- Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, often accompanied by azotemia and oliguric acute renal failure.
- Caused by the rapid release of the intracellular contents of tumor cells into the systemic circulation.
- Most commonly seen following treatment of hematologic malignancies of high cellular burden and chemosensitivity, such as lymphomas and leukemias.
First described in 1929, tumor lysis syndrome (TLS) defines a well-established constellation of potentially fatal metabolic derangements that can occur most commonly following chemotherapy for certain hematologic malignancies such as acute lymphoblastic leukemia or high-grade non-Hodgkin's lymphoma (NHL) (Table 13–1). Less commonly, TLS complicates the treatment of other hematologic malignancies such as chronic lymphocytic leukemia, acute myeloid leukemia, plasma cell disorders including multiple myeloma or isolated plasmacytomas, Hodgkin's lymphoma, and low- or intermediate-grade NHL. Finally, TLS has been reported anecdotally in the setting of solid tumors such as testicular cancer, breast cancer, and lung cancer. Although usually seen after the administration of cytoreductive chemotherapy, TLS can occur spontaneously prior to initiation of any treatment and also may be seen following other therapies such as radiation, corticosteroids, interferon-α, rituximab, and tamoxifen.
Table 13–1. Characteristic Laboratory Abnormalities Encountered in Tumor Lysis Syndrome and Their Clinical Consequences. |Favorite Table|Download (.pdf)
Table 13–1. Characteristic Laboratory Abnormalities Encountered in Tumor Lysis Syndrome and Their Clinical Consequences.
Rapid expulsion of intracellular potassium into the circulation due to cell lysis
Adverse muscle (skeletal and cardiac) and neurologic manifestations: Muscle cramps/weakness, paresthesias, ventricular arrhythmia
Calcium gluconate, insulin/glucose, sodium bicarbonate, inhaled β-agonist, potassium-binding resins, dialysis
Release of intracellular phosphate with cell lysis (compounded by reduced renal phosphorus clearance) leads to a rapid rise in phosphorus and drop in calcium due to the precipitation of calcium–phosphorus complexes
Muscle cramps, tetany, arrhythmias, seizures; exacerbation of acute renal failure through calcium–phosphorus complex deposition in renal interstitium and tubules (ie, acute nephrocalcinosis)
Phosphate binders, dialysis
Calcium gluconate (only in symptomatic patients exhibiting neuromuscular irritability)
Uric acid ↑
Cell lysis leads to increased levels of purine nucleotides into the circulation that are metabolized to uric acid
Renal failure (uric acid nephropathy)
Hydration, alkalization of urine, xanthine oxidase inhibitors, urate oxidase, dialysis
Decreased GFR from urate crystal tubular obstruction, acute nephrocalcinosis, ± concomitant ATN or volume depletion
Oligoanuria, uric acid crystalluria, urine uric acid/creatinine ratio >1, radiographic hydronephrosis (rare)
Force diuresis with intravenous fluids and/or diuretics, increased uric acid solubility, decreased uric acid production, dialysis
This oncologic emergency is characterized by the acute onset of hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, often associated with acute renal failure (ARF). TLS results from the rapid release of the intracellular contents of tumor cells (ie, uric acid, phosphate, potassium) into the systemic circulation that overwhelms physiologic metabolic pathways that maintain homeostasis. Not all patients with cancer develop TLS, and the incidence varies depending on the patient ...