Tumour Lysis Syndrome

On this page
  1. Direct answer
  2. What you must remember
  3. A lymphoma patient, step by step
  4. Where the exam tries to catch you
  5. Frequently asked questions
  6. Related topics

Direct answer

Tumour lysis syndrome is a metabolic emergency caused by the rapid release of intracellular contents when tumour cells die, most often after chemotherapy for leukaemia or lymphoma. It produces hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia, which can cause acute kidney injury and arrhythmias. Risk depends on tumour type, bulk and renal function, and management is early hydration, allopurinol or rasburicase, and close electrolyte monitoring.

What you must remember

  • Mechanism: lysis of tumour cells releases potassium, phosphate, uric acid and lactate dehydrogenase into the circulation.
  • High-risk tumours: Burkitt lymphoma, lymphoblastic leukaemia or lymphoma with a high white count, and bulky disease.
  • Laboratory criteria: two or more abnormal values within days either side of therapy, including uric acid about 8 mg/dL, potassium 6 mmol/L or more, or calcium about 7 mg/dL or less.
  • Prophylaxis: generous intravenous hydration and allopurinol, which blocks uric acid formation but does not clear uric acid already present.
  • Rasburicase: recombinant urate oxidase that converts uric acid to allantoin rapidly, reserved for high-risk or established hyperuricaemia.
  • G6PD testing: check before rasburicase, because deficiency causes haemolysis and methaemoglobinaemia.
  • Phosphate trap: do not give calcium for asymptomatic hypocalcaemia when phosphate is high, since calcium phosphate precipitation can injure the kidney.

A lymphoma patient, step by step

A 41-year-old man with high-grade B-cell lymphoma has a bulky abdomen, an LDH four times normal and a uric acid of 9 mg/dL before chemotherapy.

  1. Start prophylaxis early: Hydration starts 24 to 48 hours before treatment, allopurinol is given, and rasburicase is chosen because uric acid is already high.
  2. Check G6PD and handle the sample: G6PD is normal. Blood for uric acid must be drawn into chilled tubes and the laboratory told, because rasburicase degrades uric acid in the sample.
  3. Recognise clinical tumour lysis syndrome: After the first cycle he has potassium of 6.4 mmol/L, phosphate of 2.9 mmol/L, calcium of 1.6 mmol/L and a creatinine that has climbed from 1.0 to 2.2 mg/dL. These values make clinical tumour lysis syndrome.
  4. Protect the heart: An electrocardiogram is done, intravenous calcium gluconate protects the myocardium, and insulin with dextrose and salbutamol shift potassium into cells.
  5. Restore volume first: Fluids continue, and a loop diuretic is used only after volume is restored.
  6. Leave asymptomatic calcium alone: Asymptomatic hypocalcaemia is not replaced.
  7. Reserve dialysis: Dialysis is reserved for refractory hyperkalaemia, volume overload or oliguria.

Where the exam tries to catch you

Examiners separate prevention from clearance, and the traps usually sit in the drug choice or the calcium.

  • Trap: using allopurinol for an established high uric acid level. Correct: allopurinol prevents new uric acid formation, whereas rasburicase clears uric acid that already exists.
  • Trap: replacing calcium for hypocalcaemia that coexists with hyperphosphataemia. Correct: routine calcium replacement worsens phosphate precipitation, so calcium is reserved for symptoms, arrhythmia or hyperkalaemia treatment.
  • Trap: alkalinising the urine to protect the kidney. Correct: urinary alkalinisation has fallen out of routine use because it promotes calcium phosphate deposition and does not reliably help.
  • Trap: giving rasburicase without checking G6PD. Correct: G6PD deficiency is the classic contraindication, and it is often tested for in patients from populations where it is common.

Frequently asked questions

Which malignancies carry the highest risk of tumour lysis syndrome?

Burkitt lymphoma, acute lymphoblastic leukaemia and other high-grade lymphomas carry the highest risk of tumour lysis syndrome, especially with high tumour burden or a raised LDH. Risk is greater when renal function is already impaired. Stratifying risk before chemotherapy guides the choice of prophylaxis.

What is the role of rasburicase in tumour lysis syndrome?

Rasburicase is a recombinant urate oxidase that converts uric acid to allantoin, lowering uric acid faster than allopurinol. It is used for high-risk patients or established hyperuricaemia. Its blood samples must be handled carefully because it degrades uric acid in the tube.

Why is rasburicase contraindicated in G6PD deficiency?

Rasburicase generates hydrogen peroxide, and G6PD deficiency leaves red cells unable to cope with oxidant stress. This causes haemolysis and methaemoglobinaemia in affected patients. G6PD status must therefore be checked before rasburicase is given.

Should hypocalcaemia be corrected in tumour lysis syndrome?

Hypocalcaemia in tumour lysis syndrome is usually left untreated unless it causes symptoms, arrhythmia or seizures. Routine calcium replacement can precipitate calcium phosphate in tissues and worsen kidney injury. Calcium gluconate is used separately to stabilise the myocardium during hyperkalaemia.

How is hyperkalaemia treated in tumour lysis syndrome?

Hyperkalaemia in tumour lysis syndrome is treated with intravenous calcium to protect the myocardium, insulin with dextrose and salbutamol to shift potassium into cells, and removal of potassium by dialysis if refractory. Serial electrocardiograms guide urgency.

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