Medical Management

The potential severity of complications resulting from the development of TLS necessitates measures for prevention in high-risk patients and prompts treatment in the event that symptoms arise. Recognition of risk factors, close monitoring of at risk-patients and appropriate intervention are the key to preventing or managing tumor lysis syndrome. A cardinal sign is hyperuricemia, leading to uric acid nephropathy. Other signs are hyperkalemia, hyperphosphatemia and secondary hypocalcemia.

Treatment options of hyperkalemia include sodium polystyrene sulfonate (kayexalate), hypertonic glucose and insulin, diuretics (furosemide), and sodium bicarbonate (2040 mEq/L IV fluid; bolus with 0.51.0 mEq/kg for pH <6.5.) . If the patient has symptomatic hyperkalemia, the healthcare provider may order I.V. regular insulin and to redistribute potassium, shifting it intracellularly.

Hyperphosphatemia is managed with phosphate binders such as aluminum hydroxide given in limited dosages to avoid aluminum toxicity. For asymptomatic hyperphosphatemia, initial treatment consists of eliminating phosphate from intravenous solutions, maintaining adequate IV hydration because it maintains renal blood flow and promotes urinary excretion of uric acid and phosphate. , and the administration of phosphate binders. Treatment of hyperphosphatemia reduces dietary phosphate intake and includes phosphate binders such as aluminum hydroxide and aluminum carbonate.

When recurrent hypocalcemia is present, a continuous intravenous infusion of calcium gluconate can be initiated. Care must be taken because increased calcium might increase the risk of calcium phosphate precipitation in the tissues and consequential obstructive uropathy. Hypocalcemia should be managed by first treating hyperphosphatemia. If the hypocalcemia does not resolve and he patient is experiencing seizures or cardiac symptoms, seizures precautions and IV calcium gluconate are

Antihyperuricemic agents: Allopurinol -One approach to preventing or managing TLS associated hyperuricemia is to block the conversion of xanthine and hypoxanthine to uric acid. Allopurinol is a xanthine analog which, when converted in vivo to oxypurinol, acts as a competitive inhibitor of xanthine oxidase, thereby blocking the conversion of the purine metabolites to uric acid. -Use of Allopurinol has been shown to decrease the formation of uric acid and to reduce the incidence of obstructiove uropathy caused by uric acid precipitation in patients at risk for developing TLS.

Recombinant urate oxidase(rasburicase) -Rasburicase is administered for 5 to 7 days, and chemotheraphy could be started 4h after initiation of treatment. A recombinant urate oxidase enzyme, rasburicase converts existing uric acid to allantoin, which is 5 to 10 times more soluble in urine than uric acid. Rasburicase differs from allopurinol since it can affect existing plasma uric acid; allopurinol affects only the future production of uric acid by inhibiting

REMEMBER!

Alkalinization is recommended during allopurinol treatment, but is not required with rasburicase because there was a controversy before that alkalinization may increase precipitation of calcium phosphate in renal tubules; it also interferes with renal tubular reabsorption of phosphorus.

 Fluid

and hydrations

-Hydrations is the first and most important line of prevention. IV fluid should be 3000 mL/m/24 h or more(amount may vary depending on age and comorbidities) and continued for several days to maintain a urine output of more than 100 cc/m/hour and urine specific gravity of less than 1.010. It is especially important to work with physicians and residents to ensure that the patient receives no additional potassium during hydration, even if the patients potassium level is normal, because the patient will be exposed to an elevated level of potassium when lysis begins.

Additional Treatment
Hemofiltration/dialysis