How are electrolyte imbalances managed in tumor lysis syndrome (TLS)?

Management of Electrolyte Imbalances in Tumor Lysis Syndrome

Electrolyte abnormalities in TLS should be managed aggressively with a tiered approach based on severity: mild asymptomatic imbalances require conservative measures (hydration, diuretics, oral binders), while severe or symptomatic cases demand immediate interventions including insulin-glucose therapy for hyperkalemia, cautious calcium replacement only for symptomatic hypocalcemia, and early dialysis for refractory cases. 1

Hyperkalemia Management

Mild Hyperkalemia (<6 mmol/L, Asymptomatic)

• Correct with aggressive hydration, loop diuretics, and sodium polystyrene 1 g/kg either orally or by enema 1
• Maintain urine output at least 100 mL/hour in adults (3 mL/kg/hour in children <10 kg) 1
• Check hemodynamic status and hydration level before administering loop diuretics 1

Severe Hyperkalemia (≥6 mmol/L or Symptomatic)

• Administer rapid insulin 0.1 units/kg plus glucose (25% dextrose 2 mL/kg) 1
• Give calcium carbonate 100-200 mg/kg/dose and sodium bicarbonate to stabilize myocardial cell membrane and correct acidosis 1
• Perform continuous ECG monitoring in all hyperkalemic patients 1

Critical Pitfall: Hyperkalemia is the most hazardous acute complication that can cause sudden death from cardiac arrhythmias and requires quick, aggressive treatment 2

Hyperphosphatemia Management

Mild Hyperphosphatemia (<1.62 mmol/L or <5 mg/dL)

• Does not require treatment, or treat with aluminum hydroxide 50-100 mg/kg/day divided in 4 doses orally or by nasogastric tube 1

Severe Hyperphosphatemia (>6 mg/dL)

• Consider prophylactic dialysis before development of overt uremic symptoms 1
• High serum phosphate concentrations and calcium phosphate complexes deposited in renal interstitium exacerbate kidney damage 1

Hypocalcemia Management

Asymptomatic Hypocalcemia

• Do not treat asymptomatic hypocalcemia 1
• Calcium gluconate is not recommended for mild hypocalcemia as it leads to increased tissue and renal precipitation of calcium phosphate 1

Symptomatic Hypocalcemia (Tetany, Seizures)

• Infuse a single dose of calcium gluconate 50-100 mg/kg and cautiously repeat if necessary 1
• Calcium gluconate is potentially useful supportive therapy for hyperkalemia-induced cardiac arrhythmias 1

Critical Pitfall: Avoid routine calcium replacement in mild hypocalcemia, as this promotes calcium phosphate precipitation in kidneys and tissues, worsening renal injury 1

Monitoring Requirements

High-Risk TLS Patients (Before Development)

• Monitor LDH, uric acid, sodium, potassium, creatinine, BUN, phosphorus, and calcium every 12 hours for the first three days, then every 24 hours 1

Established TLS Patients

• Monitor vital parameters (heart rate, blood pressure, urine output, respiratory rate), serum uric acid, electrolytes (phosphate, calcium, potassium), and renal function every 6 hours for the first 24 hours, then daily 1
• Assess blood cell count, serum LDH, albumin, serum osmolality, blood gases, acid-base equilibrium, ECG, and body weight every 24 hours 1

Indications for Dialysis

Initiate renal replacement therapy for persistent hyperkalemia, severe metabolic acidosis, volume overload unresponsive to diuretic therapy, and overt uremic symptoms (pericarditis, severe encephalopathy) 1

Prophylactic Dialysis Considerations

• Consider before overt uremic symptoms develop in response to severe, progressive hyperphosphatemia (>6 mg/dL) or severe symptomatic hypocalcemia 1
• Intermittent hemodialysis effectively removes uric acid (clearance 70-100 mL/min) and phosphate, reducing plasma uric acid by approximately 50% with each 6-hour treatment 1
• Continuous renal replacement therapies (CRRT) provide better hemodynamic stability, azotemia control, and fluid management compared to intermittent hemodialysis, though no comparative outcome studies exist 1

Critical Pitfall: Peritoneal dialysis is seldom used due to lower efficiency in removing solutes (uric acid, urea) and electrolytes (potassium, phosphate) compared to hemodialysis and CRRT 1

Urine Alkalinization Controversy

• Urine alkalinization has been progressively abandoned, particularly since rasburicase availability 1
• Alkalinization increases calcium phosphate precipitation and reduces xanthine solubility without providing advantages in improving biochemical abnormalities 1
• Do not alkalinize urine in patients receiving rasburicase therapy unless other clinical conditions require it 1