Case Report: A 56-year-old Caucasian woman with history of moderate alcohol intake presented with sudden-onset, severe abdominal pain with nausea and dizziness for a few hours. On examination, she was afebrile, hypotensive, tachycardic, and icteric. There were multiple spider angiomata over the chest. She had tenderness and guarding in the epigastrium and left upper quadrant without rigidity. Rectal vault had brown stool that was guaiac negative. Lab data were: hemoglobin 7.6 mg/dL (down from 14 mg/dL six months ago); platelet 238,000/μL; total bilirubin 7.7 mg/dL; AST 135 IU/L; albumin 2.6 g/dL; and INR 1.3. CT abdomen showed an enlarged echogenic liver and a normal-appearing pancreas. Spleen had a rupture postero-inferiorly with resultant perisplenic hematoma. After taking resuscitative measures, an urgent exploratory laparotomy showed splenic rupture in multiple pieces, still connected to the hilum with massive hemoperitoneum of 1.5 L and hepatomegaly. A splenectomy and wedge liver biopsy was done. Liver histopathology showed extensive steatosis (80-90%), ballooning degeneration, severe cholestasis, Mallory-hyaline, and mixed inflammatory infiltrate. Trichrome stain highlighted extensive sinusoidal and portal fibrosis with focal areas of bridging fibrosis. Splenic histopathology showed capsular disruption with subcapsular and intraparenchymal hemorrhage, and acute inflammation. Etiological work-up for liver disease and splenic rupture including serum copper, viral panel, hemochromatosis screen, alpha-1 antitrypsin, autoimmune panel, monospot, leukemia, and lymphoma panel was negative. Cause of her splenic rupture was felt to be related to portal hypertension from alcoholic steatohepatitis and early cirrhosis. Discussion: Non-traumatic splenic rupture (NSR) is a rare, but life threatening condition. Diagnosis is often suspected based on clinical symptoms. Paracentesis with aspiration of fresh blood is useful to diagnose intraperitoneal hemorrhage. Abdominal ultrasound is especially useful in hemodynamically unstable patients. CT can shows grade of splenic damage severity and intraperitoneal free fluid. In a review of 845 cases of NSR, the spleen was normal in 7%. The major pathologic etiological groups were neoplastic (30%), infectious (27%), and inflammatory (20%). In our patient, we ascribed the splenic rupture to congestion resulting from steatohepatitis. This patient had patent portal and splenic vein, ruling out congestion due to thrombosis. This is a unique case for rarity of atraumatic splenic rupture as presenting manifestation of steatohepatitis with early changes of bridging fibrosis.