Tumor lysis syndrome overview

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Natural History, Complications and Prognosis
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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.