Synopsis
Estimate lysis risk before anticancer treatment, prevent avoidable metabolic injury and reverse hyperkalaemia, phosphate accumulation, urate burden and renal failure before arrhythmia, seizure or death.
- TLS is rapid release of tumour-cell potassium, phosphate and nucleic acid; phosphate lowers calcium and purines become urate, threatening heart, brain and kidney.
- Risk is determined before treatment from cancer type and sensitivity, burden, LDH, tumour count, baseline urate, renal function, hydration, obstruction and planned therapy.
- First-line baseline and serial tests are potassium, phosphate, calcium, urate, creatinine, bicarbonate and LDH with ECG and strict fluid balance when risk is important.
- Low-risk patients usually need surveillance and hydration; intermediate risk commonly adds allopurinol; high risk needs monitored hydration, rasburicase and frequent blood tests under the current BSH pathway.
- Allopurinol prevents formation of further urate but does not remove existing uric acid; rasburicase rapidly converts existing urate and is preferred for high-risk prophylaxis or established TLS.
- Rasburicase is contraindicated in G6PD deficiency because haemolysis and methaemoglobinaemia can occur; post-dose urate samples need pre-chilled tubes and transport on ice.
- Do not alkalinise urine routinely, add potassium or phosphate to maintenance fluid, or give calcium merely to normalise an asymptomatic low result while phosphate is high.
- Treat severe hyperkalaemia immediately and involve renal medicine early for oliguria, overload, recurrent potassium, severe phosphate or persistent metabolic rebound.
Key red flags
ECG change, muscle weakness, bradycardia or ventricular arrhythmia with rising potassium requires immediate hyperkalaemia treatment before formal TLS criteria are completed.
Tetany, laryngospasm, seizure or QT prolongation with low calcium needs monitored calcium, while asymptomatic hypocalcaemia during high phosphate is usually not corrected.
Falling urine output, rapidly increasing creatinine, pulmonary oedema or biochemical rebound despite urate treatment requires urgent renal replacement discussion.
Bulky, rapidly proliferating and highly treatment-responsive cancer with high LDH or renal impairment needs prophylaxis before steroids, antibodies, targeted therapy or chemotherapy.
TLS can occur spontaneously before treatment or after a first small treatment exposure, so timing alone cannot rule it out.
Weakness, paraesthesia, bradycardia, broad QRS, absent P waves or ventricular arrhythmia is an immediate resuscitation problem.
Perioral tingling, spasm, tetany, seizure, laryngospasm or QT prolongation indicates clinically important calcium reduction.
Oliguria, rising creatinine, hypertension, pulmonary oedema, nausea or encephalopathy signals accumulating solute and fluid burden.
Investigation priorities
Identify the biochemical syndrome and immediately dangerous electrical effect.
Management branches
A responsive malignancy is about to receive systemic therapy, corticosteroid prephase, radiotherapy or another rapid tumour-reducing intervention.
- Classify tumour and patient risk from diagnosis, burden, LDH, tumour count, renal reserve, urate, hydration, obstruction and planned treatment.
- Correct volume depletion, stop avoidable nephrotoxins and potassium or phosphate supplements and choose ambulatory, ward or higher-acuity monitoring appropriate to risk.
- Use surveillance and hydration for selected low risk, add renal-adjusted allopurinol for intermediate risk and use rasburicase with close monitoring for high risk under the BSH pathway.