TABLE 40-1 Laboratory Values in Tumor Lysis Syndrome | ||||||||||||||
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TABLE 40-2 Common Signs and Symptoms of Tumor Lysis Syndrome | |||||||||||||||||||||||||||||||||
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Tumor Lysis Syndrome
Tumor Lysis Syndrome
Kristen L. Ambrosio
I. Definition:
Tumor lysis syndrome (TLS) is an oncologic emergency in which metabolic imbalance occurs as a consequence of tumor cell kill, causing rapid release of normal intracellular products.
A. Death of malignant cells results in large amounts of intracellular contents such as potassium, phosphorus, and nucleic acids being released into circulation.
B. The syndrome includes hyperkalemia, hyperphosphatemia, and hyperuricemia (from the conversion of nucleic acid to uric acid).
1. This may lead to hyperuricemia-induced acute renal failure.
2. Hypocalcemia results from the binding of increased phosphorus with calcium to form calcium phosphate salts (Table 40-1).
C. Timing
1. The syndrome may occur spontaneously (autolysis) or begin 1 to 5 days after the initiation of therapy (chemotherapy, radiation therapy, or biologic therapy).
2. It ends in about 5 to 7 days, when cell lysis resolves.
D. TLS can be anticipated, treated, and even prevented before life-threatening complications develop.
II. Etiology
A. Cancers with a high growth fraction (rapidly dividing and more sensitive to antineoplastic therapy), large size (especially bulky abdominal tumors), and elevated lactate dehydrogenase (indirectly indicates tumor burden) commonly cause TLS.
1. Lymphomas (especially Burkitt’s, bulky disease, or treatment with rituximab)
2. Multiple myeloma—has been reported even with a single dose of corticosteroids and is thought to be more prevalent when concomitant renal dysfunction is also present.
3. Leukemias—patients who present with lymphoblasts (eg, acute lymphocytic leukemia) have four times more intracellular organic and inorganic phosphates, putting them at even greater risk to develop tumor lysis syndrome (Ezzone, 1999).
4. Small-cell lung cancer, due to rapid proliferation rate.
5. Other malignancies in which TLS has been a reported complication—breast cancer (particularly treated with biologic therapy), hepatocellular cancer after chemoembolization, choriocarcinoma, testicular cancer, gastric cancer, pancreatic cancer, malignant melanoma
B. Volume depletion enhances electrolyte concentration, especially hyperkalemia and hyperphosphatemia.
C. Renal insufficiency places the patient at higher risk for tumor lysis syndrome because the kidneys are the route of elimination for potassium, uric acid, and phosphorus.
III. Patient Management
A. Assessment: Table 40-2 lists the common signs and symptoms of TLS affecting cardiovascular, renal, neuromuscular, and gastrointestinal systems. These systems are affected due to the electrolyte abnormalities, hyperuricemia, and acidosis produced when intracellular components are released into the serum.
B. Diagnostic Parameters
1. Serum tests
a. The serum chemistry panel indicates increased potassium, phosphorus, uric acid, blood urea nitrogen, and creatinine, and decreased calcium. Magnesium may also be decreased in response to elevated serum phosphorus levels. Some institutions differentiate between serum electrolyte profiles and comprehensive metabolic panels that include phosphorus and uric acid.
b. Arterial blood gas analysis may be performed to assess the severity of acidosis that has occurred due to excess uric acid or renal insufficiency.
2. Other tests: Electrocardiogram (ECG) is performed routinely to assess the severity of ECG waveform changes that have occurred due to hyperkalemia or hypocalcemia (Figs. 40-1 and 40-2).
C. Treatment (Table 40-3)
1. TLS may be prevented in high-risk people with aggressive hydration and conservative diuresis. Dilution of electrolytes reduces the severity of imbalance and, in normally functioning kidneys, enhances excretion. Diuretics must be administered cautiously to avoid volume depletion and dangerously low calcium and magnesium levels.
2. Medications are administered to prevent or reduce the severity of specific metabolic defects (eg, phosphate-binding antacids to reduce phosphorus, allopurinol to decrease uric acid levels).
3. Hydration with a balanced intravenous (IV) fluid such as dextrose 5% and 0.9% normal saline at a rate of 250 to 500 mL/h is recommended once TLS has been confirmed. The solution may be changed to dextrose with bicarbonate in the presence of severe acidosis.
4. Renal replacement therapy (dialysis therapies) may be indicated for electrolyte abnormalities despite preventive therapies, or when renal failure is induced.
