Chapter 171 Tumor Lysis Syndrome
INTRODUCTION
Tumor lysis syndrome (TLS) is a constellation of metabolic abnormalities that may be observed in veterinary oncology patients.1,2 Clinically significant TLS is seen most often shortly after cancer treatment and is associated with significant morbidity and mortality.2-4 The precise incidence of TLS is not defined in veterinary oncology, but is likely rare because only sporadic cases are reported.5-7 The severity and nature of the metabolic alterations are often variable depending on the timing and intensity of therapy, the enormity of tumor lysis, and the hydration and renal status of the patient. The risk factors, pathogenesis, metabolic complications, and therapeutic strategies of TLS are discussed in this chapter.
RISK FACTORS
TLS is seen most commonly in veterinary patients with chemotherapy-responsive and radiation-responsive diseases, such as lymphoma or lymphoid leukemias. TLS usually is noted within a short time after treatment, typically hours to a few days, but onset can be as long as 5 to 7 days after treatment.5 Patients at highest risk include those with dehydration or advanced disease and with rapid induction of remission after treatment.5-7
The dose-response curves for most cytotoxic chemotherapy agents are sigmoidal in shape, suggesting that small reductions in dosage can translate into large reductions in efficacy.8 Given that TLS is a rare syndrome in veterinary patients, this author does not recommend routine dosage reduction or changes in protocol schedules to prevent TLS unless the patient has all of the aforementioned risk factors.
PATHOGENESIS AND METABOLIC COMPLICATIONS
The pathogenesis of TLS is related to rapid tumor cell destruction, which may result in release of intracellular ions and metabolic byproducts into the extracellular environment and systemic circulation. The metabolic complications of TLS are therefore characterized by hyperphosphatemia, hyperkalemia, and metabolic acidosis with or without azotemia.1,5 The hyperphosphatemia can secondarily induce hypocalcemia.
Acute renal failure is a common sequela of TLS and the pathophysiology is likely multifactorial.9 Not only do hyperphosphatemia and hyperuricemia result from TLS, they also contribute to the oliguric acute renal failure in these patients. Causes may include tubular precipitation of calcium phosphate and nucleic acid metabolites (and secondary intraluminal tubular obstruction), intravascular volume depletion, and poorly understood malignancy-associated nephrotoxins. A diagram of the purine metabolism pathway is shown in Figure 171-1 and is discussed further in the Treatment section.
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