Tumor lysis syndrome overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2] Nazia Fuad M.D.
Synonyms and keywords: TLS; Laboratory Tumor Lysis Syndrome; LTLS; Clinical Tumor Lysis Syndrome; CTLS
Overview
Tumor lysis syndrome (TLS) is cosidered to be an oncologic emergency that develops after chemotherapy or radiotherapy. Tumor lysis syndrome is more common in highly proliferative lymphomas and leukemias, and sometimes even without treatment. As evident by its name, tumor cells breakdown with chemotherapy releases potassium, nucleic acids, and phosphorus into the circulation, resulting in hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, and acute renal failure. The complications of tumor lysis syndrome include nausea, vomiting, diarrhea, anorexia, hematuria, tachycardia, and muscle cramps. Screening for tumor lysis syndrome is not recommended. However, patients with malignancies undergoing treatment or with acute renal failure should be considered for tumor lysis syndrome workup. The essential component in TLS treatment include aggressive hydration and diuresis, treating hyperuricaemia with allopurinol prophylaxis and rasburicase and close monitoring of electrolyte abnormalities.
Classification
Tumor lysis syndrome is classified according to the 1993 Hande-Garrow classification system into two groups i.e. laboratory tumor lysis syndrome (LTLS) and clinical tumor lysis syndrome (CTLS).
Pathophysiology
Tumor lysis syndrome (TLS) is cosidered to be an oncologic emergency that develops after chemotherapy or radiotherapy. Tumor lysis syndrome is more common in highly proliferative lymphomasand leukemias, and sometimes even without treatment. As evident by its name, tumor cells breakdown with chemotherapy releases potassium, nucleic acids, and phosphorus into the circulation, resulting in hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, and acute renal failure. Hyperuricaemia results from rapid release and catabolism of intracellular nucleic acids. Hyperphosphataemia results from the rapid release of intracellular phosphorous from malignant cells. The malignant cells contain as much as four times the amount of organic and inorganic phosphorous as compared to normal cells. Hyperkalaemia results from breakdown of tumor cells and then becomes exacerbated by the development of renal failure. Hypocalcaemia results from hyperphosphataemia and the precipitation of calcium phosphate crystals in the renal tubules. When the calcium phosphorus levels rises up there is a significant risk of calcium phosphate deposition in the kidney and other tissues. This secondarily leads to systemic hypocalcaemia.
Causes
Development of tumor lysis syndrome is the result of initiation of chemotherapy or radiotherapy in cancer patients. The most common causes of tumor lysis syndrome are Burkitt's lymphoma, acute lymphoblastic leukemia, acute myeloid leukemia and chemotherapy including methotrexate. Sometimes it can occur spontaneously without administration of treatment primarily in patients with non-Hodgkin lymphoma (NHL) or acute leukemia.
Tumor Lysis Syndrome Differential Diagnosis
Tumor lysis syndrome must be differentiated from other diseases that cause hyperuricemia, hyperkalemia, and hyperphosphatemia, such as acute kidney injury.
Epidemiology and Demographics
The exact incidence of tumor lysis syndrome has not been established. There is no racial or sex predilection for tumor lysis syndrome.
Risk Factors
The most potent risk factor in the development of tumor lysis syndrome after initiating chemotherapy is kidney disease. Other risk factors include dehydration, hematologic tumors, and solid tumors.
Screening
Screening for tumor lysis syndrome is not recommended. However, patients with malignancies or acute renal failure should be considered for tumor lysis syndrome workup.
Natural History, Complications and Prognosis
If left untreated, patients with tumor lysis syndrome may progress to develop nausea, vomiting, diarrhea, anorexia, hematuria, palpitations, and muscle cramps. Common complications of tumor lysis syndrome include hyperkalemia, hypocalcemia, and hyperphosphatemia. Prognosis is generally good, if not associated with acute renal failure.
Diagnosis
Diagnostic Criteria
The diagnosis of tumor lysis syndrome is based on the Cairo–Bishop criteria, which includes uric acid, potassium, phosphorous, and calcium.
History and Symptoms
Symptoms of tumor lysis syndrome include nausea, vomiting, diarrhea, oliguria, confusion, delirium, and seizure.
Physical Examination
Common physical examination findings of tumor lysis syndrome include edema, cardiac arrhythmia, and tetany.
Laboratory Findings
Laboratory findings consistent with the diagnosis of tumor lysis syndrome include high serum uric acid, potassium, phosphorus, and low calcium.
ECG
Electrocardiogram (ECG) may be helpful in the diagnosis of arrhythmias associated with tumor lysis syndrome.
Chest X Ray
There are no chest x-ray findings associated with tumor lysis syndrome. However, chest x-ray may be useful to detect mediastinal tumors.
Abdominal CT
There are no CT findings associated with tumor lysis syndrome. However, abdominal CT may be useful to detect abdominal tumors or renal masses.
Abdominal MRI
There are no MRI findings associated with tumor lysis syndrome. However, abdominal MRI may be useful to detect abdominal tumors or renal masses.
Abdominal Ultrasound
There are no ultrasound findings associated with tumor lysis syndrome. However, abdominal ultrasound may be useful to detect abdominal tumors or renal masses.
Other Imaging Studies
There are no other imaging studies available for the diagnosis of tumor lysis syndrome.
Other Diagnostic Studies
There are no other diagnostic studies available for the diagnosis of tumor lysis syndrome.
Treatment
Medical Therapy
Tumor lysis syndrome is a medical emergency and requires prompt treatment. Patients who develop TLS should receive intensive care with continuous cardiac monitoring and measurement of electrolytes, creatinine, and uric acid every four to six hours. Special attention should be given to correct the electrolyte abnormalities. Hyperurecemia should be treated with rasburicase at 0.2 mg/kg with repeated doses as needed, to wash out the obstructing uric acid crystals with fluids with or without a loop diuretic, and then the appropriate use of renal replacement therapy is also required
Surgery
There is no surgical intervention for the management of tumor lysis syndrome.
Primary Prevention
Effective measures for the primary prevention of tumor lysis syndrome include intravenous hydration and administration of either allopurinol or rasburicase.
Secondary Prevention
There are no secondary preventive measures available for tumor lysis syndrome.
Cost-Effectiveness of Therapy
The cost-effectiveness of administration of a singe low dose (3 mg) of rasburicase for tumor lysis syndrome prevention in cancer patients may be superior to the daily intravenous allopurinol.