Abstract: |
Tumor lysis syndrome (TLS) is an oncometabolic emergency that is triggered by lysis of tumor cells either after cytotoxic therapy or spontaneously, which results in the release of large amounts of potassium, phosphate, and uric acid into the systemic circulation. These metabolites can overwhelm normal homeostatic mechanisms in the body leading to hyperkalemia, hyperphosphatemia, hyperuricemia, secondary hypocalcemia, and their associated clinical manifestations. TLS can lead to acute kidney injury via crystal dependent (uric acid and/or calcium phosphate crystal deposits in renal tubules) and crystal independent mechanisms, resulting in increased morbidity and mortality. TLS is most commonly seen in patients being treated for hematologic malignancies such as non--Hodgkin's lymphoma and acute lymphoblastic leukemia but may also occur in highly proliferative and sensitive solid tumors. With the advent of novel and effective new therapies for a variety of hematologic malignancies, the incidence of TLS is expected to increase. Identifying patients at risk and instituting preventative measures are key to minimize the clinical consequences of this syndrome. The cornerstone of management includes intravenous hydration, diuretics as needed, hypouricemic agents (allopurinol, rasburicase), close monitoring of electrolytes, and renal replacement therapy when indicated. In this chapter, we discuss the etiology, definition, pathophysiology, prophylaxis, and management of TLS, with an emphasis on high-risk patients who require intensive care support. © Springer Nature Switzerland AG 2020. All rights reserved. |