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Contrast-Enhanced CT of Small Hypovascular Hepatic Tumors

Effect of Lesion Enhancement on Conspicuity in Rabbits

¹ The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287.
² Department of Surgery, The Johns Hopkins Medical Institutions, Baltimore, MD 21287.

Received March 3, 1999; accepted after revision July 1, 1999.

 
Address correspondence to E. K. Fishman.

Received the 1999 American Roentgen Ray Society Executive Council Award at the annual meeting of the American Roentgen Ray Society, New Orleans, May 1999.

E. K. Fishman is a member of the Siemens Spiral CT Advisory Board.

Supported in part by the American Cancer Society (grant IRG 11-35).

Abstract

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OBJECTIVE. The purpose of this study was to evaluate the effect of lesion enhancement on the conspicuity of small hypovascular hepatic tumors in an animal model.

MATERIALS AND METHODS. Seven VX2 hepatic tumors in five rabbits were imaged. Dynamic contrast-enhanced CT was performed at a single level centered over the lesions at 5-sec intervals for 119 sec after injection of 2 ml/kg IV contrast material at 2 ml/sec. Attenuation was measured over time within regions of interest in the tumor and normal liver, aorta, inferior vena cava, and portal vein. Lesion conspicuity, defined as the difference between the attenuation of the uninvolved liver and neoplasm, was calculated.

RESULTS. The mean diameter of the tumors on CT was 10 mm (range, 6-15 mm). The tumors appeared as low-attenuation lesions with progressive enhancement during the arterial phase and early portal phase. Peak mean lesion attenuation was 60 ± 27 H (enhancement, 23 H) at 64 sec. Peak mean lesion conspicuity was 80 ± 18 H at 39 sec, occurring 10 sec before the peak mean hepatic attenuation of 135 ± 15 H (enhancement, 67 H) at 49 sec. Relative lesion conspicuity paralleled relative enhancement of the liver throughout the imaging period.

CONCLUSION. Although low-level tumor enhancement during the arterial phase and early portal phase reduced the conspicuity of small hypovascular tumors in this animal model, our results support the use of maximum liver enhancement as a marker for peak lesion conspicuity.

Introduction

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Despite the established role of helical CT for liver tumor detection, detection of lesions measuring 1 cm or less continues to be problematic [1, 2]. Although volume-averaging effects reduce the sensitivity of CT for small lesions [3], there is also evidence that small tumors enhance to a greater degree than large tumors [4] and that, therefore, tumor contrast enhancement kinetics may play a role in the poor sensitivity of CT for lesions measuring 1 cm or less. On CT, most metastatic liver lesions are hypovascular and are best imaged during the portal phase of contrast enhancement—that is, when these lesions appear lower in attenuation than the enhancing normal liver parenchyma [5, 6]. Because the conspicuity of a liver tumor is defined by the difference between the attenuation of the normal liver parenchyma and that of the tumor, hypovascular tumor enhancement decreases lesion conspicuity and is potentially as important to tumor detection as the enhancement of uninvolved liver. Although tumor enhancement is known to vary with tumor type (i.e., hypervascular versus hypovascular), the enhancement kinetics of malignant hepatic tumors are poorly understood.

A large body of research has been published aimed at understanding the contrast enhancement kinetics of the normal liver [5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19]. Many investigators have plotted the enhancement of the liver and aorta as a function of time with various injection protocols to characterize the time and degree of peak hepatic enhancement and the equilibrium phase, at which point these two curves become parallel. Foley [6] has suggested that during the equilibrium phase lesion conspicuity decreases. The first assumption underlying this concept is that the enhancement of hypovascular tumors is negligible before the equilibrium phase and therefore lesion conspicuity is primarily a function of the enhancement of surrounding normal liver. The second assumption is that lesion conspicuity decreases during the equilibrium phase because contrast material accumulates within the tumor [5, 6]. These assumptions are widely accepted and serve as the basis for current contrast enhancement protocols. However, the studies in which the enhancement of hepatic tumors was actually measured [20, 21, 22] were not performed with a degree of temporal resolution that was sufficient to optimize scanning technique using modern subsecond helical scanners and multidetector scanners [23], which can image the entire liver in a matter of seconds. In patient studies, the entire liver is typically imaged, thus limiting temporal resolution for evaluating the enhancement of any individual lesion.

An animal model provides a means of addressing this issue by allowing dynamic contrast enhancement studies at a single level centered over the tumor of interest. The purpose of this study was to evaluate the effect of lesion enhancement on the conspicuity of small hypovascular hepatic tumors in an animal model.

