Evaluation of a Patient with Liver Mass

Educational Objectives

The goal of this program is to improve evaluation of liver mass. After hearing and assimilating this program, the clinician will be better able to:

1. Differentiate among hemangiomas, hepatocellular adenomas, and cystic lesions.
2. List the predominant features of focal nodular hyperplasia.

Summary

Focal liver lesions (FLLs): prevalence ranges from 15% to 20%, and these lesions are typically detected through quick imaging, eg, ultrasonography or contrast-enhanced portal venous phase computed tomography (CT); clinical decisions are based on pretest probability; develop a clinical index of suspicion; underlying liver disease is the biggest risk factor for serious liver lesions; rule out hepatocellular carcinoma (HCC) or cholangiocarcinoma in patients with FLLs with cirrhosis or significant portal hypertension; patients without advanced liver disease are more likely to have benign lesions

The pretest probability: involves a thorough medical history and physical examination (PE); it assesses for liver disease risk factors, eg, fatty liver disease, chronic viral hepatitis, alcohol use disorder, presence of cirrhosis; other than primary liver lesions are common; evaluate the history of malignancy (primarily liver-metastasizing lesions) and medications relevant to the diagnostic strategy (especially for solid liver lesions, eg, hepatocellular adenoma (HCA), focal nodular hyperplasia [FNH]); hormonal medications and a history of foreign travel can affect the diagnostic approach; evaluate clinical symptoms; PE helps detect hepatomegaly or specific liver masses; check for liver enzymes or signs of liver synthetic dysfunction first; tumor markers are checked when the clinical index of suspicion for malignancy is high

Evaluation: liver-specific cross-sectional imaging is usually recommended (focusing on perfusion characteristics); avoid ordering another CT with intravenous contrast; get a CT liver mass protocol to assess the late arterial phase, portal venous phase (differentiate solid lesions), and the delayed phase; the hepatobiliary phase helps determine if lesions have bile acid uptake; cross-sectional imaging study — choose magnetic resonance imaging (MRI) or CT depending on availability, comfort, and the experience of the radiologist; patient factors include body habitus, claustrophobia, and medical implants; consult a radiologist, hepatobiliary surgeon, or a multidisciplinary tumor board when the lesion is unclear; may require invasive testing (eg, biopsy)

Recommendation from the American College of Gastroenterology: obtain a thorough history and clinical examination, and set up pretest probability; workup for serious liver lesions in patients at high risk for HCC or cholangiocarcinoma; consider imaging strategies (eg, positron emission tomography) in patients with a history of malignancy and metastatic lesion

Hemangioma: the most common benign liver lesions; they occur in ≈20% of the population (primarily in women); no strong hormonal association; usually present since birth (may grow over time); mostly small and solitary (can be multiple); large hemangiomas (>10 cm) can cause symptoms; can cause consumptive coagulopathy (similar to disseminated intravascular coagulation); diagnosis — imaging is used; biopsy is not needed (can cause bleeding); the imaging phenotypes vary; flash filling or capillary hemangioma — small lesions that fill up in the arterial phase and hold onto it even in the postcontrast or venous phase; classical cavernous hemangioma — larger lesions that slowly fill with blood from the periphery to the center and hold onto it in the postcontrast phase; sclerosing hemangioma — has a central scar and can cause capsular retraction; resembles an early-developing HCC or intrahepatic cholangiocarcinoma (may require a biopsy)

Management: small and asymptomatic; no need for surveillance; lack of malignant potential; hormonal therapy changes needed; complications are rare, eg, rupture, hemorrhage, consumptive coagulopathy; refer to a hepatobiliary surgeon for resection or local regional therapy

Hepatocellular adenoma: a benign proliferation of mature hepatocytes; more common in women, with a strong hormonal component (women [eg, oral contraceptive pills] and men [especially those using anabolic steroids]); associated with fatty liver disease and glycogen storage disease; usually asymptomatic; higher risk for complications compared with hemangiomas, eg, hemorrhage (especially if large); more peripherally based; risk for malignant transformation (in a particular subset)

Adenoma types: ≈80% are hepatic nuclear factor 1 (HNF1) type or Janus kinase 2 activated (less likely to cause bleeding or growth complications); adenomas with β-catenin mutations (common in men) pose a high risk for malignant transformation, requiring immediate intervention

Imaging phenotypes of adenomas: inflammatory adenoma — radiologists can distinguish lesions with classical features; a bright appearance on T1 imaging and an atoll sign on T2 imaging (dark central area and lighter peripheral area); these lesions do not share malignant features, eg, capsular washout and retraction like other serious lesions; common in women, especially those with obesity or who use OCPs; HNF1 adenomas — usually multiple; often found with underlying fatty liver disease; appear dark (fatty infiltration) in out-of-phase imaging on MRI; can exhibit malignant features, eg, portal venous washout and capsule; β-catenin mutated lesions — common in men and are most concerning; share similar T1 and T2 hyperintensity features; a biopsy may help rule out HCC

