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Background: Tumor lysis syndrome is a very serious and sometimes life-threatening complication of cancer therapy. It can be defined as a pattern of metabolic abnormalities resulting from spontaneous or treatment-related tumor necrosis or fulminant apoptosis. The metabolic abnormalities observed in patients with tumor lysis syndrome include hyperkalemia, hyperuricemia, and hyperphosphatemia with secondary hypocalcemia. These can lead to renal failure. Occasionally, tumor lysis syndrome is accompanied by a coagulopathy.
Pathophysiology: Tumor lysis syndrome can be precipitated before the initiation of therapy or up to 5 days after the start of chemotherapy, especially with tumors that have a high growth fraction and high sensitivity to chemotherapy. Burkitt lymphoma and T cell acute lymphoblastic leukemia are most frequently associated with this complication. It has also been observed in association with solid tumors, such as hepatoblastoma and stage IV neuroblastoma. In 1980, Cohen et al identified risk factors that predispose patients to metabolic derangements, such as bulky abdominal disease, elevated pretreatment uric acid level, elevated lactate dehydrogenase level, and poor urine output. Lysis of tumor cells results in rapid release of potassium, uric acids (from nucleic acids), and phosphorus, leading to hyperkalemia, hyperuricemia, and hyperphosphatemia with secondary hypocalcemia. These can subsequently lead to renal failure. These complications may result in multiple organ failure and death.
The kidneys primarily excrete uric acid, phosphorus, and potassium. Uric acid (pKa = 5.4) is soluble at physiologic pH, but it can precipitate in an acidic environment of renal tubules, leading to crystallization in collecting ducts and the ureters and causing obstructive uropathy. Calcium phosphate is precipitated in the renal tubules and microvasculature as the in vivo calcium-phosphorus solubility product exceeds 60-70 because of hyperphosphatemia. Note that the phosphorus content of the lymphoblasts is 3-4 times the content of normal lymphocytes. Symptomatic hypocalcemia may result from hyperphosphatemia. Hyperkalemia results from release of intracellular potassium and is further aggravated by renal failure and metabolic acidosis.
Medical Care: Identification of patients at risk and initiation of preventive interventions are the focus of medical and nursing management.
Ongoing monitoring is necessary to promote early response to changes in patient condition and to minimize adverse events. This requires frequent blood sampling in the initial period of clinical instability or potential instability. Testing at 4- to 8-hour intervals may be required in a patient at high risk for tumor lysis syndrome. Additionally, the patient's intake and output, weight, and blood pressure must be carefully monitored at close intervals.
Metabolic stability must be achieved, even before treatment proceeds.
Prevention of renal failure entails hydration, alkalinization, and metabolic correction using medications.
Hydration is the most critical factor. Patients should receive 2-3 times the maintenance fluid volume as 5% dextrose in 0.2% NaCl. This should be monitored to maintain a urine output of at least 3 mL/kg/h for children younger than 9 years and approximately 90 mL/m 2 /h in older children. With adequate fluids, diuresis may be assisted with furosemide or mannitol. Avoid adding potassium to intravenous fluids.
Sodium bicarbonate of 75-100 mEq/L (100-125 mEq/m 2 ) should be added to IV fluids to achieve a urinary pH of 7-7.5 and urine specific gravity of 1.010 to enable efficient excretion of uric acid in soluble form.
Vigorous alkalinization is no longer required after allopurinol has been started and the uric acid level is returned to the reference range to decrease the potential problems with hypocalcemia and hyperphosphatemia.
Surgical Care: Patients with tumor lysis syndrome may need surgical intervention in the form of dialysis catheter placement in cases of extreme hyperkalemia or renal failure.
Consultations: Effective management of patients with tumor lysis syndrome requires a team approach on part of medical and nursing staff. Treat patients with tumor lysis syndrome in an intensive care unit with the active participation of the oncologist, intensivist, nephrologist, and general surgeon.
Further Inpatient Care:
Most patients with acute renal failure can be managed conservatively, but consider peritoneal dialysis or hemodialysis if conservative management is ineffective.
Dialysis may be indicated if the following apply. The decision to initiate dialysis is not usually based on a single laboratory study abnormality but on the constellation of findings and the likelihood of further clinical deterioration. Each of the laboratory findings below is much more worrisome in the setting of oliguria or anuria.
Worsening hyperuricemia (serum uric acid >10 mg/dL and increasing): Elevated uric acid in the absence of other abnormalities does not usually require dialysis.
Symptomatic hypocalcemia
Serum phosphorus (>10 mg/dL or persistent symptomatic hypocalcemia)
Uncontrolled hypertension and hypervolemia
Significant elevation of serum creatinine and blood urea nitrogen in the setting of other metabolic abnormalities or decreasing urine output: Elevation of these parameters of renal function in the absence of other abnormalities is not usually an indication to start dialysis.
Hemodialysis is preferred over peritoneal dialysis because it corrects metabolic disturbances very rapidly. Peritoneal dialysis clears uric acid with only 10% of the efficiency of hemodialysis and is also contraindicated in abdominal tumors. Chemotherapy can be reinstated with the initiation of dialysis. Dialysis is usually required for 4-11 days, until the patient's own kidney function has recovered.
Many centers employ modalities such as leukophoresis, exchange transfusion, or low-dose steroids to reduce the metabolic consequences of massive tumor lysis, which occurs often in a setting of a high leukocyte count. None of the above methods has been subjected to any controlled analysis. However, North American protocols are increasingly using steroids, and patients are allowed for registration after 48 hours of steroid therapy. Leukophoresis is often considered at leukocyte counts of greater than 100,000/mm 3 in patients with acute myelogenous leukemia (AML) or greater than 400,000 in patients with acute lymphoblastic leukemia (ALL), and it may be more successful at correcting leukostasis than preventing tumor lysis syndrome.
Transfer:
Manage patients with complicated tumor lysis syndrome in an intensive care setting. Once hemodynamically stable, patients can be transferred to a regular floor with rigorous monitoring.
Complications:
Tumor lysis syndrome can be complicated by several problems that may be severe and life threatening in a patient who has the potential to attain full remission. Therefore, evaluating high-risk patients frequently by clinical assessment and biochemical monitoring is of paramount importance.
The metabolic disturbances encountered during tumor lysis syndrome may be responsible for CNS complications, such as seizures.
Cardiac complications, such as ventricular arrhythmias leading to multiple organ failure and death, may result from hyperkalemia.
The course of tumor lysis syndrome may be complicated by acute renal failure, as described above.
Vigorous prophylactic management, anticipation, and the prompt treatment of detected metabolic problems are essential for the optimal management of high-risk patients.
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