Tumor lysis syndrome history and symptoms
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
History and Symptoms
Hyperkalemia. Potassium is mainly an intracellular ion. High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 7mmol/dL) [normal 3.5-5.0 mmol/dL] and they include
- severe muscle weakness or paralysis
- cardiac conduction abnormalities (can be fatal)
Hyperphosphatemia. Like potassium, phosphates are also predominantly intracellular. Hyperphosphatemia causes acute renal failure in tumor lysis syndrome, because of deposition of calcium phosphate crystals in the renal parenchyma.
Hypocalcemia. Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to):
- tetany
- seizures
- mental retardation / dementia
- parkinsonian (extrapyramidal) movement disorders
- papilledema
- emotional instability / agitation / anxiety
- myopathy
Hyperuricemia. Uric acid is a breakdown product of DNA, converted by xanthine oxidase from xanthine and hypoxanthine, which are in turn purine breakdown products. Uric acid is more toxic to tissues than (hypo)xanthine. Uric acid nephropathy has been a dominant cause of acute renal failure but with the advent of allopurinol and uricase treatment, hyperphosphatemia has replaced this as the main cause of acute renal failure. Oddly, gout is not a feature of tumor lysis syndrome; the high uric acid levels that cause gout probably need to be present for an extended period of time before the putative crystals can develop.