Tumor lysis syndrome
From WikiLectures
Tumor lysis syndrome occurs after the lysis of a large number of circulating tumor cells, typically leukemic blasts. It belongs to oncological emergent conditions. This massive breakdown is most often caused by malignancy therapy with cytostatics or antibodies. Cell cytoplasm is washed out into the circulation. These are mostly leukocytes that release biologically active substances - interleukins, which cause metabolic disruption. To remove these metabolites, the filtering capacity of the kidneys is exceeded, creatinine and urea rise. Potassium is released from the cells and hyperkalemia occurs.
Ethiology[edit | edit source]
- often begins after starting cytotoxic treatment in patients with hemato-oncological diseases (ALL, AML or NHL)
Diagnosis[edit | edit source]
- LAB: ↑kreatinin (AKI), ↑K+, ↓Ca2+
- KO: ↑LEU (50-100x10^9/l), they could be ↓Hb a ↓Tro
- Urine: urate crystals
- EKG: arrhythmia
- Markers of cell lysis: ↑LDH, ↑uric acid, ↑PO43-
Clinical picture[edit | edit source]
- renal failure - AKI: edema, oliguria, lethargy
- hypercalemia: cardiac arrhythmia, nausea, diarrhea
- hypocalcemia: spasms
Therapy[edit | edit source]
- fluid management
- Low risk: p.o. / i.v. hydratation, fluid balance monitoring
- High risk: agressive IV therapy, hyperhydratation F1/1,
- monitor urine output → peculiarly start forced diuresis (furosemide);
- prevention and treatment of urate nephropathy
- Alopurinol/Milurit, Rasburicasa
- correction of electrolyte balance
- hypercalemia: ECG motoring, glucose with insuline
- hyperphosphatemia: Sevelamer (phosphate binders)
- hypocalcemia: 10% Calcium gluconicum
Links[edit | edit source]
Related articles[edit | edit source]
Bibliography[edit | edit source]
- KLENER, Pavel. Vnitřní lékařství. 3. edition. Galén, 2006. ISBN 80-7262-430-X.
