Pathophysiology and clinical features

Rapid lysis of large numbers of tumour cells releases intracellular ions and metabolites into the circulation causing numerous metabolic abnormalities to develop rapidly:

• Hyperuricaemia due to metabolism of nucleic acid purines; (solubility decreased by high acidity); may cause arthralgia and renal colic.

• Hyperkalemia due to rapid cell lysis; often earliest sign of TLS; aggravated by renal failure; may cause paraesthesiae, muscle weakness and arrhythmias.

• Hyperphosphataemia due to rapid cell lysis,; precipitates calcium phosphate in tissues (insolubility exacerbated by overzealous alkalinisation),

• Hypocalcaemia secondary to hyperphosphataemia; may cause paraesthesiae, tetany, carpo-pedal spasm, altered mental state, seizures and arrhythmias.

• Acute renal failure predisposed by volume depletion and pre-existing dysfunction; due to uric acid nephropathy, acute nephrocalcinosis and precipitation of xanthine; oliguria leads to volume overload and pulmonary oedema; uraemia causes malaise, lethargy, nausea, anorexia, pruritus and pericarditis; may require dialysis; usually reversible with prompt therapy.

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