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AJR 2002; 179:81-85
© American Roentgen Ray Society


Original Report

Hemodynamic Characterization of Focal Nodular Hyperplasia Using Three-Dimensional Volume-Rendered Multidetector CT Angiography

Giuseppe Brancatelli1,2, Michael P. Federle1, Sanjeev Katyal1 and Vibhu Kapoor1

1 Department of Radiology, Division of Abdominal Imaging, University of Pittsburgh Medical Center, 200 Lothrop St., Pittsburgh, PA 15213.
2 Present address: Department of Radiology, University of Palermo, Italy.

Received December 13, 2000; accepted after revision January 15, 2002.

 
Address correspondence to M. P. Federle.


Abstract
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Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 
OBJECTIVE. The goal of this study was to show the ability of three-dimensional multidetector CT angiography to display the angioarchitecture of focal nodular hyperplasia.

CONCLUSION. CT angiography with volume rendering shows the anomalous feeding artery and hepatic draining veins that are characteristic of focal nodular hyperplasia. These features may be helpful in distinguishing focal nodular hyperplasia from other lesions.


Introduction
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Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 
Because helical CT scanning of the abdomen during a rapid bolus injection of contrast medium has become standard practice, hypervascular hepatic lesions are recognized frequently. Although the possibility of a hypervascular primary or metastatic hepatic neoplasm must be considered, many of these lesions prove to be focal nodular hyperplasia. Focal nodular hyperplasia is a benign neoplasm that is present in 3-5% of the general population and seems to develop as a hyperplastic response to a localized vascular abnormality [1]. Because focal nodular hyperplasia is rarely symptomatic and has no malignant potential, differentiation from other hypervascular hepatic masses is important. Improvements in CT and MR imaging have allowed accurate diagnosis of focal nodular hyperplasia in many cases, although many patients still undergo multiple imaging studies, percutaneous biopsy, and even surgery because the radiologists failed to make a confident diagnosis. Focal nodular hyperplasia lesions are usually nearly isoattenuating to the liver on unenhanced, portal venous phase, and delayedenhanced CT scans and are homogeneously hyperattenuating on arterial phase CT scans. A central fibrous scar is highly characteristic, but it is identified in only 50% of cases [2].

The angioarchitecture and pathophysiology of focal nodular hyperplasia have been studied extensively by pathologists and hepatologists and have been found to differ substantially from the angioarchitecture of hepatocellular carcinoma and other malignant hepatic neoplasms [1]. Focal nodular hyperplasia is supplied by an enlarged anomalous hepatic artery; its venous drainage is always into the hepatic veins [1]. Conversely, the efferent vessels in hepatocellular carcinoma are almost exclusively drained into the portal vein system [3]. Several investigators have concluded that unequivocal visualization of hepatic venous drainage from a hypervascular hepatic mass would be useful in diagnosing focal nodular hyperplasia [3,4,5].

Although multiphasic thin-section helical CT often shows blood vessels within or surrounding hypervascular liver masses, it is often difficult to recognize the origin and path of vessels on a series of transverse CT scans. The purpose of this article is to show the ability of three-dimensional (3D) multidetector CT angiography using volume rendering to display the hemodynamics and angioarchitecture of focal nodular hyperplasia, features that should prove useful in distinguishing the lesions from malignant masses.


Subjects and Methods
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Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 
Between July 1999 and October 2000, four women (age range, 37-45 years; mean age, 42 years) who were being evaluated for a known or suspected hepatic tumor had a hypervascular liver lesion found on helical CT that was subsequently proven to be focal nodular hyperplasia. The liver lesion was first detected on CT, which was requested to evaluate abdominal pain (n = 3) or possible metastatic breast carcinoma (n = 1). None of the patients had cirrhosis or viral hepatitis. Proof of focal nodular hyperplasia was by liver resection (n = 1), focal uptake of 99mTc diethyl-iminodiacetic acid (n = 1), and the stable size of the lesion for 1 and 4 years (n = 2). The CT protocol was designed to allow optimal characterization of the hypervascular liver lesion on transverse and 3D volume-rendered images. All CT examinations were performed on a Lightspeed QX/i scanner (General Electric Medical Systems, Milwaukee, WI). After a series of unenhanced 7-mm sections through the liver, all patients received IV contrast medium ([ioversol] Optiray 350; Mallinckrodt, St. Louis, MO) at a rate of 5 mL/sec and a volume of 125 mL. Arterial dominant phase images were initiated at a time determined by contrast bolustracking software to coincide with peak aortic enhancement with a scan delay of 13-25 sec. Portal venous dominant phase imaging was initiated 40 sec after the initiation of the arterial phase images (range, 53-65 sec).

