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Microbial contamination of the liver parenchyma leading to hepatic abscess (HA) can occur via the bile ducts or vessels (arterial or portal) or directly, by contiguity. Infection is usually bacterial, sometimes parasitic, or very rarely fungal. In the Western world, bacterial (pyogenic) HA is most prevalent; the mortality is high approaching 15%, due mostly to patient debilitation and persistence of the underlying cause. In South-East Asia and Africa, amebic infection is the most frequent cause. The etiologies of HA are multiple including lithiasic biliary disease (cholecystitis, cholangitis), intra-abdominal collections (appendicitis, sigmoid diverticulitis, Crohn's disease), and bile duct ischemia secondary to pancreatoduodenectomy, liver transplantation, interventional techniques (radio-frequency ablation, intra-arterial chemo-embolization), and/or liver trauma. More rarely, HA occurs in the wake of septicemia either on healthy or preexisting liver diseases (biliary cysts, hydatid cyst, cystic or necrotic metastases). The incidence of HA secondary to Klebsiella pneumoniae is increasing and can give rise to other distant septic metastases. The diagnosis of HA depends mainly on imaging (sonography and/or CT scan), with confirmation by needle aspiration for bacteriology studies. The therapeutic strategy consists of bactericidal antibiotics, adapted to the germs, sometimes in combination with percutaneous or surgical drainage, and control of the primary source. The presence of bile in the aspirate or drainage fluid attests to communication with the biliary tree and calls for biliary MRI looking for obstruction. When faced with HA, the attending physician should seek advice from a multi-specialty team including an interventional radiologist, a hepatobiliary surgeon and an infectious disease specialist. This should help to determine the origin and mechanisms responsible for the abscess, and to then propose the best appropriate treatment. The presence of chronic enteric biliary contamination (i.e., sphincterotomy, bilio-enterostomy) should be determined before performing radio-frequency ablation and/or chemo-embolization; substantial stenosis of the celiac trunk should be detected before performing pancreatoduodenectomy to help avoid iatrogenic HA.

Introduction. Response Evaluation Criteria in Solid Tumors, version 1.1 (RECIST 1.1), may underestimate activity and does not predict survival in patients with hepatocellular carcinoma (HCC) treated with sorafenib. This study assessed the value of alternative radiological criteria to evaluate response in HCC patients treated with sorafenib. Patients and Methods. A retrospective blinded central analysis was performed of computed tomography (CT) scans from baseline and the first tumor evaluation in consecutive patients treated with sorafenib over a 2‐year period in a single institution. Four different evaluation criteria were used: Choi, European Association for the Study of the Liver (EASL), modified RECIST (mRECIST), and RECIST 1.1. Results. Among 82 HCC patients, 64 with Barcelona Clinic Liver Cancer stage B‐C were evaluable with a median follow‐up of 22 months. Median duration of sorafenib treatment was 5.7 months, and median overall survival was 12.8 months. At the time of the first CT scan, performed after a median of 2.1 months, Choi, EASL, mRECIST, and RECIST 1.1 identified 51%, 28%, 28%, and 3% objective responses, respectively. Responders by all criteria showed consistent overall survival >20 months. Among patients with stable disease according to RECIST 1.1, those identified as responders by Choi had significantly better overall survival than Choi nonresponders (22.4 vs. 10.6 months; hazard ratio: 0.43, 95% confidence interval: 0.15–0.86, p = .0097). Conclusion. Choi, EASL, and mRECIST criteria appear more appropriate than RECIST 1.1 to identify responders with long survival among advanced HCC patients benefiting from sorafenib.

DW MR imaging was more sensitive for the detection and characterization of liver metastases from NETs than T2-weighted FSE and dynamic gadolinium-enhanced MR imaging and should be systematically performed.

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Budd-Chiari syndrome (BCS) is defined by clinical and laboratory signs associated with partial or complete impairment of hepatic venous drainage in the absence of right heart failure or constrictive pericarditis. Primary BCS is the most frequent type and is a complication of hypercoagulable states, in particular myeloproliferative neoplasms. Secondary BCS involves tumor invasion or extrinsic compression. Most patients present with chronic BCS including a non-cirrhotic, dysmorphic, chronic liver disease with various degrees of fibrosis deposition. Acute BCS is rare, and patients present with hepatomegaly, ascites, and hepatic insufficiency. The diagnosis is based on imaging. Imaging features include (1) direct signs, in particular occlusion or compression of the hepatic veins and/or the inferior vena cava and venous collaterals and (2) indirect signs, in particular morphological changes in the liver with hypertrophy of the caudate lobe and delayed nodule formation. Ultrasound and magnetic resonance imaging are the gold standard for diagnosis. The aim of this review is to provide an overview of the role of imaging in the diagnosis of BCS.

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Hepatic steatosis is a common condition, the prevalence of which is increasing along with non-alcoholic hepatic steatosis. In imaging, it can present in a typical homogeneous or heterogeneous way. Some forms create traps in imaging, whether localised steatosis is concerned or areas which have been spared by steatosis, and the purpose of this paper is to explain and illustrate them. The role of different imaging methods is described while emphasizing the importance of MRI.