Materials and Methods

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Animal Tumor Model
The animal research care and use committee at our institution approved this study protocol. The VX2 tumor model used in this study was initially a virus-induced papilloma first seen in the domestic rabbit in 1937 [24]. As a result of sequential transplantations, the tumor line became increasingly anaplastic. The VX2 tumor in the rabbit is an established animal model for oncologic imaging studies of the liver [4, 25]. VX2 carcinoma, which was initially obtained from EG & G Mason Research Institute (Worchester, MA), has been carried for approximately the last 15 years at our institution by repeated transfer of tumor every 14-21 days via intramuscular or subcutaneous implantation into the thighs of New Zealand white male rabbits.

Five New Zealand white rabbits weighing 3.38-4.24 kg were used in this study. Before tumor implantation and imaging, rabbits received an intramuscular injection of acepromazine maleate and ketamine hydrochloride (Ketaject; Phoenix Scientific, St. Joseph, MO). Intravenous access was then acquired via a marginal ear vein. Animals were intubated with a noncuffed endotracheal tube and placed on a small-animal ventilator (model 55-0798; Harvard Apparatus, South Natick, MA). Anesthesia was maintained using IV sodium pentothol.

A tumor was implanted into the liver of each of the five rabbits using a midline laparotomy. Hepatic tumors were created by injecting fragments of VX2 tumor measuring approximately 1 mm³ into the right (n = 2), left (n = 1), or both (n = 2) lobes of the liver using a 16-gauge angiocath, with the needle removed, and a guidewire as a pusher.

CT
CT was performed 13-24 days after implantation using a Somatom Plus 4 scanner (Siemens, Iselin, NJ). Before imaging, the animals were anesthetized, intubated, and placed on the small-animal ventilator. They were paralyzed using IV pancuronium immediately before imaging; paralysis was reversed after imaging was completed using IV neostigmine methylsulfate and atropine sulfate. Animals were weighed before imaging to determine the appropriate dose of contrast material based on 2 ml/kg.

An initial unenhanced helical study of the entire liver was performed using the following parameters: 3-mm collimation, 3-mm/sec table speed in the craniocaudal direction, 0.75-sec gantry rotation, 292 mA, and 120 kVp. Ventilation was suspended for the entire helical study. Axial reconstructions were performed every 4 mm using 180° linear interpolation. The level of the lesions was determined from the unenhanced helical study; dynamic contrast-enhanced examination was performed at that level after IV injection of 8-9 ml of nonionic iodinated contrast material (iohexol, 300 mg I/ml; dose, 2 ml/kg of body weight; iodine, 2.4-2.7 g) at 2 ml/sec via an ear vein using a power injector. Once the contrast material had been injected, dynamic scanning was begun using 2-mm collimation, 143 mA, 140 kVp, and a 100- to 164-mm field of view. Scans were obtained at 5-sec intervals from 9 to 119 sec after the initiation of the contrast injection, with delayed images of up to 199 sec. During imaging, ventilation was suspended for approximately 20-sec intervals alternated with 8-sec periods of hyperventilation. Periods of ventilation were varied between animals to ensure that sufficient data were available for all time points.

Image Analysis
CT data sets were transferred to a freestanding Sparc20 workstation (Sun Microsystems, Mountain View, CA) running MagicView software (Siemens). A radiologist carefully measured the attenuation within the regions of interest containing 21 or 37 pixels in the aorta, inferior vena cava, and portal vein; in three locations in the right, middle, and left liver distant from the tumor; and in the center of the tumor. Focal areas of low attenuation within the tumors that were suggestive of necrosis were avoided. Areas containing beam-hardening artifacts or volume averaging with adjacent structures were avoided in all measurements. Attenuation values that could not be measured because of respiration were estimated using linear interpolation of adjacent values. The resulting attenuation data from all animals were averaged for each time point and plotted as a function of time. Tumor conspicuity at each time point was calculated by subtracting the mean lesion attenuation from the mean liver attenuation.

Definitions
The arterial phase of hepatic enhancement is the period between the rapid upslope in aortic enhancement that is due to contrast material bolus and the later rapid increase in enhancement of the portal vein. During the arterial phase, hepatic enhancement primarily results from the contrast material that is supplied by the hepatic artery. The portal phase of hepatic enhancement is the period between the rapid upslope in portal vein enhancement that is due to the contrast material bolus and the onset of the equilibrium phase, which we discuss later in this article. During the portal phase, hepatic enhancement primarily results from the contrast material that is supplied by the portal vein; peak hepatic enhancement occurs during this phase. The equilibrium phase of hepatic enhancement is the point at which the attenuation curves for the aorta and liver become parallel and decline at an equal rate [6, 7]. Conspicuity is the attenuation of normal liver parenchyma minus the attenuation of the tumor of interest.

