Abstract
Tumor lysis syndrome (TLS) is an oncological emergency characterized by the massive destruction of malignant cells and the release of their contents into the extracellular space, which might occur spontaneously or post-chemotherapy. According to the Cairo&Bishop Classification, it can be defined by both laboratory criteria: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia (two or more); and clinical criteria: acute kidney injury (AKI), convulsions, arrhythmias, or death. We report the case of a 63-year-old man with a previous medical history of colorectal carcinoma and associated multiorgan metastasis. The patient was initially admitted to the Coronary Intensive Care Unit, five days after the chemotherapy session, on suspicion of Acute Myocardial Infarction. Upon admission, he presented without significant elevation of myocardial injury markers, but with laboratory abnormalities (hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia) and clinical symptoms (sudden sharp chest pain with pleuritic characteristics and electrocardiographic anomalies suggesting uremic pericarditis, and acute kidney injury), all consistent with TLS. The best approach to established TLS is aggressive fluid therapy and a decrease in uric acid levels. Rasburicase proved to be notoriously more effective, both in terms of prevention and treatment of established TLS, thus consisting of the first-line drug. However, in the present case, rasburicase was not available at the hospital level, so a decision was made to initiate treatment with allopurinol. The case evolved with slow but good clinical evolution. Its uniqueness resides in its initial presentation as uremic pericarditis, scarcely described in the literature. The constellation of metabolic alterations from this syndrome translates into a spectrum of clinical manifestations that can go unnoticed and ultimately may prove to be fatal. Its recognition and prevention are crucial for improving patient outcomes.