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Original Report |
1
Department of Diagnostic Radiology, Fukuiken Saiseikai Hospital, 7-1,
Wadanaka-cho, Funabashi, Fukui 918-8503, Japan.
2
Department of Radiology, Kanazawa University Hospital, 13-1, Takara-machi,
Kanazawa 920-8641, Japan.
3
Department of Radiology, Kaga Central Hospital, 65, Hakkenmichi, Daishoji-cho,
Kaga 922-0436, Japan.
Received August 31, 1999;
accepted after revision November 15, 1999.
Address correspondence to S. Miyayama.
Abstract
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CONCLUSION. Single-level dynamic CT during hepatic arteriography revealed not only centrifugal blood supply through the fibrous stellate scar, but also the drainage to dilated veins in or near the focal nodular hyperplasia nodule and directly to the hepatic sinusoid in the surrounding liver.
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Focal nodular hyperplasia has characteristic imaging findings, including specific vascular structures such as a spoke-wheel pattern and a stellate fibrous scar [2,3,4,5,6]. The diagnosis of focal nodular hyperplasia can be made if imaging reveals these characteristic features. However, sometimes it is difficult to diagnose small focal nodular hyperplasia lesions [6, 7].
Recent advances in imaging techniques, including the development of CT with slipring technology and CT arteriography, have enabled the analysis of the hemodynamics of hepatic nodules [8]. We examined three patients with small focal nodular hyperplasia with single-level dynamic CT during hepatic arteriography (CTHA). We describe the characteristic hemodynamics of focal nodular hyperplasia.
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-fetoprotein were negative. All lesions were examined with
sonography and dynamic CT; however, angiography was performed because
characteristic features of focal nodular hyperplasia did not appear. Single-level dynamic CTHA was performed, followed by angiography and conventional CTHA. After a 5-French angiographic catheter was positioned in the common hepatic artery, the patients underwent CT. Conventional CTHA was performed using an Xvigor or Xvision scanner (Toshiba Medical Systems, Tokyo, Japan) with a 5-mm collimation, a 7-mm pitch, and a 5-mm reconstruction, convering the entire liver in a single breath-hold. The appropriate craniocaudal level for single-level dynamic CHTA was determined on the basis of conventional CTHA images. In two patients, single-level dynamic CTHA was performed with 16 ml of IV diluted iopamidol (Iopamiron 370; Schering, Berlin, Germany) administered with a power injector (Auto Enhance A-50; Nemoto Kyorindo, Tokyo, Japan) at a rate of 2 ml/sec in the common hepatic artery. In one patient, CTHA was performed with 10 ml of IV iopamidol administered with a power injector at a rate of 1 ml/sec in the common hepatic artery. Scanning (220-250 mAs; 120 or 135 kVp) began immediately before the injection of contrast material, and a 30-sec continuous scan with a 3-mm collimation was obtained in a single breath-hold. Images were reconstructed at 1-sec intervals with a small field of view targeted to the lesion.
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In two patients, the diagnosis of focal nodular hyperplasia was made with sonographically guided core biopsy. In the remaining patient, for whom the nodule could not be detected on sonography, the diagnosis was established based on radiocolloid single-photon emission CT findings and clinical follow-up at 25 months.
Single-level dynamic CTHA revealed the contour and hemodynamics of all focal nodular hyperplasia nodules (Figs. 1A,1B,1C,1D,2A,2B,2C,3A,3B). Immediately after the injection of contrast material, we could clearly identify a feeding artery in each lesion. The feeding artery entered the central part of the lesion through a fibrous scar, and branches radiated toward periphery. A definite pattern of centrifugal filling and dense enhancement of the nodule, except for the central stellate fibrous scar, was revealed in all patients. In all lesions, the central scar, which radiated peripherally and subdivided the mass into lobules of various size, was clearly seen as a low attenuation area from 3-5 sec (mean, 4 sec) to 11-23 sec (mean, 16 sec) after the start of injection. The fibrous scar gradually became isodense with the surrounding nodule 12-24 sec (mean, 17 sec) after the start of injection. Additionally, a dilated vessel in or near the central fibrous scar and at the junction with the normal liver tissue was revealed in all lesions; it probably represented a vein because it opacified after the definite visualization of the feeding arteries. The vein began to opacify at 7-12 sec (mean, 9 sec), and opacification lasted the duration of scanning. In all lesions, the contour of the nodule changed from irregular to smooth in the late phase of scanning.