For the arterial phase images, we used a collimator width of 1.25 mm and a table speed of 7.5 mm per rotation (high-speed mode; pitch, 6). For the portal venous phase, we used a collimator width of 2.5 mm and a table speed of 15.0 mm per rotation.

Three-dimensional volume-rendered reconstructions were performed using a free-standing workstation (Advantage Windows; General Electric Medical Systems). All reconstructions were performed by a radiologist experienced in 3D postprocessing techniques, and each procedure required approximately 20 min. Volumes of interest were selected manually from the axial source images to include only the aorta, celiac axis, hepatic artery, draining veins, and lesion. CT angiograms were then reconstructed using the volume-rendering algorithm with lower thresholds of 70-140 H. Display parameters including width, level, opacity, and brightness were chosen subjectively. The volume-rendered images were obtained in projections selected to best depict the course of the hepatic vasculature. Standard projections performed in all cases included right anterior, oblique, inferior, posterior, and lateral projections.

The reconstructed axial images and the 3D volume-rendered reconstructions were reviewed by two radiologists, and the arterial supply and venous drainage to and from the lesion were recorded as part of the official CT report.


Results
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Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 
A single focal nodular hyperplasia lesion was found in three patients, and two lesions were found in a fourth patient. The lesions ranged in diameter from 1 to 9 cm. All lesions were hypo- to isoattenuating on unenhanced CT. All lesions appeared homogeneously and brightly enhancing on the arterial dominant phase, and all were isoattenuating on the portal venous dominant phase (Figs. 1A,1B,1C and 2A,2B,2C,2D). One patient underwent 6-min delayed scanning, with the lesion remaining isoattenuating to the liver. A central scar was shown in two lesions, and it was isoattenuating to the surrounding focal nodular hyperplasia on unenhanced images and hypoattenuating on both arterial and portal venous phases. The scar was hyperattenuating to the liver and the focal nodular hyperplasia on delayed scans in one patient.



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Fig. 1A. 39-year-old woman with focal nodular hyperplasia. Early hepatic arterial phase transverse CT scan (20-sec delay) shows large homogeneously and brightly enhancing mass (solid straight arrow) with central scar (open arrow). Blood vessels (curved arrows) are evident within mass and on its surface, but their origin and course are difficult to determine.

 


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Fig. 1B. 39-year-old woman with focal nodular hyperplasia. Portal venous phase transverse CT scan (70-sec delay) reveals blood vessels (arrows), probably veins, within mass and on its surface. Mass is nearly isoattenuating to liver.

 


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Fig. 1C. 39-year-old woman with focal nodular hyperplasia. Volume-rendered CT angiogram (20-sec delay) shows focal nodular hyperplasia (FNH) lesion supplied by anomalous artery (a a) arising from hepatic artery (HA). Lesion is drained by two hepatic vein tributaries (HV).

 


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Fig. 2A. 45-year-old woman with focal nodular hyperplasia. Early arterial phase transverse CT scan (13-sec delay) shows lesion (straight arrow) is brightly and homogeneously enhancing. Blood vessels (curved arrow) are noted on surface of mass.

 


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Fig. 2B. 45-year-old woman with focal nodular hyperplasia. Portal venous phase CT scan (60-sec delay) shows mass almost isoattenuating to liver with hypoattenuating central scar (open arrow). Large blood vessels (solid arrows) are noted.

 


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Fig. 2C. 45-year-old woman with focal nodular hyperplasia. Volume-rendered CT angiogram (13-sec delay) shows multiple branches of anomalous artery (a a) spread over lesionlike spider legs. HA = hepatic artery, FNH = focal nodular hyperplasia.

 


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Fig. 2D. 45-year-old woman with focal nodular hyperplasia. Volume-rendered CT angiogram (60-sec delay) shows that multiple draining veins (arrows) coalesce to drain into right hepatic vein (RHV) and inferior vena cava (IVC).

