Management

Identification of patients at risk and institution of appropriate prophylactic measures are essential for the management of TLS. The cornerstones of therapy include aggressive hydration, maintenance of adequate urinary output (with gentle diuresis, if necessary), urinary alka-linization, frequent monitoring of electrolytes, and specific treatment of individual metabolic abnormalities.

Hyperkalemia

Several approaches for the treatment of hyperkalemia are available. Methods that reduce serum potassium level through excretion, rather than via intracellular shifts, are preferred. Elimination of potassium in infusions, use of cation exchange resins such as sodium polystyrene sulfonate, loop diuretics (especially in the fluid overloaded patient), and hemodialysis (in severe cases)26 are reasonable strategies.

Hyperphosphatemia and hypocalcemia

Reduction of serum phosphate levels with oral phosphate binders, such as aluminum hydroxide, is usually effective. Spontaneous correction of serum calcium levels is noted when hyperphosphatemia is adequately managed. In cases of severe symptomatic hypocal-cemia, cautious repletion with calcium chloride or glu-conate can be undertaken. Overzealous intravenous calcium replacement should be avoided, as this can promote metastatic calcifications.2728

Hyperuricemia

Treatment of hyperuricemia should focus on measures that prevent uric acid formation and precipitation, and augment uric acid metabolism to allantoin. Allopurinol 300 mg/day is used prophylactically to prevent uric acid synthesis from purines released as a result of leukemic cell lysis, through inhibition of xanthine oxidase. Alkalinization of urine with sodium bicarbonate infusions to a target urinary pH of 7.0 is effective in preventing uric acid deposition in the renal tubules. However, overaggressive alkalinization could foster calcium phosphate precipitation, and therefore should be done with care.27

Urate oxidase metabolizes uric acid to allantoin, which is 5- to 10-fold more soluble than uric acid29 and is readily excreted by the kidneys.30 Recombinant urate oxidase (rasburicase) has been recently approved for the treatment of hyperuricemia in pediatric patients with acute leukemia. It is extremely effective in reducing serum uric acid to low levels within a few hours of administration,31 but is used in severe cases that have failed traditional prophylactic methods, and in whom the probability of acute renal failure is very high. This therapy is initiated only when a patient's uric acid rises to >14.

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