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AJR 2005; 184:83-90
© American Roentgen Ray Society


Pictorial Essay

Transient Hepatic Attenuation Differences in Focal Hepatic Lesions: Dynamic CT Features

Hyoung Jung Kim1, Ah Young Kim1, Tae Kyoung Kim1, Jae Ho Byun1, Hyung Jin Won1, Kyoung Won Kim1, Yong Moon Shin1, Pyo Nyun Kim1, Hyun Kwon Ha1 and Moon-Gyu Lee1

1 All authors: Department of Radiology, Asan Medical Center, University of Ulsan College of Medicine, 388-1, Poongnap-dong, Songpa-Ku, Seoul, South Korea.

Received March 9, 2004; accepted after revision June 14, 2004.

 
Address correspondence to A. Y. Kim.


Introduction
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 
The widespread use of dual-phase dynamic CT has led to an improvement in the characterization and detection of focal hepatic lesions by highlighting the dynamic contrast-enhancement features. Transient hepatic attenuation difference (THAD) is an attenuation difference of the liver appearing during bolus-enhanced dynamic CT and not corresponding to mass [1]. THAD is generally seen as an area of high attenuation on the hepatic arterial phase image that returns to normal attenuation on the portal venous phase image. THADs that are associated with hepatic tumors are generally characteristic of malignant tumors. However, benign focal lesions, such as hemangiomas, focal nodular hyperplasia, pyogenic abscesses, and focal eosinophilic necrosis, may accompany THADs. Hepatic hemodynamic alterations caused by liver cirrhosis and aberrant blood supply may show findings similar to those of THADs in focal hepatic lesions.


Malignant Focal Hepatic Lesions
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 
Hepatocelluar Carcinoma
Hepatocellular carcinoma (HCC) is the most common primary hepatic tumor associated with the THAD. Okuda et al. [2] reported that arterioportal shunts occurred in 63% of cases of HCC (second-order and larger portal vein in 41% and third-order and smaller branch in 22%). Various routes, such as the transplexal, transsinusoidal, transvasal, or transtumoral route, may be the communication between the hepatic artery and the portal vein. However, if a HCC is located in the peripheral portion of the liver and is small, it rarely compromises the portal or hepatic vein and may show THAD through the transtumoral route (Figs. 1A, 1B, and 1C). In a study using dynamic CT and focused on HCCs less than 3 cm, Byun et al. [3] noted THAD in only 4% of the tumors.



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Fig. 1A. 40-year-old man with hepatocellular carcinoma (HCC). Hepatic arterial phase CT scan shows small high-attenuation tumor (arrow) in posterior segment and homogeneous high-attenuation area (arrowheads) peripheral to tumor. It is difficult to estimate extent of tumor on hepatic arterial phase image.

 


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Fig. 1B. 40-year-old man with hepatocellular carcinoma (HCC). Portal venous phase CT scan shows discrete extent of HCC (arrow) because transient hepatic attenuation difference no longer exists.

 


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Fig. 1C. 40-year-old man with hepatocellular carcinoma (HCC). Hepatic angiogram shows opacification of portal vein branch (arrow) near tumor through transtumoral route.

 

Peripheral Cholangiocarcinoma
When cholangiocarcinoma is located adjacent to the hilar portion of the liver, it frequently shows THAD of lobar distribution on hepatic arterial phase images (Figs. 2A, 2B, and 2C). THAD is an important indirect sign of vascular invasion. Peripheral cholangiocarcinoma may have a risk of vascular involvement, especially in the peripheral branch of the portal vein (Figs. 3A and 3B). The reported incidence of THAD in peripheral cholangiocarcinoma on dynamic CT is from 29% to 45% [4, 5].



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Fig. 2A. 53-year-old man with cholangiocellular carcinoma. Hepatic arterial phase CT scans show diffuse high attenuation in left lobe (A) and low-attenuation mass with peripheral rim enhancement (B). Left portal vein is partially obliterated by tumor (arrow, B). Transient hepatic attenuation difference (THAD) on hepatic arterial phase CT scan is due to increased arterial flow as compensation for compromised portal vein flow.

