Focal steatosis (focal fatty infiltration) is an area of localized triglyceride accumulation in liver parenchyma and is not a true mass or neoplasm. It results from focal intracellular fat (triglyceride) accumulation in normal hepatocytes. It occurs in typical locations: segment 4 (adjacent to falciform ligament), gallbladder fossa, periportal bifurcation area, and subcapsular region. The most important diagnostic feature is the absence of mass effect — hepatic veins and portal vein branches pass through the lesion with normal course, the lesion does not displace or compress vessels. Signal drop on opposed-phase images on chemical shift MRI (in-phase/opposed-phase) is pathognomonic. Prevalence is high and is associated with metabolic syndrome, obesity, diabetes, and alcohol use. No treatment is required; however, differentiation from mass lesions is critical.
Age Range
20-80
Peak Age
50
Gender
Equal
Prevalence
Very Common
Focal steatosis is a focal form of intracellular triglyceride accumulation in hepatocytes. The pathophysiological mechanism is related to the dual blood supply of the liver: differences in blood flow between the hepatic artery and portal vein cause hepatocytes in certain regions to be exposed to different metabolic environments. Typical locations such as adjacent to the falciform ligament and gallbladder fossa receive systemic venous blood rather than insulin-rich portal blood due to aberrant gastric or cystic venous drainage; hepatocytes in these regions are exposed to different hormonal and metabolic signals, leading to focal fat accumulation. The cause of signal drop on opposed-phase imaging is the coexistence of water and fat protons within the same voxel — on opposed-phase, the signals of these protons cancel each other (intravoxel signal cancellation). On CT, focal steatosis appears as a hypodense area because fat lowers X-ray attenuation. On US, fat accumulation changes acoustic impedance creating a hyperechoic area. The absence of mass effect reflects that the lesion does not disrupt hepatocyte architecture — only the intracellular composition changes.
Marked signal drop in the focal area on opposed-phase images compared to in-phase on chemical shift MRI — intravoxel signal cancellation due to intracellular fat accumulation. This finding, combined with absence of mass effect and typical location, is pathognomonic for focal steatosis diagnosis.
On chemical shift MRI (in-phase and opposed-phase T1-weighted gradient echo sequences), marked signal drop in the lesion on opposed-phase images compared to in-phase. The amount of signal loss is proportional to intracellular fat content — maximum signal cancellation occurs at 50% fat content. Surrounding normal parenchyma is not affected by this phase difference (if it does not contain fat). India ink artifact is not seen at the lesion margin because fat is intracellular — water and fat coexist within the same voxel.
Report Sentence
Marked signal drop is observed in the indicated area of the liver on opposed-phase images compared to in-phase, consistent with intracellular fat accumulation (focal steatosis); no mass effect detected.
Focal hypodense area on non-contrast CT — lower density than surrounding normal parenchyma. Normal liver density is 55-65 HU, while density drops to 30-40 HU in the focal steatosis area. Geographic (map-like) irregular margins are typical — does not show round/oval mass shape. Hepatic and portal vein branches pass through the lesion with normal course (no mass effect). In contrast phases, the lesion enhances at the same rate as surrounding parenchyma — no enhancement difference occurs.
Report Sentence
Focal hypodense area with geographic irregular margins in liver segment 4 on non-contrast CT with hepatic veins passing through with normal course; consistent with focal steatosis.
Focal hyperechoic area on B-mode US — brighter than surrounding normal parenchyma. Seen with geographic margins in typical location (segment 4, gallbladder fossa). No posterior acoustic shadowing. Hepatic and portal vein branches pass through the lesion with normal course (no mass effect). Homogeneous internal echo pattern — does not show internal heterogeneity like a solid mass. In the setting of diffuse steatosis, the focal steatosis area may show the same echogenicity as parenchyma and be indistinguishable.
Report Sentence
Focal hyperechoic area with geographic margins at typical location in the liver on US with vascular structures passing through normally; consistent with focal steatosis.
On standard T1-weighted images, the focal steatosis area appears isointense or mildly hyperintense relative to surrounding parenchyma. Mild T1 hyperintensity is expected because fat protons have short T1. However, on fat-suppressed (fat-sat) T1 sequences, signal drop is observed in the focal steatosis area — the area becomes hypointense due to suppression of fat protons. This finding strengthens the diagnosis when evaluated together with chemical shift.
