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Original Research |
1 Department of Radiology, Gifu University School of Medicine, 1-1 Yanagido,
Gifu 501-1194, Japan.
2 Department of Radiology Services, Gifu University School of Medicine, Gifu,
Japan.
3 Department of Physiology and Neuroscience, Kanagawa Dental College, Yokosuka,
Japan.
4 Department of Diagnostic Radiology, National Cancer Center Hospital, Tokyo,
Japan.
Received December 13, 2004;
accepted after revision May 9, 2005.
Address correspondence to S. Goshima
(gossy{at}par.odn.ne.jp).
Abstract
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SUBJECTS AND METHODS. CT images (2.5-mm collimation, 5-mm thickness with no intersectional gap) detected an increase in the CT value of 50 H in the lower thoracic aorta. The images were obtained after an IV bolus injection of 2 mL/kg of nonionic iodine contrast material (300 mg I/mL) at 4 mL/s in 171 patients, who were prospectively randomized into three groups with scans commencing at 5, 20, and 45 seconds; 10, 25, and 50 seconds; and 15, 30, and 55 seconds for the first (acquisition time: 4.3 seconds), second (4.3 seconds), and third (9.1 seconds) phases, respectively, after a bolus-tracking program. CT values of the aorta, spleen, proximal portal veins, liver parenchyma, and hepatic veins were measured. Increases in CT values from unenhanced to contrast-enhanced CT were assessed using a contrast enhancement index (CEI). Spleen-to-liver and HCC-to-liver contrasts were also assessed. A qualitative degree of contrast enhancement in each organ was prospectively assessed by two independent radiologists.
RESULTS. At 10-15 seconds, the CEI of the aorta reached 300-336 H and that of the spleen reached 97-108 H without significant enhancement of liver parenchyma (15-25 H). The CEI of the proximal portal veins moderately increased (75-104 H) at 10-15 seconds, but no significant enhancement of hepatic veins was observed (24-51 H). The CEI of liver parenchyma peaked (59-63 H) at 45-55 seconds, when the CEIs of the aorta (117-125 H) and spleen (73-82 H) decreased. Spleen-to-liver contrast (81-84 H) was highest at 10-20 seconds and HCC-to-liver contrast (39-44 H) was highest at 10-15 seconds. The qualitative results correlated well with quantitative results.
CONCLUSION. The optimal scan delays for hepatic arterial and portal venous phases after the bolus-tracking program detected threshold enhancement by 50 H in the lower thoracic aorta for the detection of hypervascular HCCs were 10-15 and 45-55 seconds, respectively.
Keywords: contrast media • CT technique • liver
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Several researchers have investigated timedensity profiles for various doses, concentrations, and injection rates of contrast material using single-detector helical CT. Foley et al. [8] reported that hepatic enhancement increased to more than 50 H 60 seconds after initiation of monophasic IV injection of contrast material with a 50-g iodinated load at 3 mL/s. Tublin et al. [9] reported that peak enhancement of the liver occurred 63 and 87 seconds after initiating contrast material injection of 150 mL of 300 mg I/mL at rates of 5.0 and 2.5 mL/s, respectively. Also, Lee et al. [12] reported that the optimal duration for the hepatic arterial dominant phase was from 36 to 56 seconds after the injection of 150 mL of contrast material at a rate of 3 mL/s, but added that no optimal fixed delay time is appropriate for all patients. These previous studies evaluated the time-density profiles from the initiation of contrast medium injection without incorporating circulation time difference in individual patients, which significantly influence peak enhancement time [7, 13, 14].
With the advent of MDCT, the acquisition time for whole liver imaging is fewer than 5-10 seconds. Such a short acquisition time provides an opportunity to capture peak enhancement in visceral organs by optimizing contrast medium injection and scan protocols. However, an off-timing scan markedly increases the risk of suboptimal contrast enhancement. A bolus-tracking technique has become widely available and may be indispensable for the optimization of scan timing in individual patients to compensate for the variability of circulation time between patients. Although several researchers have investigated the importance of bolus-tracking [15-17], no previous reports on the optimization of scan delay for the bolus-tracking technique have, to our knowledge, been available. Therefore, the purpose of our study was to optimize scan delays for hepatic arterial and portal venous phases for bolus-tracking techniques in MDCT of the liver.
