Tumour lysis syndrome

The tumour breakdown syndrome occurs after lysis of large numbers of circulating tumour cells, typically leukaemic blasts. It is one of the oncological emergent conditions. This massive breakdown is most often caused by cytostatics or antibodys therapy of the malignancy. The cytoplasm of the cells leaches into the circulation. Most of the time, it is leukocytes that release biologically active substances - interleukins, which cause metabolic disruption. To remove these metabolites, the filtration capacity of the kidney is exceeded, creatinine and urea rise. The cells release potassium and hyperkalemia develops.

Ethiology

 * often begins after the initiation of cytotoxic therapy in patients with haemato-oncological disease (ALL, AML or NHL)

Diagnosis

 * LAB: ↑kreatinin (AKI), ↑K+, ↓Ca2+


 * BC: ↑LEU (50-100x10^9/l), can be ↓Hb a ↓Tro
 * Urine: urate crystals
 * ECG: arrhytmia
 * Markers of cell lysis: ↑LDH, ↑urine acid, ↑PO43-

Clinical picture

 * renal failure - AKI: oedema, oliguria, lethargy
 * hyperkalemia: cardiac arrhythmias, nausea, diarrhea
 * hypocalcemia: spasms

Therapy

 * fluid management
 * Low risk: p.o. / i.v. hydration, fluid balance monitoring
 * High risk: aggressive IV therapy, hyperhydration F1/1,
 * monitor urine output → possibly initiate forced diuresis (furosemide);


 * prevention and treatment of urate nephropathy
 * Alopurinol/Milurite, Rasburicase
 * correction of electrolyte balance
 * hyperkalemia : ECG motorisation, glucose with insulin
 * hyperphosphatemia: Sevelamer (phosphate binders)
 * hypocalcemia: 10% Calcium gluconicum

Related articles

 * Basic diagnostic tests in hematooncology

Literature used



 * KLENER, Pavel. Vnitřní lékařství. 3. vydání. Praha : Galén, 2006.  ISBN 80-7262-430-X.