Presentation of TLS
| Hyperuricaemia | Nucleic acids within rapidly dividing cancer cells are metabolised to insoluble uric acid | Deposition within renal tubules results in uric acid nephropathy (oliguric AKI) |
| Hyperphosphataemia | Cancer cells have higher PO4 levels than normal tissues. Intracellular phosphate is released into bloodstream. Can precipitate with calcium and deposit as calcium phosphate in tissues | Deposits in renal tubules cause AKI
Deposits in skin can cause gangrene Deposits in the heart can cause arrhythmias |
| Hyperkalaemia | Intracellular potassium is released by cell breakdown, and worsened in concurrent TLS-driven AKI | Most dangerous electrolyte abnormality; can cause cardiac arrhythmias and sudden cardiac death |
| Hypocalcaemia (and hypomagnesaemia) | Calcium precipitates with phosphate as calcium phosphate and is depleted | Neuromuscular irritability; paraesthesias, muscle twitching, tetany, Trousseau’s sign, Chvostek’s sign, laryngospasm, bronchospasm
Hypotension Cardiac failure |
| AKI/renal failure | May be due to precipitation of uric acid crystals or calcium phosphate within renal tubules | Creatinine rise, oliguria, symptoms of uraemia (itch, nausea, vomiting, confusion, coma) |
| Metabolic acidosis | Related to declining renal function; acidosis then promotes uric acid crystallisation and can, in turn, worsen AKI | Nausea, vomiting, fatigue
Raised respiratory rate |
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