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We excluded 38 patients from our study for the following reasons: five patients had numerous recurrent tumors after treatment, 15 patients had undergone partial hepatectomy for malignant hepatic tumors, six had undergone total splenectomy, four had diffuse or segmented fatty liver of a severe degree, and eight experienced technical failure related to contrast medium injection, breath-holding, or a machine problem during CT examination. These patients were excluded from the study population because hepatic vascular alterations caused by numerous tumors or preceding surgery, abnormal hepatic density, or artifacts might have adversely affected our evaluation of contrast enhancement. The remaining 171 patients comprising 102 men and 69 women (age range, 18-92 years; mean, 63.1 years) constituted the study population.
The study population contained 27 patients with HCC in cirrhosis, three with HCC in noncirrhotic livers, 17 with liver metastases (from colorectal [n = 8], gastric [n = 4], pulmonary [n = 3], duodenal [n = 1], and uterine cervical [n = 1] cancers), eight with chronic hepatitis, three with cavernous hemangiomas, and 113 with extrahepatic primary neoplasms and healthy livers (gastric [n = 27], colorectal [n = 26], lung [n = 20], uterine [n = 12], lymphoma [n = 5], esophageal [n =4], ovarian [n = 3], malignant melanoma [n = 2], cholangiocarcinoma [n = 2], breast [n = 2], renal [n = 2], pancreatic [n = 2], laryngeal [n = l], cholelithiasis [n = 1], acute pancreatitis [n = 1], chronic pancreatitis [n = 1], urinary stone [n = 1], and an unknown fever [n = 1]).
Contrast Material Injection and Scan Protocols
A CT scanner (LightSpeed Ultra, GE Healthcare) with an 8 x 2.5 mm
detector configuration was used, in which eight interspaced helical data sets
were collected from eight detector rows. The high-speed mode used for first-
and second-phase CT in our study was equivalent to a helical pitch of 1:1.35
with a table speed set at 27 mm per rotation (0.5 seconds). The high-quality
mode used for the third-phase CT was equivalent to a pitch of 1:0.875 with a
table speed set at 17.5 mm per rotation (0.7 seconds). These scanning
parameters were selected to scan the entire liver as rapidly as possible
without impairing image quality. Transverse images were reconstructed and
displayed as 40 sections of 5-mm-thick images with no intersectional gap for
each phase set.
All patients were administered nonionic iodine contrast material containing 300 mg I/mL (Omnipaque 300, Daiichi Pharmaceutical) using a power injector (Autoenhance A-50, Nemotokyorindo) at a rate of 4 mL/s through a 21-gauge plastic IV catheter placed in an upper extremity vein, typically in an antecubital vein. The volume of contrast material delivered was 2 mL/kg of body weight in patients ranging in weight between 38-75 kg (n = 165), but was fixed at 150 mL for patients weighing between 76-86 kg (n = 6), which resulted in a total volume of contrast material of 76-150 mL (mean, 112 mL).
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Patients were randomized into three groups so that scans were commenced at 5, 20, and 45 seconds; 10, 25, and 50 seconds; and 15, 30, and 55 seconds for the first (acquisition time, 4.3 seconds), second (acquisition time, 4.3 seconds), and third (acquisition time, 9.1 seconds) phases, respectively, after the trigger. This trigger threshold level was set to increase the CT value by 50 H at the lower thoracic aorta just above the level of the diaphragmatic dome. The aortic transit time of contrast material was also calculated as the time from initiation of contrast material administration to the trigger point determined by the bolus-tracking program. Figure 1 illustrates the timing schemes used for the three imaging protocols. The first- and second-phase scans were completed during a single breath-hold, and the third-phase scan was commenced after a 20-second breathing interval. The equilibrium phase scan was commenced 160 seconds after the trigger in all patients, although these images were not evaluated in the current study.
