- An MRI or triple-phase CT should be obtained in patients with cirrhosis with an ultrasound showing a lesion of >1cm.
- Patients with chronic liver disease, especially with cirrhosis, who present with a solid FLL are at a very high risk for having HCC and must be considered to have HCC until otherwise proven.
- A diagnosis of HCC can be made with CT or MRI if the typical characteristics are present: a solid FLL with enhancement in the arterial phase with washout in the delayed venous phase should be considered to have HCC until otherwise proven.
- If an FLL in a patient with cirrhosis does not have typical characteristics of HCC, then a biopsy should be performed in order to make the diagnosis.
- MRI or CT should be obtained if CCA is suspected clinically or by ultrasound.
- A liver biopsy should be obtained to establish the diagnosis of CCA if the patient is non operable.
Suspected hepatocellular adenoma
- Oral contraceptives, hormone-containing IUDs, and anabolic steroids are to be avoided in patients with hepatocellular adenoma.
- Obtaining a biopsy should be reserved for cases in which imaging is inconclusive and biopsy is deemed necessary to make treatment decisions.
- Pregnancy is not generally contraindicated in cases of hepatocellular adenoma < 5 cm and an individualized approach is advocated for these patients.
- In hepatocellular adenoma ≥ 5 cm, intervention through surgical or nonsurgical modalities is recommended, as there is a risk of rupture and malignancy.
- If no therapeutic intervention is pursued, lesions suspected of being hepatocellular adenoma require follow-up CT or MRI at 6- to 12-month intervals. The duration of monitoring is based on the growth patterns and stability of the lesion over time.
- Clinical variants of hepatocellular adenoma
- Liver adenomatosis.
- Multiple adenomas, defined as between > 3 and ≥ 10 lesions, are collectively referred to as liver adenomatosis. These multiple lesions have identical clinical, histological, and radiographic features as hepatocellular adenomas and are managed in the same manner.
- Telangiectatic hepatocellular adenoma
- Previously known as telangiectatic focal nodular hyperplasia, telangiectatic hepatocellular adenoma (THCA) has recently been reclassified as a subcategory of inflammatory hepatocellular adenoma. THCA should be managed as aggressively as hepatocellular adenomas as they are likely to be symptomatic, prone to hemorrhage, and may contain focal areas of necrosis. The high likelihood of hemorrhage combined with an unknown potential of transformation to HCC makes surgery the recommended treatment.
- Liver adenomatosis.
Suspected hemangioma
- An MRI or CT scan should be obtained to confirm a diagnosis of hemangioma.
- Liver biopsy should be avoided if the radiologic features of a hemangioma are present.
- Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with a hemangioma.
- Regardless of the size, no intervention is required for asymptomatic hepatic hemangiomas. Symptomatic patients with impaired quality of life can be referred for surgical or nonsurgical therapeutic modalities by an experienced team.
Suspected focal nodular hyperplasia
- An MRI or CT scan should be obtained to confirm a diagnosis of FNH. A liver biopsy is not routinely indicated to confi rm the diagnosis.
- Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with FNH.
- Asymptomatic FNH does not require intervention.
- Annual US for 2-3 years is prudent in women diagnosed with FNH who wish to continue OCP use. Individuals with a firm diagnosis of FNH who are not using OCP do not require follow-up imaging.
- Liver biopsy is required to confirm the diagnosis of NRH.
- Pregnancy and the use of oral contraceptives or anabolic steroids are not contraindicated in patients with an NRH.
- Asymptomatic NRH does not require intervention.
- Management of NRH is based on diagnosing and managing any underlying predisposing disease processes.
- A hepatic cyst identified on US with septations, fenestrations, calcifications, irregular walls, or daughter cysts should prompt further evaluation with a CT or MRI.
- Asymptomatic simple hepatic cysts should be observed with expectant management.
- Aspiration of asymptomatic, simple hepatic cysts is not recommended.
- Symptomatic simple hepatic cysts may be managed with laparoscopic deroofing rather than aspiration and sclerotherapy, dictated based on availability of local expertise.
- Routine fluid aspiration is not recommended when BCA is suspected because of limited sensitivity and the risk of malignant dissemination.
