INTRODUCTION: Budd-Chiari syndrome (BCS) is any process that inhibits hepatic venous outflow. It is caused by malignancy in 10% of all cases, either through hepatic vein / inferior vena cava (IVC) thrombosis and / or vascular compression due to mass effect. Clinical suspicion should remain high when abdominal pain, jaundice, and hepatomegaly are present with elevated transaminases, alkaline phosphatase, and bilirubin. This is a rare case of acute BCS caused by metastatic small cell lung carcinoma (SCLC) compressing the IVC. CASE DESCRIPTION/METHODS: A 61 y/o male with hypertension, dyslipidemia, asthma, and nonalcoholic fatty liver disease presented to the ED for URI symptoms refractory to antibiotics and steroids. He denied weight changes, hemoptysis, nausea, abdominal pain, sick contacts, and recent travel. The patient reported 22 years of second-hand smoke exposure as a police officer. He denied alcohol, tobacco, or illicit drug use. On exam he had a firm, distended abdomen. Laboratory exam showed: WBC: 18.8 103/µL, lactate: 2.8 mmol/L, BUN: 25 mg/dL, Tbili: 3.0 mg/dL, AST: 637 U/L, ALT: 606 U/L, ALP: 362 U/L, and LDH: 11173 U/L. Autoimmune, infectious, and toxicology workup was negative. Abdominal US and CT revealed hypoechoic liver masses and hilar / mediastinal lymphadenopathy. His liver biopsy identified a primary small cell carcinoma. The patient developed severe elevation of transaminases and acute kidney injury. RUQ tenderness, hepatomegaly, and jaundice correlated with worsening liver and kidney tests (Figures 1, 2). Abdominal CT revealed extra-luminal tumor compression of the IVC (Figure 3). The oncologist began carboplatin / etoposide in the ICU with rapid improvement of his labs and symptoms. The final diagnosis was stage IV SCLC complicated by BCS. The patient expired six months later. DISCUSSION: BCS caused by primary lung carcinoma (PLC) is rare; less than a dozen cases are reported in the literature. Prompt diagnosis of PLC allowed for targeted chemotherapy, which reduced tumor burden, improved symptoms, prevented acute liver and renal failure, and prolonged life. Rapid treatment may have prevented ascites by restoring hepatic venous pressures. Clinical suspicion of BCS should be based on physical exam and lab findings even with negative doppler US or CT. Past cases showed post-mortem tumor invasion of hepatic vasculature despite negative imaging. The overall prognosis for stage IV SCLC is poor, making early immunohistochemical analysis, tumor identification, and treatment method paramount.