Results

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The mean diameter of the seven hepatic tumors imaged was 10 mm (range, 6-15 mm). The apparent tumor size did not change over time on contrast-enhanced images. The tumors appeared as focal hepatic lesions with low attenuation relative to the normal hepatic parenchyma on both unenhanced and contrast-enhanced studies (Fig. 1A, 1B, 1C). During the arterial phase of hepatic enhancement, peripheral rim enhancement was seen in six (86%) of seven tumors. The rim enhancement was highly variable, ranging from imperceptible to a dense rind of enhancement (Fig. 1A, 1B, 1C). Arterial phase rim enhancement resolved during the portal phase in all cases.

View larger version (106K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —New Zealand White rabbit with liver containing two small VX2 carcinomas measuring 6 mm (right lobe) and 7 mm (left lobe). Unenhanced CT scan shows two subtle lesions within liver.

View larger version (118K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —New Zealand White rabbit with liver containing two small VX2 carcinomas measuring 6 mm (right lobe) and 7 mm (left lobe). Arterial phase CT scan obtained 24 sec after start of contrast material injection shows ring enhancement surrounding lesions.

View larger version (130K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —New Zealand White rabbit with liver containing two small VX2 carcinomas measuring 6 mm (right lobe) and 7 mm (left lobe). Portal phase CT scan obtained 54 sec after start of contrast material injection shows peak lesion conspicuity. Both lesions are of low attenuation relative to enhancing normal liver.

The peak mean hepatic attenuation of 135 ± 15 H (enhancement, 67 H) occurred at 49 sec (Fig. 2). At baseline before infusion of contrast material, the tumors measured 37 ± 13 H. Peak mean lesion attenuation was 60 ± 27 H (enhancement, 23 H) at 64 sec. Tumor enhancement began during the arterial phase and continued through the early portal phase; tumor enhancement plateaued during the mid portal phase and appeared to change minimally during the late portal phase and equilibrium phase, which began at approximately 100 sec (Fig. 3). The peak mean aortic attenuation of 910 ± 274 H (859 H enhancement) occurred at 19 sec after the initiation of the injection of contrast material. Peak mean portal vein attenuation was 231 ± 58 H (enhancement, 189 H) at 29 sec. Peak mean inferior vena cava attenuation was 271 ± 37 H (enhancement, 223 H) at 29 sec. A difference of less than 10 H between the attenuation of the aorta and inferior vena cava, (the definition of the equilibrium phase of enhancement proposed by Burgener and Hamlin [9]) occurred at 29 sec—well before peak hepatic enhancement and peak lesion conspicuity (Fig. 2).

View larger version (22K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2. —Graph shows conspicuity (•) and attenuation of tumor (*), liver (), aorta (), inferior vena cava (x), and portal vein () plotted against time after initiation of contrast material injection. Peak aortic attenuation of 910 H at 19 sec is not included on graph. Peak conspicuity occurs when attenuation of aorta and portal vein are equal.

View larger version (28K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3. —Graph shows relationship of conspicuity (•) and attenuation of tumor (*), liver (), aorta (), and portal vein () versus phases of hepatic enhancement. Tumors progressively enhance during arterial and early portal phases of hepatic enhancement, plateauing in late portal phase and equilibrium phase. Conspicuity is substantially decreased by onset of equilibrium phase.

Maximum lesion conspicuity occurred before maximum hepatic enhancement in four (57%) of seven lesions and at the time of peak hepatic enhancement in the remaining three lesions (43%). Peak mean lesion conspicuity was 80 ± 18 H at 39 sec, thus occurring 10 sec before the peak mean hepatic enhancement. The mean lesion conspicuity at peak hepatic enhancement was 76 ± 17 H—that is, 4 H (5%) less than peak conspicuity. Peak conspicuity occurred at approximately the same time that attenuation within the aorta and portal vein became equal (39 sec) (Fig. 2). The attenuation curves for the aorta and portal vein were nearly identical after this point. Relative conspicuity paralleled relative hepatic enhancement throughout the imaging period (Fig. 4).

View larger version (21K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4. —Graph shows relative tumor conspicuity () and liver enhancement ([UNK]) as percentage of maximum values versus time after contrast material injection. Although peak conspicuity occurs slightly before peak hepatic enhancement, conspicuity curve parallels liver enhancement curve throughout imaging.

