A 52-year-old man ingested "Tusanqi powder" at a dose of 5 g one to two times daily because of an injury sustained from a fall. Eight days later, he developed fatigue, abdominal distension, and abdominal pain. His coagulation indices were as follows: PT: 19.0 s, prothrombin activity (PTA): 42%, and international normalized ratio (INR): 1.87. On biochemical testing, his results were as follows: estimated value of the glomerular filtration rate: 98.47 mL/min/1.73 m2, TBIL: 108.9 micromol/L, direct bilirubin (DBIL): 65.4 micromol/L, ALB: 26.0 g/L, globulin: 33.4 g/L, ALT: 645 U/L, AST: 477 U/L, ALP: 148 U/L, and GGT: 251 U/L. The CT scan showed that the density of the liver parenchyma was unevenly reduced. The liver parenchyma in the arterial and venous phases showed a characteristic "map-like" appearance and uneven enhancement, and the hepatic veins were thin and unclear. Enlarged lymph nodes in the porta hepatis were observed. A liver biopsy was performed on the 10th day of the disease. Early pathological changes were observed in the specimen of the patient who underwent liver biopsy during the acute stage. Hepatocytes exhibited hemorrhagic necrosis and were fused into sheets. As hepatocytes separated, numerous red blood cells infiltrated the perisinusoidal space, and the perisinusoidal space expanded and compressed the hepatic sinus. The sinus cavity and perisinusoidal space fused and became indistinguishable, and the hepatic sinusoid appeared dilated and congested. Hemorrhagic necrosis was observed on HE staining (Figure 2). After the diagnosis of HSOS was established, treatment with low-molecular-weight heparin combined with warfarin was initiated; however, the condition of the patient continued to deteriorate. Complications, such as hepatic encephalopathy, hepatorenal syndrome, and gastrointestinal bleeding, occurred, and the patient died on the 30th day of the disease.