Paediatrics: Acute care: biochemistry

Acute care: biochemistry

Tumour lysis syndrome

This involves lysis of malignant cells on starting chemotherapy, releasing intracellular contents, exceeding renal excretory capacity and physiologi-cal buffering mechanisms. Abnormalities include:

·  Hyperuricaemia.

·  Hyperkalaemia.

·  Hyperphosphataemia and reciprocal hypocalcaemia.

·  Dehydration, leading to risk of acute renal failure.

Mainly seen in ALL, NHL (especially B cell), occasionally AML, rarely solid tumours (e.g. germ cell, neuroblastoma). May occur spontaneously or be precipitated by single dose of steroids or chemotherapy. Risk is increased with high white count, bulky disease, pre-existing renal impairment or infiltration.

Management

Key is prevention and monitoring.

·  Hyperhydration: e.g. 2.5% or 5% dextrose in 0.45% saline at 3.0L/m²/ day 24h before starting treatment, and continued for least 48hr after treatment started. Avoid added potassium.

·  Ensure good renal output, with diuretic (furosemide) if necessary.

·  Allopurinol reduces urate precipitation, use urate oxidase in high risk cases.

·  Hyperkalaemia: may need treatment with salbutamol, calcium resonium, dextrose/insulin, haemofiltration.

·  Hyperphosphataemia/hypocalcaemia: increase fluids; haemofiltration in extreme cases; avoid calcium unless symptomatic (tetany, seizures).

Other biochemical disturbances

Hypercalcaemia

Rarely complicates malignancy (usually disseminated), e.g. rhabdomyosar-coma. Manage with hyperhydration (normal saline) and frusemide; bispho-sphonates more effective than steroids or calcitonin.

Renal toxicity

Due to chemotherapy or antibiotics.

·  Cisplatin (glomerular function, Mg²⁺ loss), ifosfamide (tubular losses of Mg²⁺, PO₄²⁺, bicarbonate), high dose methotrexate.

·  Amphotericin B (glomerular toxicity and heavy potassium loss), aminoglycosides, vancomycin.

Particular care needed when any of these drugs used in combination.