Synopsis
Predict tumour lysis before anticancer therapy, recognise its biochemical pattern and clinical consequences, sequence hydration, urate-lowering therapy, electrolyte treatment and renal support safely, and monitor high-risk children closely enough to prevent irreversible organ injury.
- The classic laboratory pattern is hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia with rising urea and creatinine after or even before therapy.
- Risk-assess every new high-grade haematological malignancy before corticosteroid, chemotherapy or radiotherapy; prevention is safer than treating established lysis.
- First-line tests are potassium, phosphate, corrected and ionised calcium, urate, urea, creatinine, LDH, bicarbonate, glucose and FBC, with ECG and continuous monitoring when abnormalities or symptoms are present.
- First-line prevention for high or very high risk is specialist-controlled IV hydration without added potassium or phosphate, strict input and output, frequent weights and protocol-selected urate-lowering therapy.
- Rasburicase is the treatment of choice for established TLS and very high urate risk because it degrades existing uric acid rapidly; it should be available within 1 hour of prescription.
- A paediatric treatment regimen is rasburicase 0.2 mg/kg IV over 30 minutes once daily, with duration set by biochemical response and the oncology protocol.
- Rasburicase is contraindicated in G6PD deficiency because of haemolysis and methaemoglobinaemia risk; assess ancestry and prior results during risk planning and use the specialist alternative when deficient.
- Allopurinol prevents new uric acid formation but does not remove existing urate; it suits selected lower-risk prophylaxis and requires renal and mercaptopurine interaction review.
- Do not routinely combine allopurinol with rasburicase or alkalinise urine; alkalinisation promotes calcium-phosphate and xanthine precipitation.
- After rasburicase, collect urate into the specified tube, place it on ice immediately and transport rapidly, because ongoing ex-vivo urate breakdown gives a falsely low result.
- Treat symptomatic, not asymptomatic, hypocalcaemia unless a specialist protocol directs otherwise; calcium can worsen calcium-phosphate deposition.
- Escalate early for dialysis when hyperkalaemia, phosphate rise, symptomatic hypocalcaemia, oliguria, uraemia or fluid overload is refractory.
Key red flags
Potassium rise or ECG change demands immediate hyperkalaemia treatment; the absence of ECG change does not make important hyperkalaemia safe.
Oliguria despite adequate perfusion, rising creatinine, fluid overload or severe hypertension requires urgent nephrology and critical-care involvement.
Paraesthesia, cramps, carpopedal spasm, tetany, seizure or prolonged QT indicates symptomatic hypocalcaemia and requires carefully monitored calcium treatment.
Rapidly rising phosphate, calcium–phosphate burden or persistent hypocalcaemia can cause nephrocalcinosis and dialysis-requiring renal failure.
High-burden leukaemia or lymphoma, renal infiltration, pre-existing kidney injury, dehydration, high LDH or marked leucocytosis predicts lysis before treatment begins.
Unexpectedly low urate after rasburicase may be a sample-handling artefact unless blood was chilled immediately and analysed rapidly.
Investigation priorities
Detect potassium, phosphate, calcium, urate and renal changes before and during cytoreductive therapy.
Management branches
A new malignancy or cytoreductive treatment has potential for rapid cell lysis.
- Classify tumour burden, proliferation, sensitivity, LDH, white count, renal function and hydration risk.
- Start protocolised potassium- and phosphate-free hydration with strict balance and weight monitoring when indicated.
- Use allopurinol for selected lower-risk prophylaxis or rasburicase for the highest-risk plan after G6PD assessment.
- Locate the child where frequent laboratory testing, intensive care and dialysis are accessible.