Tumor lysis syndrome (TLS)
Tumor lysis syndrome is a metabolic oncologic emergency in which massive tumor cell breakdown, spontaneous or chemotherapy-induced, releases potassium, phosphate, and nucleic acids into the blood, producing hyperuricemia, hyperkalemia, hyperphosphatemia, and secondary hypocalcemia that can precipitate acute kidney injury, arrhythmia, seizure, and death. Risk-stratified prophylaxis with hydration plus allopurinol or rasburicase before chemotherapy, and aggressive correction of electrolytes with renal replacement therapy when needed, are the cornerstones of management.
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What this article covers
- Overview
Tumor lysis syndrome (TLS) is a metabolic oncologic emergency caused by the release of tumor cell contents into the bloodstream, either spontaneously or as a result of treatment, producing…
- Epidemiology
Occurs most commonly in acute leukemia and high-grade non-Hodgkin lymphoma, particularly Burkitt lymphoma, where the combination of large tumor burden and exquisite chemosensitivity produces rapid, massive cell death.
- Risk factors
Large tumor burden and high proliferative rate, the dominant determinant of TLS risk, reflected in bulky disease, high white blood cell count, or elevated lactate dehydrogenase.
- Pathophysiology
Rapid lysis of malignant cells, most often triggered by cytotoxic chemotherapy, releases a large intracellular potassium and phosphate load into the bloodstream, directly raising serum potassium and phosphate.
- Clinical features
Gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia): often the earliest nonspecific symptoms, typically emerging within hours to a few days of starting chemotherapy in a high-risk patient.
- Differential diagnosis
Cytokine release syndrome (after CAR T-cell therapy or other immunotherapy): fever, hypotension, and tachycardia with a temporal relationship to cellular immunotherapy rather than cytotoxic…
- Diagnosis
TLS is confirmed by the laboratory pattern of hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia arising in a patient with a large-burden, chemosensitive tumor around the time of…
- Management
First, stratify risk and start prophylaxis before chemotherapy: intermediate-risk: IV hydration plus allopurinol 300 mg PO once daily, starting 1-2 days before chemotherapy, continued 3-7 days after or until values normalize.
- Complications
Acute kidney injury, from uric acid and calcium-phosphate crystal precipitation in the renal tubules, the most common organ complication and often the trigger for renal replacement therapy.
- Prognosis
Prompt recognition and risk-stratified prophylaxis prevent the great majority of clinically significant TLS, particularly in patients correctly identified as high risk before chemotherapy begins.
- Prevention
Risk-stratify every patient before starting chemotherapy for a bulky, chemosensitive hematologic malignancy, and start prophylaxis before, not after, the first dose.
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- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Non-Hodgkin lymphoma
Non-Hodgkin lymphoma is a heterogeneous group of B-cell (about 85%) and T-cell lymphoid malignancies that spread noncontiguously and often involve extranodal sites, ranging from indolent follicular lymphoma to aggressive diffuse large B-cell lymphoma to highly aggressive Burkitt lymphoma. Diagnosis requires excisional or core biopsy with flow cytometry and cytogenetics, Ann Arbor staging with PET-CT, and treatment is subtype-specific, from observation to R-CHOP to intensive Burkitt regimens with aggressive tumor lysis and CNS prophylaxis.