The hyperkalemia associated with tumor lysis syndrome may be accentuated by associated renal insufficiency or renal failure and may cause electrocardiographic alterations and potentially fatal cardiac arrhythmia. The major manifestation of hyperphosphatemia is secondary hypocalcemia caused by precipitation of calcium phosphate in the soft tissues and the kidney. Hypocalcemia may lead to alterations in mental status, neuromuscular irritability, carpopedal spasm, and seizures. Treatment Anticipation and controlled management of tumor lysis are the keys to preventing the syndrome. Patients who are at risk should be hospitalized and fully hydrated, with ongoing diuresis before, during, and after treatment, and should undergo frequent electrolyte monitoring.
Diuresis minimizes the renal sludging from high urinary loads of uric acid, xanthine, and phosphate.
Pretreatment with allopurinol blocks the conversion of hypoxanthine and xanthine to uric acid and minimizes the uric acid sludging in the kidney caused by xanthine crystals. Alkalinization of the urine with sodium bicarbonate infusion increases the solubility of urinary uric acid and decreases the risk of urate nephropathy. Patients at risk for tumor lysis syndrome should not receive supplemental potassium and should be monitored for development of hyperkalemia. Patients who have either symptomatic hypocalcemia or the electrocardiographic changes associated with hypocalcemia should be treated with an infusion of calcium gluconate. The hypocalcemia may persist beyond the period of observed hyperphosphatemia.