Magnetic resonance imaging (MRI) is frequently used as the definitive imaging test to characterize focal hepatic lesions and avoid percutaneous biopsies. In this role, the interpreting radiologist must try to offer a specific histologic diagnosis when possible or when this is not possible, narrow the differential diagnosis to facilitate patient management. The differential diagnosis of a focal hepatic lesion in a non-cirrhotic liver is broad and encompasses a spectrum of pathology that spans from benign lesions which do not require any further workup to primary malignant tumors and metastatic disease. In this regard, an experienced radiologist can recognize the specific MRI characteristics of a focal hepatic lesion using an “Aunt Minnie approach” by integrating the different features of the lesion on T1- and T2-weighted imaging, diffusion weighted imaging (DWI), and multiphasic contrast enhanced acquisitions. However, this approach requires experience and can be challenging in the setting of diffuse liver disease (e.g. steatosis, iron deposition), when the signal intensity of the background liver is abnormal. Alternatively, a stepwise approach to imaging interpretation can help narrowing the differential diagnosis into clinically useful categories such as hepatocellular versus non-hepatocellular origin and benign vs malignant lesions. In this lecture, we will review the imaging characteristics of the most commonly encountered hepatic lesions in patients without a history of cirrhosis. We will review the appearance of masses of hepatocellular origin such as focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) and the phenotypic characterization of the latter using MRI to distinguish among three molecularly distinct subtypes (i.e. a) inflammatory hepatocellular adenomas, b) hepatocyte nuclear factor 1 alpha (HNF-1α)–mutated hepatocellular adenomas, and c) β-catenin–mutated hepatocellular adenomas). The advantages and limitations of extracellular versus hepatocellular contrast agents to distinguish FNH and HCA will be discussed. Examples of pitfalls in image interpretation using hepatocellular contrast agents will be presented. Further, the imaging characteristics of hepatic lesions of non-hepatocellular origin will be discussed. Specifically, we will review the imaging features that allow to narrow the differential diagnosis to the most common benign lesions in this group (e.g. cyst, hemangioma, hamartomas, and abscess) versus pre-malignant lesions (e.g. cystadenoma) and malignant lesions (e.g. cystadenocarcinoma, metastasis, cholangiocarcinoma). Some of the MRI findings that suggest a specific malignant process will be presented. During this talk we will emphasize some of the key technical aspects in the clinical MRI protocol that facilitate the diagnosis of these entities and the rationale for selecting some MRI acquisition strategies over others. For example, we will discuss the advantages of the breath-hold imaging acquisitions versus respiratory compensation strategies with respiratory bellows and navigators. Furthermore, we will discuss the use of multi-shot versus single-shot T2-weighted echo train imaging on the image interpretation of patients with focal hepatic lesions and the impact of such acquisitions on the characterization of some of the key features of common hepatic lesions including their signal intensity, presence of internal architecture, and edge sharpness. Similarly, the implications of different acquisition schemes for DWI on image interpretation for patients with focal liver lesions will be presented with special emphasis on the effect of these on the calculation of the apparent diffusion coefficient (ADC) for lesion characterization. We will review the potential advantage of novel acquisition strategies with free-breathing and high-temporal resolution contrast enhanced techniques. This talk will be constructed using a practical 4-step diagnostic algorithm that facilitates the characterization of focal liver lesions. First, this approach will be presented for patients without obvious underlying liver disease. Then, alternative criteria for patients with underlying diffuse hepatic steatosis will be discussed using other organs such as the spleen as the reference organ for signal intensity. Finally, examples of pitfalls in imaging interpretation such as artifacts, atypical presentations of common disease (sclerosed hemangioma, metastasis), uncommon hepatic lesions (i.e. inflammatory pseudotumors, parasitic infections, angiomyolipomas, epithelioid hemangioendothelioma), and pseudo-lesions (e.g. fatty sparing, perfusion abnormalities) that can mimic focal hepatic lesions will be presented. At the end of this talk, the audience will be able to describe the MRI features that distinguish a focal hepatic lesion of hepatocellular versus non-hepatocellular origin and the imaging characteristics of focal nodular hyperplasia and different types of hepatocellular adenoma both on pre-contrast images and contrast enhanced MRI using extracellular and hepatocellular contrast agents. Moreover, the audience will be able to diagnose the most common non-hepatocellular tumors and identify the MRI features associated with malignancy in a focal hepatic lesion.

Acknowledgements

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References

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