Management: need definitive treatment; women with small and asymptomatic adenomas <5 cm — low risk for bleeding and malignant transformation; managing risk factors and intervening, eg, stopping hormonal therapy, weight loss (in obesity) can help regress or eliminate adenomas; women with adenomas >5 cm — the first step is risk factor assessment and intervention; assess after a timeline (usually 6 mo) and continue if there is a response (lesions become <5 cm); need definitive treatment (if no response, eg, resection, embolization [if resection is not possible]); men with adenomas — often have β-catenin mutations with a high risk for malignant transformation; genetic mutation causes 50% to 80% of cases; surgical resection or embolization is recommended; risk factor assessment is important as lesions may recur or new ones may grow

Preconception counseling: lesions >5 cm are associated with a high risk for growth and complications during pregnancy; consider definitive treatment for lesions <5 cm with high risk for growth, peripherally based, or intralesional hemorrhage; order ultrasonography every 6 to 12 wk; a resection or embolization procedure at 26 wk is recommended if the lesion attained the threshold size of 6.5 cm and has high-risk features; perform surgical intervention during pregnancy in case of serious complication; stabilize the patient, and embolization can slow the bleeding rate if rupture occurs outside the pregnancy period

Focal nodular hyperplasia (FNH): hepatic tissue proliferation associated with a localized vascular abnormality; predominantly in women (without hormonal predisposition); has no malignant potential; an area that actively absorbs bile acid can help differentiate it from adenoma in MRI sequences; asymptomatic; conservative management; surveillance imaging or hormonal therapy changes not needed; surgical intervention is reserved for symptomatic cases

Cystic lesions: simple hepatic cysts, the most common type, are thin-walled, fluid-filled structures lined by cuboidal bile duct epithelial cells; single or multiple; start at birth (grow with age); slight female predominance (no hormonal contribution); benign; appear as anechoic cysts with no internal vascularity and septations on ultrasonography; bright appearance on T1 imaging; can grow and are asymptomatic; single or multiple cysts in the liver (without any evidence of a generalized cystic disease) can be left untreated; no routine surveillance is necessary; unroofing of the cyst or aspiration may be needed for large cysts compressing the stomach or causing early satiety, which are recommended over injection, sclerotherapy, and aspiration (higher risk for recurrence)

Hydatid cysts: caused by a parasitic infection (Echinococcus granulosus); limited geographical area presence; humans are accidental intermediate hosts (exposed to the parasite by ingesting infected animal meat or eggs); different imaging phenotypes based on how active and long the disease has been; classic presentations include multiple cysts within the liver that can have internal septations; calcifications may occur depending on chronicity; may occur in unexpected sites, eg, the mesentery or lungs; management — combination of medical therapy and surgical intervention; albendazole and mebendazole for a few months before and after intervening on the cysts can help prevent complications; consider surgical intervention with enucleation or complete removal of the cyst; conservative therapy is needed in complex cases; may consider a multidisciplinary discussion

Readings

Bajenaru N, Balaban V, Savulescu F, et al. Hepatic hemangioma — Review. J Med Life. 2015;8(Spec Issue):4–11; Frenette C, Mendiratta-Lala M, Salgia R, et al. ACG Clinical guideline: Focal liver lesions. Am J Gastroenterol. 2024;119(7):1235-1271. doi:10.14309/ajg.0000000000002857; Gavara CG, Lopez-Andujar R, Ibanez TB, et al. Review of the treatment of liver hydatid cysts. World J Gastroenterol. 2015;21(1):124–131. doi:10.3748/wjg.v21.i1.124; LeGout JD, Bolan CW, Bowman AW, et al. Focal nodular hyperplasia and focal nodular hyperplasia–like lesions. RadioGraphics. 2022;42(4). doi:10.1148/rg.210156; Wang X, Zhang X. Hepatocellular adenoma: Where are we now? World J Gastroenterol. 2022;28(14):1384–1393. doi:10.3748/wjg.v28.i14.1384.

Disclosures

For this program, members of the faculty and planning committee reported nothing relevant to disclose.

Acknowledgements

Dr. Hassan was recorded at the 13th Annual Western Michigan Liver Round-Up, held on October 11, 2024, in Grand Rapids, MI, and presented by the University of Michigan Health. For information on future CME activities from this presenter, please visit medschool.umich.edu/offices/cme. Audio Digest thanks the speakers and presenters for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0.75 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0.75 CE contact hours.

Lecture ID:

GE390302

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.