Tumor lysis syndrome (TLS) is a life-threatening metabolic emergency most commonly associated with hematologic malignancies and is rarely reported in solid tumors.We describe spontaneous TLS in a woman in her late 70s with chronic kidney disease, diabetes mellitus, and atrial fibrillation who presented with vasopressor-dependent shock and was found to have a large necrotic mediastinal mass with mediastinal lymphadenopathy and bilateral pulmonary nodules.Endobronchial ultrasound-guided transbronchial needle aspiration of mediastinal lymph nodes demonstrated malignancy favoring small cell carcinoma.She had received no anticancer therapy.Available pre-bronchoscopy laboratory measurements included potassium 4.5 mEq/L, phosphorus 3.0 mg/dL, uric acid 4.0 mg/dL, and calcium 8.8 mg/dL, without the characteristic biochemical pattern of TLS.Subsequently, she developed progressive hyperkalemia, hyperphosphatemia, modest hypocalcemia, severe metabolic acidosis, oliguria progressing to anuria, and worsening renal failure.Uric acid increased to a documented peak of 12 mg/dL, and lactate dehydrogenase reached 3,608 U/L.Rasburicase was administered, and continuous renal replacement therapy was initiated; however, the patient developed refractory shock and progressive multiorgan failure and died.This case highlights spontaneous tumor lysis syndrome (STLS) as a rare but potentially fatal complication of a bulky thoracic malignancy with cytology favoring small cell carcinoma, particularly in the setting of markedly impaired renal reserve.Bronchoscopy serves as a temporal landmark in the biochemical evolution of TLS, but a causal relationship cannot be established, and pre-existing shock, acute kidney injury, and possible sepsis were important concurrent contributors.
No takes yet. Share an insight, caveat, or question.
Rana et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: