A 30-year-old Caucasian male with, no prior medical history, presented at the Emergency Department with acute right upper quadrant pain, high grade fever (38.5 C) and vomit.
Laboratory tests revealed marked leukocytosis (WBC: 19810/ml) and abnormal liver function tests (AST/ALT: 218/280 IU/L, ALP/gamma-GT: 123/147 IU/L, TBil: O,84 mg/dl). Serology profile for hepatitis B or C was negative. A previous history of alcohol abuse was not documented.
Abdominal US revealed a 7 cm hyperechoic lesion at the right liver lobe.
Computed tomography demonstrated a single lesion, located in segments V and VI, with hemorrhagic features. After contrast administration the lesion appeared to be encapsulated with peripheral enhancement, a necrotic core and contrast wash out at the venous phase. These findings were suspicious for adenoma or HCC although fever and leukocytosis suggested a possible infectious process. No dilatation of the intra- or the extra-hepatic biliary ducts was noted. A lateral displacement of the gallbladder was documented (Figure 1).
The patient was admitted and initially treated with systemic broad spectrum antibiotics. However blood cultures and antibodies for Echinococcus and Entamoeba histolytica were negative.
Tumor markers including CA 19-9, a-Fetoprotein and CEA were within normal range.
A CT-guided core-needle biopsy was performed and revealed numerous lymphocytes and necrotic material but not atypia. Gram stain and Tissue cultures were negative.
The patient was treated with intravenous antibiotics for 7 days until fever subsides with complete white cell count normalization and followed by CT scan two weeks later. Due to high suspicion for a malignant process, anatomic liver resection including segments V and VI was performed. Intraoperatively, the liver had a normal appearance and a solid mass, well encapsulated without gallbladder invasion was identified.
Pathology was associated with hemorrhagic infarct and extensive hepatocellular necrosis, due to sinusoidal portal vein thrombosis. Furthermore hepatoportal sclerosis and non-cirrhotic portal vein fibrosis was identified. An eosinophil granular matter combined with calcifications, cholesterol, foam cells, and some inflammatory cells was noted.
The patient had an uneventful course, discharged the 6th postoperative day and remains well 6 months postoperatively.