Quantitative Image Analysis
Mean CT values (H) in the aorta, spleen, right and left proximal portal
veins, liver parenchyma, and hepatic veins were measured in all patients on
the CT console monitor by using a circular region-of-interest cursor ranging
in size from 5 to 30 mm in diameter on the unenhanced, first-, second-, and
third-phase images. CT values in the aorta were measured in areas just above
the level of diaphragmatic dome; in the spleen, they were measured in one area
covering as much area of splenic parenchyma as possible; in the proximal
portal veins, values were measured in two areas (in the right and left
proximal portal branches) and then averaged; in the liver parenchyma, they
were measured in three areas (the right anterior segment, the right posterior
segment, and the left lobe of the liver) and then averaged; and in the hepatic
veins, they were measured in three areas (the right, middle, and left hepatic
veins) and then averaged. Focal hepatic or splenic lesions, blood vessels,
bile ducts, calcifications, and artifacts were carefully excluded from all
measurement areas.
We performed a subanalysis of 30 patients who had 36 untreated HCCs ranging
from 5 to 75 mm (mean, 16.4 mm). The 30 patients included 21 men and 9 women
ranging in age from 54 to 92 years (mean, 69 years) who had chronic liver
damage caused by type B (n = 5) or type C (n = 22) hepatitis
or with no underlying liver disease (n = 3). Proof of the untreated
HCC was obtained with definitive surgery (n = 6), percutaneous liver
biopsy (n = 12), or measurement of substantially increased
-fetoprotein or proteins induced by vitamin K antagonism (PIVKA-II)
levels, with follow-up CT or MRI showing the progression of hepatic tumors
(n = 12). CT values were measured on unenhanced, first-, second-, and
third-phase images. A circular cursor was placed to encompass as much of the
HCC as possible. When the lesion was too small to accurately place a cursor,
the image was magnified up to three times.
Quantitative degrees of contrast enhancement were expressed as contrast enhancement indexes (CEIs), which were calculated by subtracting CT values on unenhanced images from those on contrast-enhanced images. Spleen-to-liver contrast was assessed as a CT value difference, by subtracting the CT value of the liver from that of the spleen. HCC-to-liver contrast was similarly assessed by subtracting a CT value of the liver from that of the HCC.
Qualitative Image Analysis
Two independent gastrointestinal radiologists prospectively reviewed the
first-, second-, and third-phase images separately versus unenhanced images.
Images were evaluated subjectively by the two interpreters, who were blinded
to patient clinical information. Each interpreter evaluated images in terms of
the degree of contrast enhancement in anatomic structures: the proper hepatic
artery in the porta hepatis, spleen, proximal portal veins, liver parenchyma,
and hepatic veins. Interpreters used a four-point scale: a score of 0 was
assigned when an organ showed virtually no enhancement, 1 for minimal to mild
enhancement, 2 for moderate enhancement, and 3 when an organ was maximally
enhanced. The degree of splenic enhancement moiré pattern was also
assessed, using a four-point scale: a score of 0 for no moiré pattern,
1 for a mild pattern, 2 for a moderate pattern, and 3 for a prominent pattern.
A splenic enhancement moiré pattern was defined as a heterogeneous
enhancement of the spleen, which is believed to be caused by its unique
anatomic structure, with variable rates of flow through the cords of red and
white pulp.
Each interpreter also evaluated HCC depiction for the hepatic arterial enhancement and washout degree. Interpreters used a four-point scale: a score of 0 was assigned when a HCC showed no arterial enhancement or washout, 1 for minimal to mild enhancement, 2 for moderate enhancement, and 3 for marked arterial enhancement or clear washout. When a disagreement occurred, consensus was reached by discussion.
Statistical Analysis
Analysis of variance and multiple comparisons with the Scheffé
criterion [19] were used to
evaluate the following determinants in the three groups; patient age; patient
body weight; aortic transit time; spleen-to-liver contrast; and CEIs of the
aorta, spleen, proximal portal veins, liver parenchyma, and hepatic veins. The
Kruskal-Wallis test and multiple comparisons with the Scheffé criterion
were used to evaluate qualitative scores obtained as categoric data.
To assess interobserver variability at interpreting images, kappa statistics were used to measure the degree of agreement. A kappa value of up to 0.20 stood for slight agreement, 0.21-0.40 for fair agreement, 0.41-0.60 for moderate agreement, 0.61-0.80 for substantial agreement, and 0.81 or greater for almost perfect agreement.