 

In the arterial phase, one or more anomalous feeding arteries to each lesion were identified (Figs. 1A,1B,1C and 2A,2B,2C,2D). The arteries branched into a spiderlike series of vessels on the surface of the focal nodular hyperplasia (Fig. 2A,2B,2C,2D); the course of the vessels within the focal nodular hyperplasia could not be visualized on the volume-rendered images. Anomalous draining veins were identified that could be followed into or toward larger hepatic veins and not into portal vein branches (Fig. 2A,2B,2C,2D). In the patient with the smaller lesions, an anomalous draining vein could not be identified (Fig. 3).



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Fig. 3. 43-year-old woman with focal nodular hyperplasia. Volume-rendered CT angiogram (20-sec delay) shows large focal nodular hyperplasia lesion (FNH) supplied by multiple branches of anomalous artery (a a) arising from hepatic artery (HA). Small lesion (FNH) is supplied by single artery.

 

For comparison, we illustrate the portal venous drainage of hepatocellular carcinoma (Fig. 4A,4B).



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Fig. 4A. 70-year-old woman with cirrhosis and hepatocellular carcinoma. Portal venous phase transverse CT scan shows 5-cm hypoattenuating lesion in segment VIII of liver.

 


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Fig. 4B. 70-year-old woman with cirrhosis and hepatocellular carcinoma. Maximum-intensity-projection off-axial CT scan shows two enhancing vessels (straight arrows) at periphery of mass draining lesion and joining right branch of portal vein (curved arrow). On biopsy, mass was well-differentiated hepatocellular carcinoma.

 


Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 
Multiphasic multidetector CT allows greater spatial and temporal or hemodynamic characterization than conventional or single-detector helical CT, which can result in a more confident and specific diagnosis of focal hepatic lesions. Many of these features, such as uniform hypervascularity and a central scar, are evident on transverse CT sections and have been reported to result in a more frequent and confident diagnosis of focal nodular hyperplasia [6]. The ability to acquire a volume of CT data with near-isotropic voxels (the same in the x, y, and z planes) offers further possibilities to characterize the shape and hemodynamics of focal liver masses. Graphics workstations and software packages are now affordable accessories to multidetector CT scanners and have become more user-friendly for radiologists and technologists.

The relatively minor alterations of our standard biphasic CT liver protocol and the moderate amount of time necessary to perform the 3D reconstructions provided unique insights into the angioarchitecture of focal nodular hyperplasia in these four patients. Prior attempts to study the hemodynamics of focal nodular hyperplasia have been quite invasive and labor-intensive. Transcatheter angiography was more widely used in the past to detect and characterize liver tumors, but few cases of focal nodular hyperplasia were studied and were generally characterized merely as hypervascular masses supplied by an enlarged anomalous artery [7]. Miyayama et al. [8] coupled hepatic arteriography with single-level dynamic CT and showed arteries and veins in or near the central stellate scar and at the junction of the focal nodular hyperplasia and normal liver tissue. They noted that blood (contrast media) occasionally drained from the focal nodular hyperplasia nodule into surrounding hepatic sinusoids producing an enhanced capsulelike rim. Their CT technique did not allow depiction of the shape or number of focal nodular hyperplasia lesions or the pattern of feeding or draining vessels beyond the focal nodular hyperplasia.

Fukukura et al. [3] studied 29 surgically resected focal nodular hyperplasia lesions and three autopsy specimens with angiography; in the autopsy cases, they studied the injection of colored gelatin into the hepatic artery and portal vein. They concluded that focal nodular hyperplasia is supplied by an anomalous enlarged hepatic artery and is neither supplied nor drained by the portal vein. Rather, venous drainage of focal nodular hyperplasia was exclusively into the hepatic vein branches [3]. Conversely, several investigators have studied the vascular supply and drainage of hepatocellular carcinoma in great detail and have found that hepatocellular carcinoma is supplied almost exclusively by the hepatic artery and is drained almost always into the portal vein [4, 9, 10]. Okuda et al. [11] showed some drainage into hepatic veins in only 1.8% of hepatocellular carcinoma.

Wanless et al. [1], who have written most extensively on the pathophysiology of hypervascular liver masses, have conducted detailed studies on the morphometry of these lesions. They report that focal nodular hyperplasia is supplied by an anomalous artery, larger than expected for its hepatic location, that branches into a spiderlike structure on or within the focal nodular hyperplasia lesion. They further report that the artery is not accompanied by a portal vein branch and that focal nodular hyperplasia drains directly to hepatic veins or first through enlarged sinusoids near its periphery [1].

