Tumour Lysis Syndrome
An oncological emergency requiring rapid recognition, risk stratification, and aggressive management
Tumour lysis syndrome (TLS) is a potentially life-threatening complication of cancer treatment, occurring when the rapid destruction of malignant cells releases large amounts of intracellular contents into the bloodstream. It is most commonly seen in haematological malignancies such as Burkitt lymphoma and acute leukaemia, particularly following initiation of cytotoxic therapy.
What is Tumour Lysis Syndrome?
TLS occurs when malignant cells are rapidly destroyed — typically by chemotherapy, radiotherapy, or corticosteroids — releasing potassium, phosphate, and nucleic acids into the circulation. The resulting metabolic disturbances (hyperkalaemia, hyperphosphataemia, hyperuricaemia, and secondary hypocalcaemia) can cause acute kidney injury, cardiac arrhythmias, seizures, and death. Prevention through risk stratification and prophylaxis is far preferable to treating established TLS.
Who is at Risk?
High-risk patients include those with bulky haematological malignancies such as Burkitt lymphoma, ALL, and AML with high white cell count, particularly when combined with pre-existing renal impairment or dehydration. LDH greater than twice the upper limit of normal is an additional risk marker. Solid tumours are generally lower risk, though exceptions occur with particularly chemo-sensitive tumours. All patients receiving cytotoxic therapy should be assessed for TLS risk before treatment begins.
Recognition and Diagnosis
The Cairo-Bishop criteria define TLS by the presence of two or more electrolyte abnormalities within three days before or seven days after cytotoxic therapy: uric acid above 476 micromol/L, potassium above 6.0 mmol/L, phosphate above 1.45 mmol/L, or calcium below 1.75 mmol/L (each defined as an absolute value or a 25% change from baseline). Clinical TLS requires additionally a rise in creatinine of 1.5 times the upper limit of normal, a cardiac arrhythmia, or a seizure. Monitoring electrolytes every 4-6 hours during high-risk treatment periods allows early detection before clinical deterioration occurs. Prompt evaluation of trends in electrolyte results — particularly rising potassium or uric acid — is essential.
Prevention and Management Principles
Aggressive IV hydration to maintain urine output above 100 mL per hour is the cornerstone of both prophylaxis and treatment. Allopurinol, started 24-48 hours before chemotherapy, reduces uric acid production and is used for intermediate-risk patients. Rasburicase rapidly breaks down uric acid and is preferred for high-risk TLS; it must not be used in patients with G6PD deficiency. Electrolyte disturbances are managed according to standard protocols: symptomatic hypocalcaemia is treated with IV calcium gluconate, though asymptomatic hypocalcaemia should not be treated in the presence of hyperphosphataemia. Refractory cases may require dialysis.
