Infiltrative hepatocellular carcinoma: what radiologists need to know.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. The macroscopic growth pattern of HCC is subdivided into three categories: nodular, massive, and infiltrative. Infiltrative HCC accounts for 7%-20% of HCC cases and is confirmed at pathologic analysis on the basis of the spread of minute tumor nodules throughout large regions of the liver. Infiltrative HCC may represent a diagnostic challenge because it is often difficult to distinguish from background changes in cirrhosis at imaging. Infiltrative HCC usually spreads over multiple hepatic segments, occupying an entire hepatic lobe or the entire liver, and it is frequently associated with portal vein tumor thrombosis. The tumor is usually ill defined at ultrasonography and shows minimal and inconsistent arterial enhancement and heterogeneous washout at contrast material-enhanced computed tomography and magnetic resonance (MR) imaging. The tumor may be more visible among the surrounding liver parenchyma at diffusion-, T1-, and T2-weighted MR imaging. Several liver diseases can mimic the infiltrative appearance of this malignancy, including focal confluent fibrosis, hepatic fat deposition, hepatic microabscesses, intrahepatic cholangiocarcinoma, and diffuse metastatic disease (pseudocirrhosis). The prognosis for patients with infiltrative HCC is poor because the tumor is often markedly advanced and associated with vascular invasion at presentation. Survival after surgical resection is decreased; thus, infiltrative HCC is a contraindication for resection and transplantation. Knowledge of the key tumor characteristics and imaging findings will help radiologists formulate a correct and timely diagnosis to improve patient management.

A multi-disciplinary model of risk factors for fatal outcome in posterior reversible encephalopathy syndrome.

PURPOSE: To evaluate the relative impact of clinical data, imaging findings, and CSF laboratory values on clinical outcome in patients with posterior reversible encephalopathy syndrome (PRES). METHODS: 47 patients with PRES who underwent a lumbar puncture were retrospectively evaluated. Fatal outcome was defined as death directly ascribed to PRES toxicity. Univariate and multivariate analyses were used to evaluate the association between fatal outcome and clinical factors (demographics, PRES etiology), imaging findings (signal abnormality severity, atypical distribution, restricted diffusion, hemorrhage, enhancement, angiographic abnormalities), and lumbar puncture results (appearance, cell count, glucose, protein, culture results). RESULTS: Nine patients (19.1%) had a fatal outcome. Odds of a fatal outcome increased nearly 5-fold with hemorrhage on imaging (Adjusted Odds Ratio (AOR) 4.8, 95% CI 3.8-6.0, p=0.03) and nearly doubled with low CSF glucose (AOR 1.9, 95% CI 1.5-2.5, p=0.02). Hypertensive encephalopathy as an etiology was associated with a fatal outcome (AOR 1.6, 95% CI 1.3-2.9, p=0.02), while toxemia of pregnancy was protective, with a 75% decreased risk (AOR 0.25, 95% CI 0.15-0.43, p=0.02). CONCLUSION: Clinical, imaging, and CSF laboratory findings all influence outcome in PRES, with a low CSF glucose, hypertensive encephalopathy, and imaging findings of hemorrhage associated with increased risk of fatal outcome.

Value of prominent flow voids without cord edema in the detection of spinal arteriovenous fistulae.

PURPOSE: To determine the prevalence of spinal dural arteriovenous fistulae (SDAVF) in patients presenting with prominent vascular flow voids on imaging without other imaging findings suggestive of SDAVF. METHODS: We retrospectively identified patients from January 1, 2005 to March 1, 2012 who underwent spinal angiography for suspected SDAVF with prominent vascular flow voids on prior imaging. We excluded patients with other major spinal pathology or other imaging findings of SDAVF including cord hyperintensity, enhancement, or expansion. We calculated the proportion of patients with positive findings for SDAVF on angiography and evaluated the prevalence of SDAVF for this finding alone and in correlation with clinical findings. RESULTS: 18 patients underwent spinal angiography for prominent flow voids on imaging without other spinal pathology or imaging findings of SDAVF. Three had a SDAVF detected on angiography. The prevalence of SDAVF in this population was low, only 17% (95% CI 6-39%). All of the patients with positive angiography findings had myelopathy, increasing the prevalence to 100% if the additional clinical finding of myelopathy was present. CONCLUSIONS: Prominent flow voids without other imaging findings suggestive of SDAVF is poorly predictive of the presence of a SDAVF, unless myelopathy is present clinically.