Presentation of TLS | Medibuddy
29th December 2024

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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