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One of the characteristic hemodynamic patterns of focal nodular hyperplasia is a centrifugal blood supply [2, 4,5,6]. One or more feeding arteries arise centrally and radiate peripherally in a spoke-wheel pattern. On angiography, the centrifugal blood supply can be detected in 57-90% of patients with large focal nodular hyperplasia lesions [5, 6]. However, in small focal nodular hyperplasia lesions, it is more difficult to detect this vascular pattern [6, 7, 9]. To detect the characteristic vascular patterns of small focal nodular hyperplasia lesions, new imaging techniques are being used. A study by Kudo et al. [7] described the usefulness of dynamic contrast-enhanced sonography with carbon dioxide microbubbles in the diagnosis of small focal nodular hyperplasia nodules. However, small focal nodular hyperplasia nodules located in the upper portion of the right lobe of the liver are often difficult to visualize on sonography. A study by Takayasu et al. [9] reported the usefulness of CT arteriography in identifying focal nodular hyperplasia nodules and characterizing their centrifugal blood supply and central low density area that corresponds to the fibrous scar. However, the study did not use continuous scanning; therefore, precise analysis of the hemodynamics of focal nodular hyperplasia was not determined.
The pattern of vascular drainage of focal nodular hyperplasia also seems to be characteristic. Microscopically, large veins with eccentric and concentric wall thickening are present in the normal liver tissue adjacent to the lesion, at the junction with the normal liver tissue, and in larger stellate scars [2, 3]. Recently, a study by Fukukura et al. [10] confirmed the drainage of focal nodular hyperplasia using gelatin injected into the hepatic artery and portal vein of cadavers. They reported that focal nodular hyperplasia nodules had two drainage pathways: one pathway was venous drainage connected directly to the central or hepatic veins surrounding the lesions, the other pathway was through the intranodular sinusoids that are connected to sinusoids in the surrounding liver. To our knowledge, the presence of large veins in focal nodular hyperplasia nodules has not been previously reported, except for reports of dilated early draining veins surrounding the focal nodular hyperplasia nodules detected on CT scans [4, 11].
Single-level dynamic CTHA was first used to examine the hemodynamics of hypervascular hepatocellular carcinoma in a study by Ueda et al. [8]. With continuous scanning, thin collimation, and a small area of interest, CTHA produces excellent time and spatial resolution. The technique also allows the delineation of blood flow in hepatic neoplasms. Continuous scanning after the intraarterial injection of contrast material enables the depiction of washout from tumors. We applied this method to evaluate the hemodynamics of small focal nodular hyperplasia.
In our study, single-level dynamic CTHA revealed the hemodynamics of focal nodular hyperplasia nodules. CTHA revealed feeding arteries and the veins in or near the central stellate scar and at the junction with normal liver tissue. These veins were consistent with those described in a study by Fukukura et al. [10]. These veins probably connect directly to the hepatic veins, although we used the continuous scan technique without table feed, so we could not confirm the connection. These veins may be the main drainage vessels of focal nodular hyperplasia nodules; however, as also described by Fukukura et al., some blood may drain from the lesion directly into the hepatic sinusoid. In all of our patients, the margins of the lesions changed from irregular to round on delayed images, a characteristic also reported by Takayasu et al. [9]. This finding might be caused by direct drainage into the sinusoids in the surrounding liver. If the blood predominantly drains from the nodule into the hepatic sinusoids, it might also induce an enhanced capsulelike rim, which was reported by Choi and Freeny [11] as an atypical finding of focal nodular hyperplasia.
Centrifugal blood supply and the presence of dilated veins in or near the nodule are two characteristic findings of focal nodular hyperplasia. If seen on single-level dynamic CTHA, these findings are useful in the diagnosis of small focal nodular hyperplasia, particularly when definite diagnosis cannot be made with other imaging techniques. We recognize that the number of patients studied in this report is small. Additionally, we know that the presence of hypovascular focal nodular hyperplasia has been reported [5]. Further studies are required before drawing more conclusions.
In summary, single-level dynamic CTHA is useful in evaluating the intranodular hemodynamics of small focal nodular hyperplasia. This technique enables radiologists to identify centrifugal blood supply and two drainage pathways: large veins in and near the lesion and direct connection to the hepatic sinusoid.
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