Report Sentence
Signal drop is observed in the relevant area on fat-suppressed T1 sequences, confirming intracellular fat content.
The focal steatosis area appears isointense or mildly hyperintense relative to surrounding parenchyma on T2-weighted images. Does not show marked T2 hyperintensity — this feature distinguishes it from hemangioma and cysts. Signal drop may be observed in the focal steatosis area on T2 fat-suppressed (STIR or fat-sat T2) sequences.
Report Sentence
The area shows isointense appearance to surrounding parenchyma on T2-weighted images with no significant T2 hyperintensity; no finding consistent with hemangioma or cyst detected.
On contrast-enhanced CT in the portal venous phase, the focal steatosis area enhances at the same rate as surrounding parenchyma — no or minimal enhancement difference. The same enhancement pattern is seen in the arterial phase. This finding is a critical criterion confirming that focal steatosis is not a real mass and its vascular architecture is not disrupted. Malignant lesions (metastasis, HCC) show different enhancement patterns.
Report Sentence
In contrast phases, the area demonstrates the same rate of enhancement as surrounding parenchyma, consistent with a pattern excluding mass lesion.
Focal steatosis does not show diffusion restriction on DWI. ADC values are close to normal liver parenchyma. This finding confirms the area is not a highly cellular neoplasm. While malignant lesions (metastasis, HCC) show marked diffusion restriction on DWI, focal steatosis shows normal diffusion.
Report Sentence
No diffusion restriction is detected in the relevant area on DWI with ADC values within normal limits; no finding favoring neoplastic process.
Criteria
Localized in segment 4 (adjacent to falciform ligament), gallbladder fossa, portal bifurcation, or subcapsular region
Distinct Features
Most common form (70-80%). Typical location facilitates diagnosis. Explained by aberrant venous drainage hypothesis. Usually no additional workup needed.
Criteria
In any liver segment outside typical locations
Distinct Features
May be confused with mass lesion. MRI chemical shift is critical for diagnosis. Opposed-phase signal drop + absence of mass effect + normal enhancement confirms diagnosis. Short-term follow-up may be considered.
Criteria
Focal fat accumulation in multiple areas — heterogeneous form of diffuse steatosis
Distinct Features
May be confused with multiple metastases. Opposed-phase signal drop in all areas, absence of mass effect, and normal enhancement are differentiating. Absence of diffusion restriction on DWI excludes metastasis.
Distinguishing Feature
Metastasis shows diffusion restriction on DWI (low ADC), focal steatosis does not. Metastasis causes mass effect (vessel displacement), focal steatosis does not. Metastasis does not show signal drop on opposed-phase. Metastasis shows different enhancement pattern (rim/heterogeneous).
Distinguishing Feature
HCC shows arterial enhancement + washout in portal venous/delayed phase; focal steatosis shows same enhancement as surrounding parenchyma. HCC causes mass effect, may show capsule. HCC shows diffusion restriction. Some HCCs may contain intratumoral fat but mass morphology and enhancement pattern are differentiating.
Distinguishing Feature
Adenoma is round/oval mass-shaped and causes mass effect; focal steatosis has geographic margins and no mass effect. Adenoma shows arterial enhancement. HNF1α adenoma may contain diffuse intracellular fat but mass morphology is present.
Distinguishing Feature
Focal sparing is normal parenchyma in a diffusely steatotic liver (no fat); focal steatosis is a fat-containing area in a normal liver. Focal sparing appears hyperdense on CT (surrounding is fatty), focal steatosis appears hypodense (surrounding is normal). On MRI, focal sparing does not show signal drop on opposed-phase while surrounding steatotic parenchyma shows signal drop.
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
no-follow-upFocal steatosis is a benign condition and requires no treatment. Diagnosis can be definitively made with MRI chemical shift imaging. No additional workup is needed when the triad of typical location + absence of mass effect + opposed-phase signal drop is present. Underlying metabolic risk factors (obesity, diabetes, dyslipidemia, alcohol) should be evaluated and managed appropriately. Short-term follow-up (3-6 months) may be considered for atypical location or suspicious morphology.
Focal steatosis is a benign pseudolesion requiring no treatment or follow-up. Evaluation of the underlying metabolic condition is recommended. It is not a true neoplasm.