Discussion

Top Abstract Introduction Materials and Methods Results Discussion References

 
In this animal model, enhancement within small hypovascular tumors during the arterial and early portal phases of enhancement resulted in reduced lesion conspicuity. Although peak tumor conspicuity occurred slightly before peak hepatic enhancement, the conspicuity of the tumors paralleled hepatic enhancement throughout the imaging period (Fig. 4). These findings support the common practice of using the time of peak hepatic enhancement as a marker for peak hypovascular lesion conspicuity.

The hypovascular tumors in this animal model enhanced well into the portal phase of hepatic enhancement. This tumor enhancement, combined with decreasing liver attenuation from peak hepatic enhancement to the onset of the equilibrium phase, resulted in a substantial decline in lesion conspicuity before the equilibrium phase of hepatic enhancement. These results confirm that helical CT protocols for imaging hypovascular liver tumors should cover the liver as rapidly as possible during peak hepatic enhancement. Acquisition that is completed just before the equilibrium phase but well after peak hepatic enhancement results in an average lesion conspicuity that is significantly diminished compared with a very rapid acquisition completed at peak lesion conspicuity. Potential strategies for imaging the liver as rapidly as possible include performing subsecond scanning, imaging with multidetector-array CT, and increasing the pitch. However, it is known that increasing the pitch increases the effective slice thickness—therefore reducing the conspicuity of small tumors because of volume-averaging effects.

Peak lesion conspicuity occurred when the attenuation in the aorta, inferior vena cava, and portal vein became equal and began to decrease together (Fig. 2). This finding corresponds to the onset of equilibrium in the concentration of the contrast material within the intravascular space. It is reasonable to postulate that lesion conspicuity increases up to that point because of differences in the relative amounts of blood being supplied by the hepatic artery and portal vein to the tumor and uninvolved liver parenchyma combined with differences in the concentration of contrast material within those two vessels. Once equilibrium between the concentrations of contrast material in the arterial system and the portal vein has been established, differences in blood supply to the tumor and liver can no longer be exploited to enhance lesion conspicuity.

The concept of an equilibrium phase of contrast enhancement has played a key role in the formulation of contrast enhancement protocols for CT detection of hypovascular liver tumors to date. Although the point at which the equilibrium phase begins has been defined differently, the underlying concept is that at later times after injection of a contrast bolus, hypovascular liver tumors become substantially less conspicuous. This phenomenon has been suggested to be a result of diffusion of contrast material into the extravascular space of the tumor [6, 7]. The concept of the equilibrium phase was defined by Burgener and Hamlin [9] as "a difference in blood iodine concentration between the aorta and inferior vena cava of less than 10 Hounsfield units." Foley [6] and Cox et al. [7] subsequently proposed an alternative definition of equilibrium as "when the two enhancement curves [aortic and hepatic] become parallel and decline at an equal rate," which they suggest occurs "when intravascular and extravascular contrast material equilibrate." In our study, equilibrium as defined by Burgener and Hamlin occurred before peak lesion conspicuity and well before peak hepatic enhancement. Our data suggest that enhancement of the tumor has plateaued and conspicuity is substantially lower than its maximum value by the onset of the equilibrium phase as defined by Foley and Cox et al.

The main potential limitation of applying the results of this study to patient care is that liver tumor enhancement characteristics in humans vary with tumor type and may differ from those seen in this animal model. Additionally, we studied a small number of hepatic tumors in a small number of animals. Larger studies are needed in humans to accurately characterize the enhancement characteristics of hepatic tumors as a function of both size and tumor type. The 100- to 164-mm field of view used in this animal study is smaller than that used in routine clinical practice. This smaller field of view provided better spatial resolution than standard scanning techniques used in human patients. Finally, the effects of the rate of contrast material administration and the total dose of contrast material administered on lesion enhancement and conspicuity were not evaluated.

In conclusion, the small hypovascular tumors in this animal model exhibited low-grade enhancement during the arterial phase and early portal phase of hepatic enhancement. Although peak tumor conspicuity occurred slightly before peak hepatic enhancement, conspicuity paralleled hepatic enhancement throughout the imaging period. Our results support the use of peak hepatic enhancement as a marker for peak lesion conspicuity. High-temporal resolution studies of tumor enhancement kinetics are needed in humans to optimize imaging protocols for detecting small hepatic tumors with modern subsecond and multidetector helical scanners.

Acknowledgments
 
We thank Nancy L. Spangler for her technical assistance.

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