2023 ARRS ANNUAL MEETING - ABSTRACTS

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E1481. Liver Lesions With Progressive Enhancement: What You Should Know About Flo!
Authors
  1. Tony Lin; Yale New Haven Hospital
  2. Jay Pahade; Yale New Haven Hospital
  3. Richard Do; Memorial Sloan Kettering Cancer Center
  4. Kathryn Fowler; UC San Diego Health
  5. Natally Maciel; Memorial Sloan Kettering Cancer Center
  6. Christine Menias; Mayo Clinic
  7. Sandeep Arora; Yale New Haven Hospital
Background
Hepatic hemangioma is the most common benign solid hepatic lesion. Radiologists are taught to recognize the classic appearance of discontinuous peripheral nodular arterial phase enhancement with “filling in” of contrast. However, not all lesions that demonstrate progressive enhancement are benign. The purpose of this exhibit is to introduce readers to other hepatic lesions which demonstrate progressive enhancement and to recognize worrisome features.

Educational Goals / Teaching Points
Major goal is to discuss progressive/delayed enhancement in various liver tumors with a focus on pathophysiology and overlap of imaging findings between benign and malignant entities. Lesions include: hemangiomas (cavernous, capillary, sclerosing, anastomosing, hepatic small vessel neoplasm), sarcomatoid mesothelioma, angiosarcoma, epithelioid hemangioendothelioma, inflammatory myofibroblastic tumor, peliosis, atypical hepatocellular carcinoma (HCC), cholangiocarcinoma/mixed tumors, rare infections and metastases.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Hemangiomas have proliferation of abnormal vessels. These demonstrate progressive enhancement due to slow filling of contrast in the vascular spaces but are usually easily differentiated from other lesions using concurrent imaging features like marked T2 hyperintensity, peripheral nodular enhancement and enhancement paralleling blood pool. Other tumors like hepatic angiosarcoma and epithelioid hemangioendothelioma also have abnormal vasculature. Many liver tumors demonstrate central necrosis (ischemia) or fibrosis in which contrast agents may progressively accumulate. Fibrosis has large extracellular spaces and acts like a “sponge” that retains contrast. Ischemic areas are associated with sluggish blood flow through which contrast is slow to leave. Many malignancies tend to be ischemic/fibrotic in their centers while having an arterialized hypercellular periphery. Therefore, the central stroma enhances in a delayed pattern following injection of contrast. By comparison, the periphery has a relatively small extracellular compartment, is characterized by brisk blood flow and does not trap the agent. Fibrosis may also be seen with nonmalignant entities like myofibroblastic tumor. Fibrotic tumors may enhance more in the delayed phase than "blood pool". Lexicon: For a formalized lexicon, we are referring to Liver Reporting and Data System (LI-RADS) v 2018, according to which delayed central enhancement is a targetoid feature of LR-M classification (probably or definitely malignant, not specific for HCC). LI-RADS suggests that progressive enhancement terminology be reserved for description of benign entities like hemangiomas and not be confused with delayed central enhancement. “Delayed” refers to all post-arterial extracellular phases, and not to the delayed phase only. “Central” refers to inner portions of the observation but is not meant to imply the geometric center.

Conclusion
Benign and malignant liver lesions can demonstrate progressive/central enhancement with overlapping features. Any lesion that cannot be classified as definitely benign should be biopsied and/or followed-up.