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Radiological Category:. Gastrointestinal. Principal Modality (1): Principal Modality (2):. MRI. Angiography. Case Report of patient RE. Submitted by:. Jesse M Proett, MS4. Faculty reviewer:. Sandra Oldham, M.D. Date accepted:. 29 August 2007. Presentation for Radiology 4001.

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Radiological Category:


Principal Modality (1):

Principal Modality (2):



Case Report of patient RE

Submitted by:

Jesse M Proett, MS4

Faculty reviewer:

Sandra Oldham, M.D

Date accepted:

29 August 2007

Presentation for Radiology 4001

case history
Case History

RE is a 62 yo man with cirrhosis and ESLD likely secondary to NASH and portal HTN. He has a MELD score of 18 and is currently on the liver transplant list. On his last appointment he was found to have an elevated AFP of 153.8 (Ref Range <15).

He had core needle biopsies of the liver on 5/4/2005 and also in 2001 in Denver. RE also had a jet ski accident in 1992 resulting in a leg fracture and additional traumas in 2002 and 2004 requiring hand and wrist surgery. There was no reported trauma to the liver other than the biopsies.


Test Your Diagnosis

Which one of the following is your choice for the appropriate diagnosis?

  • Hepatocellular Carcinoma
  • Hepatic Adenoma
  • Hemangioma
  • Focal Nodular Hyperplasia
  • Hepatic Cysts
  • Vascular Abnormality

The liver demonstrates a heterogeneous appearance, and there is some nodularity associated with its contour. Decreased intensity is noted in the left lobe in non-contrast, dynamic, and delayed images. On the dynamic images there is an area of blush seen near the dome. This is felt to represent an area of increased vascularity. There is no evidence of washout, enhancing capsule, or discrete mass lesion. The portal vein is enlarged measuring 16mm.

Findings and Differentials



  • Hepatocellular Carcinoma
  • Hepatic Adenoma
  • Hemangioma
  • Focal Nodular Hyperplasia
  • Vascular Abnormality
Hepatocellular Carcinoma

Lesion must be larger than 3cm

Hyperintense appearance in T2W images

Intense enhancement in the arterial dominant phase

Late washout

Presence of capsule

Tendency to invade the portal and hepatic veins

Rapid growth

Hepatic Adenoma

MRI characteristics are highly variable

Hyperintense on T1 and T2W images due to the presence of fat and/or glycogen

Greater enhancement on T2W images with gadolinium is highly suggestive of the diagnosis

Gadolinium enhancement is early, after which the lesion becomes isointense



Hypointense in T1W images

Hyperintense in T2W images

Smooth, well-demarcated borders

Ring-like enhancement 1 minute after contrast is given

Wash-out, which causes a heterogeneous appearance, and observation of a uniform, thick ring

Focal Nodular Hyperplasia

They are hypo- or isointense on T1W images

Mildly hyper- or isointense on T2W images

Rapid enhancement in the early arterial phase

Washout in the late phase is observed

Central scar tissue shows late enhancement


Vascular Abnormality

MRI is not the ideal modality to diagnose vascular abnormalities

Angiography is the gold standard for diagnosis.

The decreased intensity in the left lobe of the liver through both non-contrast and contrast images does indicate a possible vasculature etiology

The area of high intensity during the dynamic phase suggests increased vascularity with no evidence of a discrete mass

Hepatic US showed no evidence of abnormal blood flow on 4/29/2005 before his core needle biopsy on 5/4/2005.


A diagnosis could not be made based on the MRI.

Further evaluation is needed to rule out malignancy.

A lipiodol study was ordered to visualize a possible HCC.

Lipiodol is an embolic agent used in angiography that allows us to visualize HCC because the embolic agent stays in the mass.



Etiology Acquired Trauma - blunt or penetratingIatrogenic- interventional hepatic procedures, liver biopsies, percutaneous transhepatic cholangiography, ruptured splanchnic artery aneurysms, transhepatic catheterization of bile ducts Tumors - especially hepatocellular carcinomaLiver Transplant Other - Hemangiomas, cirrhosis, regenerating liver nodules, hepatic abscess, Budd- Chiari syndrome, hereditary hemorrhagic telangiectasia, and Ehlers-DanlosCongenital - typically presents very early in life (neonate – 10yo)



Liver biopsy - 52% of the patients who had an arteriogram performed within 1 week following liver biopsy. This rate decreased to 10% if the arteriogram was performed 3 weeks after liver biopsy. These data suggest most small, peripheral, asymptomatic fistulas caused by liver biopsy will disappear spontaneously within 1 month.Trauma - The majority of APFs are due to blunt or penetrating trauma. APFs develop more frequently from penetrating trauma. In some cases the traumatic event can be decades before the presentation of the APF.Cirrhosis - AFPs due to cirrhosis are more commonly peripheral and asymptomatic.



Ultrasound - US is a useful tool in screening patients with cirrhosis or those at risk of acquiring APFs. RE did have an US of his abdomen, and at that time there was no mention of an APF. Finding on his US on 4/29/2005 include portal vein 4.5mm with no detectable flow within the main portal vein.MRI - This is not a diagnostic study for the evaluation of APFs, but there are some subtle signs. APFs can induce focal sparing in the diffuse fatty liver through increased non-lipid-rich arterial flow and decreased lipid-rich portal flow. This means that in the area affected by the APF there can be decreased signal which is what we observed on MRI. Much in the same way gadolinium will also be shunted away from the areas affected by the APF.Angiography - This is the gold standard for diagnosing APFs. Contrast material is seen immediately entering the portal circulation.



Proposed ClassificationType 1-Small, peripheral, intrahepatic fistulas with minimal physiologic consequences- Commonly secondary to liver biopsy- Usually thrombose spontaneously <1mo- Follow with US or embolize if persistent >1mo and/or become symptomaticType 2- Larger, more central fistulas with enough flow to cause elevated portal pressures- Most are secondary to penetrating trauma- Cause portal hypertension and hepatoportal sclerosis and can progress to portal fibrosis- Treat with embolization if possible or surgery for complicated casesType 3- Diffuse intrahepatic APFs- Congenital- Cause severe portal hypertension in infancy- Refer to a specialized pediatric hepatobiliary center. Treatment may consist of hepatic artery ligation, embolization, resection, or liver transplantation



1. Guzman EA, McCahill LE, Rogers FB. Arterioportal fistulas: introduction of a novel classification with therapeutic implications. J Gastrointest Surg 2006;10:543–550.2. Bilgili Y,Firat Z, Pamuklar E, et al. Focal liver lesions evaluated by MR imaging. Diagn Interv Radiol 2006; 12:129-135.3. Bolognesi M, et al. Arterioportal fistulas in patients with liver cirrhosis: usefulness of color doppler US for screening. Radiology 2000; 216:738–743. 4. Choi BI, Lee KH, Han JK, Lee JM, et al. Hepatic arterioportal shunts: dynamic CT and MR features. Kor J Radiol 2002;3:1–15. 5. UpToDate