Tumor Lysis Syndrome

TLS results from spontaneous or treatment-related release of intracellular potassium, phosphate, and nucleic acids. Uric acid generation and calcium-phosphate deposition can contribute to acute kidney injury (AKI); hyperkalemia and hypocalcemia can cause arrhythmias or seizures. ScienceDirect+1ScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Risk is driven by disease burden, cellular proliferation and turnover, treatment sensitivity, and patient-specific clearance limitations. Large burden may include leukocytosis, bulky disease, organ infiltration, or markedly elevated lactate dehydrogenase; preexisting kidney dysfunction, dehydration, hyperuricemia, and nephrotoxin exposure increase the risk that laboratory lysis progresses to clinical TLS. BMJ+2BMJEarly treatment with rasburicase and risk of kidney replacement therapy and death in adults with tumour lysis syndrome: emulated target trial | The BMJScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Novel targeted, immune-based, and cellular therapies have made TLS less predictable than in the conventional cytotoxic chemotherapy era. Risk assessment should therefore be regimen-specific and repeated when disease burden or treatment intensity changes. Wolters Kluwer+1Wolters KluwerTumor Lysis Syndrome : New England Journal of MedicineScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

The Cairo-Bishop framework classifies laboratory TLS by abnormalities in uric acid, potassium, phosphate, and calcium occurring around treatment initiation; clinical TLS requires laboratory TLS plus a clinically important complication such as AKI, arrhythmia, seizure, or sudden death. Adult absolute laboratory thresholds cited in contemporary reviews include uric acid at least 8 mg/dL, potassium at least 6 mEq/L, and phosphate at least 4.5 mg/dL; calcium decline is a supporting abnormality. ScienceDirect+1ScienceDirectTumor Lysis SyndromeScienceDirectReview article Tumor lysis syndrome in gynecologic cancers

Interpret criteria in context. Baseline chronic kidney disease, pseudohyperkalemia, phosphate administration, hypocalcemia from other causes, sepsis-associated AKI, and obstructive uropathy can mimic or compound TLS. The central clinical question is whether rapid tumor-cell breakdown is producing a worsening metabolic pattern that exceeds renal clearance. ScienceDirect+1ScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Spontaneous TLS occurs, particularly with high tumor burden, and should be considered before therapy when hyperuricemia accompanies hyperkalemia, hyperphosphatemia, AKI, oliguria, or rapidly rising lactate dehydrogenase. BMJ+2BMJEarly treatment with rasburicase and risk of kidney replacement therapy and death in adults with tumour lysis syndrome: emulated target trial | The BMJScienceDirectTumor Lysis Syndrome - an overviewScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Allopurinol and febuxostat reduce uric acid production by inhibiting xanthine oxidase but do not remove preformed uric acid. Their greatest role is prophylaxis in patients who can start therapy before substantial hyperuricemia develops. Rasburicase enzymatically converts uric acid to allantoin and can rapidly lower existing uric acid; it is preferred for high-risk patients or established TLS with hyperuricemia when no contraindication exists. ScienceDirect+1ScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

The supplied sources describe traditional rasburicase dosing of 0.15 to 0.20 mg/kg IV daily for up to 7 days, but they also note contemporary practice variation, including reduced-dose strategies that have not been uniformly tested in randomized trials. Follow current institutional protocol and product labeling for dosing, repeat dosing, and laboratory specimen handling. ScienceDirect+1ScienceDirectTumor Lysis Syndrome - an overviewScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Do not administer rasburicase to patients with known G6PD deficiency. Hemolytic anemia and methemoglobinemia are rare but serious adverse events related to oxidative stress from hydrogen peroxide generation. When feasible, screen patients at increased likelihood of G6PD deficiency before treatment; in life-threatening TLS, the urgency of treatment requires individualized risk-benefit assessment. ScienceDirect+1ScienceDirectTumor Lysis Syndrome - an overviewScienceDirectTumor Lysis Syndrome

Admit patients with established or evolving clinical TLS for close monitoring. Treat hyperkalemia according to severity and ECG findings, restrict exogenous potassium and phosphate, manage volume carefully, and use urate-lowering therapy appropriate to urate burden and contraindications. ScienceDirect+1ScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

Treat symptomatic hypocalcemia, such as tetany, seizure, or arrhythmia, but avoid routine calcium replacement for asymptomatic biochemical hypocalcemia because added calcium can increase calcium-phosphate precipitation. The primary strategy is control of phosphate burden and restoration of renal clearance. ScienceDirect+1ScienceDirectTumor Lysis Syndrome - an overviewScienceDirectTumor Lysis Syndrome

Renal replacement therapy indications are broadly similar to other causes of AKI but the threshold is lower in TLS because solute release can be rapid and persistent. Refractory hyperkalemia, persistent severe hyperphosphatemia, symptomatic hypocalcemia attributable to phosphate excess, oliguria or anuria, uncontrolled volume overload, severe acidosis, and uremic complications should prompt urgent nephrology-directed dialysis. ScienceDirect+2ScienceDirectTumor Lysis Syndrome - an overviewScienceDirectTumor Lysis SyndromeScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel

TLS is most common in rapidly proliferating hematologic malignancies with high tumor burden, but it also occurs in solid tumors and after targeted therapy. A reported case of lenvatinib-associated TLS in hepatocellular carcinoma illustrates that clinically important TLS can occur after noncytotoxic targeted therapy; case reports establish signal recognition, not incidence or routine prophylaxis requirements. Wolters Kluwer+1Wolters KluwerLenvatinib-Induced Tumor Lysis Syndrome in... : ACG Case Reports JournalWolters KluwerTumor Lysis Syndrome : Critical Care Nurse

For patients receiving new therapies, determine whether the regimen label, disease-specific guideline, or institutional pathway has a mandated step-up schedule, hydration plan, laboratory schedule, or inpatient observation requirement. General TLS principles remain applicable, but the risk window and pace of lysis may differ by agent. Wolters Kluwer+1Wolters KluwerTumor Lysis Syndrome : New England Journal of MedicineScienceDirectExpert consensus guidelines for the prophylaxis and management of tumor lysis syndrome in the United States: Results of a modified Delphi panel