complications

Last reviewed 01/2018

The tumour lysis syndrome consists of one or more of the following conditions:

• acute renal failure
  • multifactorial pathophysiology in tumor lysis syndrome
  • two major synergistic mechanisms are volume depletion and uric acid nephropathy
• hyperuricaemia
  • develops from 48 to 72 hours following initiation of treatment
  • tumor cell lysis releases purine nucleic acids, which are subsequently metabolized into uric acid
  • malignant tumour cells carry a large burden of nucleic acid products (as a consequence of their high cellular activity and turnover)
• hyperkalaemia
  • may appear from 6 to 72 hours after the initiation of chemotherapy
  • cell lysis leads to the liberation of large amounts of intracellular potassium into extracellular fluid and consequent hyperkalaemia
  • concurrent chronic kidney disease, acute renal failure, or acidosis may exacerbate hyperkalemia - in these situations the excretory capacity of the kidney may be overwhelmed by transcellular shifts due to potassium release from lysing cells as well as acidosis
• hypocalcaemia and hyperphosphatemia
  • hyperphosphatemia may develop from 24 to 48 hours following initiation of chemotherapy. The release of intracellular phosphate following chemotherapy can exceed the renal threshold for phosphate excretion and result in hyperphosphatemia
  • note that malignant hematologic cells may contain up to four times more intracellular phosphate compared with normal mature lymphoid cells. Also acute destruction of tumor cells during chemotherapy prevents the rapid reuse of phosphate for newly synthesized tumor cells
  • when the solubility of calcium and phosphate is exceeded then precipitation of calcium phosphate occurs, possibly resulting in hypocalcemia

Reference:

1. Davidson MB et al. Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome. Am J Med. 2004 ;116(8):546-54.