Tumor lysis syndrome (TLS), an oncologic emergency, occurs when cancer treatment successfully kills cancer cells, resulting in the release of intracellular components (eg, potassium, phosphate, nucleic acids). Clients with TLS develop significant imbalances of serum electrolytes and metabolites.
TLS may result in the following life-threatening conditions:
• Hyperkalemia (>5.0 mEq/L [5.0 mmol/L]) that can cause lethal dysrhythmias
• Large amounts of nucleic acids (normally converted to uric acid and excreted by the kidneys) that can overwhelm the kidneys and cause hyperuricemia and acute kidney injury (AKI) from uric acid crystal formation
• Hyperphosphatemia (>4.4 mg/dL [1.42 mmol/L]) that can cause AKI and dysrhythmias
• Hypocalcemia (<8.6 mg/dL [2.15 mmol/L]) that can cause tetany and cardiac dysrhythmias Potassium-sparing medications (eg, spironolactone) can worsen hyperkalemia (Option 4). Loop or osmotic diuretics may be prescribed to increase urine output and lower serum potassium. Sodium polystyrene sulfonate (Kayexalate) also helps to reduce potassium.
(Options 1 and 2) Hypouricemic agents (eg, allopurinol) prevent the formation of uric acid, and aggressive fluid hydration (eg, IV normal saline) flushes out the kidneys to avoid the accumulation of toxins. Hydration therapy also dilutes serum potassium, lowering the risk for lethal dysrhythmias.
(Option 3) Health care providers often prescribe mealtime phosphate binders (eg, sevelamer, lanthanum carbonate, calcium acetate) to prevent absorption of additional nutritional phosphorus.
Tumor lysis syndrome (TLS), an oncologic emergency, occurs when cancer treatment successfully kills cancer cells, resulting in the release of intracellular components (eg, potassium, phosphate, nucleic acids). Clients with TLS develop significant imbalances of serum electrolytes and metabolites.
TLS may result in the following life-threatening conditions:
• Hyperkalemia (>5.0 mEq/L [5.0 mmol/L]) that can cause lethal dysrhythmias
• Large amounts of nucleic acids (normally converted to uric acid and excreted by the kidneys) that can overwhelm the kidneys and cause hyperuricemia and acute kidney injury (AKI) from uric acid crystal formation
• Hyperphosphatemia (>4.4 mg/dL [1.42 mmol/L]) that can cause AKI and dysrhythmias
• Hypocalcemia (<8.6 mg/dL [2.15 mmol/L]) that can cause tetany and cardiac dysrhythmias Potassium-sparing medications (eg, spironolactone) can worsen hyperkalemia (Option 4). Loop or osmotic diuretics may be prescribed to increase urine output and lower serum potassium. Sodium polystyrene sulfonate (Kayexalate) also helps to reduce potassium.
(Options 1 and 2) Hypouricemic agents (eg, allopurinol) prevent the formation of uric acid, and aggressive fluid hydration (eg, IV normal saline) flushes out the kidneys to avoid the accumulation of toxins. Hydration therapy also dilutes serum potassium, lowering the risk for lethal dysrhythmias.
(Option 3) Health care providers often prescribe mealtime phosphate binders (eg, sevelamer, lanthanum carbonate, calcium acetate) to prevent absorption of additional nutritional phosphorus.