These and other investigators [3] have concluded that the visualization of these vascular features should prove useful in distinguishing focal nodular hyperplasia from other hepatic masses including hepatocellular carcinoma. We believe the CT angiographic techniques that we have reported accomplish this goal and do so noninvasively and relatively inexpensively.

The CT angiograms provided by volume-rendered 3D modeling showed the size, number, and angioarchitecture of focal nodular hyperplasia in each of our four patients. The images showed the characteristic enlarged anomalous feeding arteries, the spiderlike branching on the surface of the focal nodular hyperplasia, and the hepatic venous drainage (Figs. 1A,1B,1C and 2A,2B,2C,2D). The portal vein supplied neither inflow nor drainage of the focal nodular hyperplasia in our cases.

Another potential benefit of the 3D display of hepatic vasculature provided by CT angiography is in planning for embolization or ligation of vessels for the rare symptomatic cases of focal nodular hyperplasia [12].

Our study has some limitations. The detection of draining veins was not possible for the smallest of the lesions shown. From our knowledge, based on our prior surgical and gross pathologic studies, the depiction of hepatic venous drainage (for focal nodular hyperplasia) or portal venous drainage (for hepatocellular carcinoma) should be a reliable criterion. Nevertheless, our study size is small, and a study of a larger group of patients may be warranted. We conclude that 3D CT angiography can provide useful information in cases of suspected focal nodular hyperplasia that may allow a more confident diagnosis and treatment in some cases.


References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
 

  1. Wanless IR, Mawdsley C, Adams R. On the pathogenesis of focal nodular hyperplasia of the liver. Hepatology 1985;5:1194 -1200[Medline]
  2. Nguyen BN, Flejou JF, Terris B, Belghiti J, Degott C. Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms. Am J Surg Pathol 1999;23:1441 -1454[Medline]
  3. Fukukura Y, Nakashima O, Kusaba A, Kage M, Kojiro M. Angioarchitecture and blood circulation in focal nodular hyperplasia of the liver. J Hepatol 1998;29:470 -475[Medline]
  4. Tanaka S, Kitamra T, Fujita M, Kasugai H, Inoue A, Ishiguro S. Small hepatocellular carcinoma: differentiation from adenomatous hyperplastic nodule with color Doppler flow imaging. Radiology 1992;182:161 -165[Abstract/Free Full Text]
  5. Ueda K, Matsui O, Kawamori Y, et al. Hypervascular hepatocellular carcinoma: evaluation of hemodynamics with dynamic CT during hepatic arteriography. Radiology 1998;206:161 -166[Abstract/Free Full Text]
  6. Carlson SK, Johnson CD, Bender CE, Welch TJ. CT of focal nodular hyperplasia of the liver. AJR 2000;174:705 -712[Free Full Text]
  7. Welch TJ, Sheedy PF 2nd, Johnson CM, et al. Focal nodular hyperplasia and hepatic adenoma: comparison of angiography, CT, US, and scintigraphy. Radiology 1985;156:593 -595[Abstract/Free Full Text]
  8. Miyayama S, Matsui O, Ueda K, et al. Hemodynamics of small hepatic focal nodular hyperplasia: evaluation with single-level dynamic CT during hepatic arteriography. AJR 2000;174:1567 -1569[Abstract/Free Full Text]
  9. Baron RL. Understanding and optimizing use of contrast material for CT of the liver. AJR 1994;163:323 -331[Abstract/Free Full Text]
  10. Matsui O, Kadoya M, Kameyama T, et al. Benign and malignant nodules in cirrhotic livers: distinction based on blood supply. Radiology 1991;178:493 -497[Abstract/Free Full Text]
  11. Okuda K, Musha H, Yamasaki T, et al. Angiographic demonstration of intrahepatic arterio-portal anastomoses in hepatocellular carcinoma. Radiology 1977;122:53 -58[Abstract]
  12. Pain JA, Gimson AE, Williams R, Howard ER. Focal nodular hyperplasia of the liver: results of treatment and options in management. Gut 1991;32:524 -527[Abstract/Free Full Text]

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