 


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Fig. 2B. 53-year-old man with cholangiocellular carcinoma. Hepatic arterial phase CT scans show diffuse high attenuation in left lobe (A) and low-attenuation mass with peripheral rim enhancement (B). Left portal vein is partially obliterated by tumor (arrow, B). Transient hepatic attenuation difference (THAD) on hepatic arterial phase CT scan is due to increased arterial flow as compensation for compromised portal vein flow.

 


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Fig. 2C. 53-year-old man with cholangiocellular carcinoma. Portal venous phase CT scan still shows diffuse high attenuation in left lobe and parenchymal atrophy. Left hepatic vein branch (arrow) is not opacified because of tumor invasion (not shown). Persistent THAD up to portal venous phase may be due to concurrent obstruction of left hepatic vein branch.

 


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Fig. 3A. 62-year-old man with cholangiocellular carcinoma. Hepatic arterial phase CT scan shows peripheral rim enhancement of tumor and associated wedge-shaped high-attenuation area (arrows) in posterior segment.

 


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Fig. 3B. 62-year-old man with cholangiocellular carcinoma. Portal venous phase CT scan shows progressive tumor enhancement and near-isoattenuation area peripheral to tumor.

 

Metastasis
To the best of our knowledge, there is no report of the incidence and pathogenesis of THAD of hepatic metastasis. However, some of the metastases may accompany the wedge-shaped high-attenuation areas on hepatic arterial phase images. Hypervascular metastases such as islet cell tumors, carcinoids, renal cell carcinoma, and breast cancer, may show THAD (Figs. 4A and 4B). If we consider that the various tumors eliciting THAD are hypervascular, it is not surprising that hypervascular metastasis shows THAD.



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Fig. 4A. 52-year-old man with metastases from neuroendocrine tumor of pancreas. Hepatic arterial phase CT scan shows two hypervascular hepatic metastases associated with peripheral wedge-shaped high-attenuation area (arrows).

 


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Fig. 4B. 52-year-old man with metastases from neuroendocrine tumor of pancreas. Portal venous phase CT scan shows near-isoattenuation areas peripheral to tumors. Upper portion of pancreatic mass is also visualized (arrows).

 


Benign Focal Hepatic Lesions
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 
Hemangioma
Hepatic hemangiomas may show THAD, probably because of an associated arterioportal shunt [6]. Although, to our knowledge, no report gives pathologic proof of the transtumoral route of an anteroportal shunt, this route may be the potential communication between the hepatic artery and the portal vein (Figs. 5A and 5B). The arterioportal shunt of a hemangioma is somewhat different from that of an HCC because most HCCs accompanying an arterioportal shunt tend to be large tumors with portal vein invasion. In small hepatic lesions less than 3 cm, the incidence of arterioportal shunt is significantly higher in a small hemangioma (21%) than in a small HCC (4%) [3].



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Fig. 5A. 63-year-old man with hemangioma. Hepatic arterial phase CT scan shows homogeneous high-attenuation mass in left lobe and concomitant transient hepatic attenuation difference (THAD). Peripheral small portal vein branch (arrow) is visualized early in area of THAD.

 


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Fig. 5B. 63-year-old man with hemangioma. On portal venous phase CT scan, THAD no longer exists.

 

Focal Nodular Hyperplasia
Focal nodular hyperplasia is supplied by an anomalous enlarged hepatic artery and is neither supplied nor drained by the portal vein. We experienced a case of focal nodular hyperplasia associated with a transient low attenuation peripheral to the tumor on the hepatic arterial phase image (Figs. 6A and 6B).



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Fig. 6A. 28-year-old man with focal nodular hyperplasia. Hepatic arterial phase CT scan shows high-attenuation mass in anterior segment. Low-attenuation area is noted peripheral to tumor (arrows). It may be assumed that anomalous enlarged hepatic artery "siphons" blood flow to peripheral portion of tumor.

 


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Fig. 6B. 28-year-old man with focal nodular hyperplasia. On portal venous phase CT scan, tumor still shows high attenuation, and subtle low-attenuation transient hepatic attenuation difference (THAD).

