Abstract: Case Reports |


Jason Huet, MD*; Roy Essig, MD
Author and Funding Information

The Ohio State University, Columbus, OH


Chest. 2008;134(4_MeetingAbstracts):c56002. doi:10.1378/chest.134.4_MeetingAbstracts.c56002
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INTRODUCTION: Tumor lysis syndrome (TLS) is a metabolic emergency characterized by hyperphosphatemia, hyperuricemia, hyperkalemia, hypocalcemia, and acute renal failure. This potentially fatal syndrome is most often seen after anti-cancer treatment of extensive, rapidly proliferating, and treatment-sensitive tumors such as aggressive lymphomas and acute leukemias. The pathophysiologic mechanism of TLS is thought to be rapid tumor necrosis leading to the release of intracellular ions and metabolic products into the bloodstream. Spontaneous TLS (STLS), which manifests prior to treatment, is exceedingly rare in solid tumors and has not been reported in small cell lung cancer.

CASE PRESENTATION: A 67-year-old white male presented with progressive hoarseness and dyspnea over the proceeding two months. A chest roentegram and subsequent chest computed tomography showed a left hilar mass causing obstruction and complete atelectasis of the left upper lobe along with extensive mediastinal lymphadenopathy. The patient underwent fiber-optic bronchoscopy which revealed an obstructing friable mass at the secondary carina of the left lung. Endobronchial biopsies showed small cell lung cancer (SCLC). He was also found to have evidence of disease in his liver and bone marrow per imaging and bone marrow biopsy respectively. On admission, prior to any treatment, the patient's chemistries showed: sodium 141 mmol/L, potassium 5.9 mmol/L, chloride 107 mmol/L, carbon dioxide 21 mmol/L, urea nitrogen 74 mg/dL, creatinine 2.29 mg/dL, phosphorus 5.1 mg/dL, calcium 9.5 mg/dL, uric acid 16.5 mg/dl, and lactate dehydrogenase (LDH) 1,221 U/L. The patient was diagnosed with STLS and was given hydration, urinary alkalinization, and rasburicase. After his chemistries stabilized he was administered one dose of cisplatin as a palliative measure. He subsequently developed oliguric renal failure requiring renal replacement therapy and respiratory failure requiring intubation and mechanical ventilation. After two weeks the patient had not improved and was made comfort care and life sustaining measures were withdrawn.

DISCUSSIONS: We report the initial case of STLS secondary to small cell lung cancer. STLS in solid tumors is very rare. This can be explained by the fact that most solid tumors have a low proliferative index and a relatively marginal response to cytotoxic therapy. SCLC is different from most solid tumors in that it has an elevated rate of cell turnover and can present with high tumor burden. Reported risk factors for TLS include a high LDH and evidence of liver metastasis. A distinction has been described between spontaneous and post-treatment TLS based on the magnitude of hyperphosphatemia. STLS is thought to have lower phosphorus levels due to its reutilization in the ongoing synthesis of new tumor cells, whereas, post-treatment TLS has higher phosphorus levels primarily from cell destruction. Despite being significantly less common, TLS in solid tumors appears to carry a higher mortality rate than that seen in hematologic malignancies.

CONCLUSION: STLS is a metabolic emergency with high morbidity and mortality. Although rare in solid tumors, the potential for STLS should be considered when caring for patients with extensive, rapidly proliferating disease and an elevated LDH. This may allow for closer appropriate monitoring and more effective prophylaxis and treatment, possibly leading to better outcomes.

DISCLOSURE: Jason Huet, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 29, 2008

2:30 PM - 4:00 PM




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