Abstract
Tumour lysis syndrome (TLS) is a potentially fatal oncological emergency characterised by rapid cellular breakdown resulting in hyperkalaemia, hyperphosphataemia, hyperuricaemia, and hypocalcaemia, with subsequent acute kidney injury, cardiac dysrhythmias, and multi-organ dysfunction. It most commonly occurs following initiation of anti-cancer therapy in highly proliferative haematological malignancies. Spontaneous tumour lysis syndrome (STLS), occurring in the absence of a therapeutic trigger, is considerably rarer, particularly in solid tumours. We report a 55-year-old female presenting with progressive abdominal distension, pain, constipation, and oliguria progressing to anuria. Investigation demonstrated a 14 × 12 cm pelvic mass with extensive peritoneal and omental metastatic disease and large-volume ascites. During admission, prior to any anti-cancer therapy, she developed severe refractory hyperkalaemia, peaking at 8.1 mmol/L, alongside hyperphosphataemia >1.45 mmol/L (peaking at 2.44 mmol/L), hyperuricaemia of ≥476 µmol/L (peaking at 784 mmol/L), ionised hypocalcaemia ≤1.12 mmol/L (1.06 mmol/L), and rapidly progressive acute kidney injury, with creatinine rising from a baseline of 54 µmol/L to 310 µmol/L. These abnormalities fulfilled the Cairo-Bishop criteria for both laboratory TLS by achieving two or more deranged serum biochemical markers or changes >25% from baseline, as well as clinical TLS with the presentation of acute kidney injury and eventual death. Histopathological and genetic assessment ultimately identified a dedifferentiated endometrial carcinoma. Despite appropriate intravenous hydration, rasburicase, and repeated correction of electrolyte abnormalities, renal function and multi-organ dysfunction progressively deteriorated. The patient died nine days after admission, before anti-cancer therapy could be commenced. It was this absence of anti-cancer therapy and the trigger for the TLS that led us to classify this patient's presentation as STLS. STLS is exceptionally uncommon in solid malignancies but may occur in aggressive tumours with a high disease burden and rapid cellular turnover. This case is particularly notable because biochemical evidence of TLS preceded biopsy and any oncological treatment, supporting a genuinely spontaneous presentation. Furthermore, conventional risk stratification classified this patient as low risk, demonstrating the limitations of existing approaches when applied to rare, aggressive solid malignancies. STLS should be considered in patients with newly diagnosed or suspected solid malignancy who develop otherwise unexplained hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia, or acute kidney injury, even before anti-cancer treatment. Early recognition and application of TLS diagnostic criteria are essential to facilitate prompt hydration, urate-lowering therapy, and correction of life-threatening metabolic abnormalities; however, it is key to note that, despite this, this condition remains to possess a poor prognosis. Greater awareness of STLS in aggressive solid tumours may enable earlier intervention and potentially improve outcomes for this fulminant condition.