 

Pyogenic Abscess
The incidence of THAD of a pyogenic abscess shows some variation according to the results of researchers (30–67%) [7, 8]. The THAD in a pyogenic abscess may be attributed to portal vein thrombosis or stenosis due to periportal inflammation [7] (Figs. 7A, 7B, and 7C) or localized hepatic venous obstruction caused by acute inflammation of the hepatic parenchyma surrounding the abscess [8]. Most THADs of pyogenic abscesses—as well as the pyogenic abscess itself—decrease in size or disappear after antibiotic treatment, which alleviates the inflammation of the portal tract (Fig. 7C).



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Fig. 7A. 45-year-old man with pyogenic abscess. Hepatic arterial phase CT scan shows wedge-shaped high-attenuation area containing target lesion in right lobe. Note partial thrombosis of portal vein branch (arrow).

 


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Fig. 7B. 45-year-old man with pyogenic abscess. On portal venous phase CT scan, transient hepatic attenuation difference (THAD) associated with pyogenic abscess disappears.

 


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Fig. 7C. 45-year-old man with pyogenic abscess. On follow-up hepatic arterial phase CT scan obtained 1 month after the scan shown in B, pyogenic abscess (arrows) is noted only on further cranial scans. THAD has also decreased and is less conspicuous.

 

Focal Eosinophilic Necrosis
Recently, imaging findings of focal eosinophilic necrosis attracted considerable attention because this condition often gives rise to a diagnostic dilemma in daily practice. It more frequently shows a fuzzy margin, subtle hypoattenuation, and a nonspheric shape than does a metastasis (Figs. 8A, 8B, and 8C). As far as we know, there is no report about the THAD in focal eosinophilic necrosis. Pathologically, it is a focal area of hepatocellular necrosis caused by severe eosinophilic infiltration of the perivascular space. Therefore, one may assume that eosinophilic infiltration of the perivascular space may be the cause of the THAD in focal eosinophilic necrosis.



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Fig. 8A. 63-year-old man with focal eosinophilic necrosis. Hepatic arterial phase serial CT scans show wedge-shaped high-attenuation area and small low-attenuation lesion (arrow) in right lobe.

 


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Fig. 8B. 63-year-old man with focal eosinophilic necrosis. On portal venous phase serial CT scans, transient hepatic attenuation difference (THAD) associated with focal eosinphilic necrosis is not present.

 


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Fig. 8C. 63-year-old man with focal eosinophilic necrosis. Follow-up hepatic arterial phase CT scan obtained 2 months after the scan shown in B does not show definite low-attenuation lesion or THAD, as was seen on previous CT scan (B).

 


Tumorous Versus Nontumorous THAD
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 
On hepatic arterial phase images, a high-attenuation focal hepatic lesion of cirrhotic liver is usually HCC. However, nontumorous THAD in a cirrhotic liver has a similar appearance. A wedge shape, a straight-line margin, and the presence of normal vessels coursing through the lesion on hepatic arterial phase images make a diagnosis of THAD very likely. Portal venous phase images have an important role because most hypervascular tumors are seen as low attenuations, whereas THADs are seen as normal attenuations on portal venous phase images (Figs. 9A, 9B, 9C, and 9D). If there is any doubt about the diagnosis of THAD on dynamic CT, MRI may solve the problem. Normal signal intensity on T1- and T2-weighted images excludes hypervascular tumor (Figs. 9C and 9D). Another important cause of THAD is the "third-inflow tract." Aberrant gastric venous drainage into the hepatic segment IV and aberrant cystic venous drainage into the gallbladder fossa are the commonly encountered third-inflow tracts. Focal hepatic lesions are not always associated with THAD and vice versa. In some cases, it is impossible to define the specific cause of THAD (Figs. 10A, 10B, and 10C).



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Fig. 9A. 40-year-old woman with idiopathic transient hepatic attenuation difference (THAD). Hepatic arterial phase CT scan shows small high-attenuation nodular lesion (arrow) in right lobe.