- Imaging characteristics suggestive of BC or BCA, such as internal septations, fenestrations, calcifications, or irregular walls, should lead to referral for surgical excision.
- Complete surgical excision, by an experienced team, is recommended if BC or BCA is suspected.
- Routine medical therapy with mammalian target of rapamycin inhibitors or somatostatin analogs is not recommended.
- Aspiration, deroofing, resection of a dominant cyst(s) can be performed based on the patient’s clinical presentation and underlying hepatic reserve.
- Liver transplantation with or without kidney transplantation can be considered in patients with refractory symptoms and significant cyst burden.
- MRI is preferred over CT for concomitant evaluation of the biliary tree and cystic contents.
- Monotherapy with antihelminthic drugs is not recommended in symptomatic patients who are surgical or percutaneous treatment candidates.
- Adjunctive therapy with antihelminthic therapy is recommended in patients undergoing PAIR or surgery, and in those with peritoneal rupture or biliary rupture.
- Percutaneous treatment with PAIR is recommended for patients with active hydatid cysts who are not surgical candidates, who decline surgery, or who relapse after surgery.
- Surgery, either laparoscopic or open, based on available expertise, is recommended in complicated hydatid cysts with multiple vesicles, daughter cysts, fistulas, rupture, hemorrhage, or secondary infection.
- Heterogeneous; hyperechoic if steatotic but anechoic center if hemorrhage
- Well demarcated with peripheral enhancement; homogenous more often than heterogeneous; hypodense if steatotic, hyperdense if hemorrhagic
- HNF1 α : signal lost on chemical shift; moderate arterial enhancement without persistent enhancement during delayed phase
- IHCA: markedly hyperintense on T2 with stronger signal peripherally; persistent enhancement in delayed phase
- β – Catenin: inflammatory subtype has same appearance as IHCA; noninflammatory is heterogeneous with no signal dropout on chemical shift, isointense of T1 and T2 with strong arterial enhancement and delayed washout
- Variable appearance
- Hypo- to isoattenuating
- T1: heterogeneous and well-defined iso- to hyperintense mass. Strongly hyperintense with persistent contrast enhancement in delayed phase
- Hyperechoic with well-defined rim and with few intranodular vessels
- Discontinuous peripheral nodular enhancement isoattenuating to aorta with progressive centripetal fi ll-in
- T1: hypointense; discontinuous peripheral enhancement with centripetal fi ll-in
- T2: hyperintense relative to spleen
- Generally isoechoic
- Central scar. Arterial phase shows homogenous hyperdense lesion; returns to pre contrast density during portal phase that is hypo- or isodense
- T1: isointense or slightly hypointense. Gadolinium produces early enhancement with central scar enhancement during delayed phase
- T2: slightly hyperintense or isointense
- Isoechoic / hyperechoic
- Nonenhancing nodules, sometimes hypodense, with variable sizes (most sub-centimeter)
- T1: hyperintense
- T2: varied intensity (hypo / iso / hyperintense)
- Anechoic, homogeneous,fluid filled. Smooth margins
- Well-demarcated, water-attenuated, smooth lesion without an internal structure. No enhancement with contrast
- Well-defined, homogeneous lesion. No enhancement with contrast.
- T1: hypointense signal intensity
- T2: hyperintense signal intensity
- Irregular walls, internal septations forming loculi
- Heterogeneous septations, internal septations, irregular papillary growths, thickened cyst walls
- May appear heterogeneous.
- T1: Hypointense signal intensity
- T2: Hyperintense signal intensity
- Multiple hepatic cysts, similar in characteristics to SHC US findings
- Multiple hepatic cysts, similar in characteristics to SHC CT findings
- Multiple hepatic cysts, similar in characteristics to SHC MRI findings
- May appear similar to SHC. Progress to develop thick, calcified walls, hyperechoic / hypoechoic contents. Daughter cysts in periphery.
- Hypodense lesion with hypervascular pericyst wall, distinct endocyst wall. Calcified walls and septa easily detected. Daughter cysts seen peripherally within mother cyst.
- T1: Hypointense signal intensity of cyst contents.
- T2: Hyperintense signal intensity of cyst contents.
- Hypointense rim on T2.
- Daughter cysts seen peripherally within mother cyst. Collapse parasitic membranes seen as floating linear structures within cyst.