Tumour Lysis Syndrome

Tumour lysis syndrome (TLS) occurs when malignant cells are destroyed so rapidly that the circulation and kidneys cannot safely process their intracellular contents. It most often follows effective cytotoxic therapy, but the risk is determined by the biology and burden of the malignancy as much as by the drug being given. Nucleic acids released from lysed cells are metabolised through hypoxanthine and xanthine to uric acid. Potassium and phosphate enter the bloodstream directly. Phosphate binds circulating calcium, producing secondary hypocalcaemia and calcium-phosphate precipitation. Uric acid and calcium-phosphate deposits can impair tubular function and renal perfusion, while the electrolyte changes disrupt excitable tissues. The clinical consequences follow that chemistry. Hyperkalaemia can produce conduction abnormalities and sudden death. Hypocalcaemia can cause muscle cramps, tetany, seizures, and arrhythmia. Hyperphosphataemia and urate accumulation worsen acute kidney injury (AKI), which then reduces clearance of potassium, phosphate, and uric acid even further. TLS is therefore a self-amplifying metabolic emergency, not simply an elevated uric acid level. A patient may initially look well while the process is developing. A rising potassium or falling urine output may be...