 


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Fig. 9B. 40-year-old woman with idiopathic transient hepatic attenuation difference (THAD). On portal venous phase CT scan, there is no definite high- or low-attenuation lesion in right lobe.

 


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Fig. 9C. 40-year-old woman with idiopathic transient hepatic attenuation difference. T1-weighted (C) and T2-weighted (D) images do not show definite focal hepatic lesion. Hepatic arterial phase CT scan (not shown) obtained 6 months later showed no interval change in small enhancing lesion in right lobe.

 


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Fig. 9D. 40-year-old woman with idiopathic transient hepatic attenuation difference. T1-weighted (C) and T2-weighted (D) images do not show definite focal hepatic lesion. Hepatic arterial phase CT scan (not shown) obtained 6 months later showed no interval change in small enhancing lesion in right lobe.

 


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Fig. 10A. 63-year-old woman with hemangioma. Hepatic arterial phase CT scan shows well-defined high-attenuation area (arrow) in dorsal aspect of segment IV.

 


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Fig. 10B. 63-year-old woman with hemangioma. On portal venous phase CT scan, dorsal aspect of segment IV shows no attenuation difference compared with other hepatic parenchyma.

 


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Fig. 10C. 63-year-old woman with hemangioma. On slightly caudal hepatic arterial phase CT scan, small dense enhancing nodule (arrow) is noted. It is impossible to determine whether transient hepatic attenuation difference (THAD) is secondary to hemangioma or to aberrant gastric vein drainage.

 


Conclusion
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 
THADs of focal hepatic lesions reflect a change in the dual blood supply of the liver adjacent to the lesions. Benign focal hepatic lesions and malignant tumors may be the causes of THADs. Radiologists should be familiar with the dual-phase CT appearances of THADs to avoid the false-positive diagnosis of pseudolesions and not to overestimate the extent of the disease.


Acknowledgments
 
We thank Bonnie Hami, department of radiology, University Hospitals Health System, Cleveland, OH, for editorial assistance in preparing the manuscript.


References
Top
Introduction
Malignant Focal Hepatic Lesions
Benign Focal Hepatic Lesions
Tumorous Versus Nontumorous THAD
Conclusion
References
 

  1. Itai Y, Hachiya J, Makita K, Ohtomo K, Kokubo T, Yamauchi T. Transient hepatic attenuation differences on dynamic computed tomography. J Comput Assist Tomogr1987; 11:461 -465[Medline]
  2. Okuda K, Musha H, Yamasaki T, et al. Angiographic demonstration of intrahepatic arterio-portal anastomoses in hepatocellular carcinoma. Radiology1977; 122:53 -58[Abstract]
  3. Byun JH, Kim TK, Lee CW, et al. Arterioportal shunt: prevalence in small hemangiomas versus that in hepatocellular carcinomas 3 cm or smaller at two-phase helical CT. Radiology2004; 232:354 -360[Abstract/Free Full Text]
  4. Kim TK, Choi BI, Han JK, Jang HJ, Cho SG, Han MC. Peripheral cholangiocarcinoma of the liver: two-phase spiral CT findings. Radiology 1997;204 : 539-543[Abstract/Free Full Text]
  5. Zhang Y, Uchida M, Abe T, Nishimura H, Hayabuchi N, Nakashima Y. Intrahepatic peripheral cholangiocarcinoma: comparison of dynamic CT and dynamic MRI. J Comput Assist Tomogr1999; 23:670 -677[Medline]
  6. Kim KW, Kim TK, Han JK, Kim AY, Lee HJ, Choi BI. Hepatic hemangiomas with arterioportal shunt: findings at two-phase CT. Radiology2001; 219:707 -711[Abstract/Free Full Text]
  7. Gabata T, Kadoya M, Matsui O, et al. Dynamic CT of hepatic abscesses: significance of transient segmental enhancement. AJR 2001;176:675 -679[Abstract/Free Full Text]
  8. Mathieu D, Vasile N, Fagniez PL, Segui S, Grably D, Larde D. Dynamic CT features of hepatic abscesses. Radiology1985; 154:749 -752[Abstract/Free Full Text]

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