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The mean CEIs of the aorta, spleen, proximal portal veins, liver parenchyma, and hepatic veins in the three patient groups are summarized in Table 2. The scan delays after the trigger-versus-mean CEI curves for the aorta are shown in Figure 2; those for the spleen, proximal portal veins, liver parenchyma, and hepatic veins are shown in Figure 3.
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The mean CEI of the aorta showed a peak (336 H, Fig. 2) at a scan delay of 10 seconds after the trigger (density of the aorta reaching 50 H when obtained at the level of the diaphragm), and then was progressively less with time (Fig. 2). The mean CEI of the spleen increased constantly at images obtained with a scan delay of 5-20 seconds, peaked (116-117 H) at a scan delay of 20-25 seconds, and then gradually reduced with a scan delay of 30 to 55 seconds (106-73 H) (Fig. 3). The mean CEI of proximal portal veins increased constantly at images obtained with a scan delay of 5 to 25 seconds, peaked (149 H) at a scan delay of 25 seconds, and then gradually reduced (Fig. 3). The mean CEI of liver parenchyma increased gradually at images obtained with a scan delay of 5 to 30 seconds, exceeded 50 H at a scan delay of 30 seconds (52 H), and then plateaued (59-63 H) at a scan delay of 45-55 seconds. The mean CEI of the hepatic veins increased constantly at images obtained with a scan delay of 20 to 30 seconds and then plateaued (121-126 H) at a scan delay of 45-55 seconds (Fig. 3).
The scan delays after the trigger-versus-mean spleen-to-liver contrast curves are shown in Figure 4. Spleen-to-liver contrast had peaked (81-84 H) at a scan delay of 10-20 seconds and decreased from a scan delay of 25 seconds. The scan delays after the trigger-versus-mean HCC-to-liver contrast curves and the mean CEI of the liver with chronic liver damage and HCCs in the 30 patients are shown in Figure 5. The HCC-to-liver contrast peaked (39-44 H) at a scan delay of 10-15 seconds, decreased from a scan delay of 25 seconds, and was below zero at a scan delay of 45-55 seconds. The mean CEI of liver parenchyma in the 30 patients with HCCs increased gradually at images obtained with a scan delay of 5 to 30 seconds, exceeded 50 H at a scan delay of 30 seconds (50 H), and then plateaued (51-59 H) at a scan delay of 45-55 seconds.
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The enhancement of liver parenchyma exceeded 50 H at a scan delay of 30 seconds after the trigger and that of the proximal portal veins peaked at a scan delay of 25 seconds after the trigger, which suggests that the optimal portal venous phase starts at a scan delay of 30 seconds after the trigger. However, at this time frame aortic and splenic enhancement were still high (179 and 106 H, respectively), which suggests that a 30-second delay after the trigger was premature for the portal venous phase, because hypervascular tumors in the liver might be continuing to enhance at this time and could be obscured. The liver parenchyma was most intensely enhanced (59-63 H) at 45-55 seconds after the trigger, splenic enhancement was reduced at the same time frame (73-82 H), and the HCC-to-liver contrast was below zero at this time. We infer that the optimal portal venous phase for the detection of hypervascular tumors may start at a scan delay of 45 seconds or even later after the trigger (Fig. 8B).
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Observation of hemodynamics in focal hepatic lesions is important in the differential diagnosis of malignant tumors. Murakami et al. [28] recommended double hepatic arterial phase imaging with MDCT for improving the detection of hypervascular HCCs and reducing false-positive lesions. To perform double hepatic arterial phase imaging, one should be able to obtain biphasic images within a single breath-hold by starting the first phase at a scan delay of 10 seconds and the second phase at a scan delay of 15-20 seconds after the trigger, depending on the time interval necessary between the two scans. Even if the portal venous phase imaging is commenced at a scan delay of 45 seconds after the trigger, patients are allowed a breathing interval of at least 20 seconds between the double hepatic arterial and portal venous phase scans.
Although we used an injection rate of 4 mL/s in all patients in our study, the contrast injection rate is a topic of debate. Bae et al. [7] reported that injection rates of more than 2 mL/s did not substantially increase peak hepatic enhancement, but they did help increase the magnitude of arterial enhancement and the temporal separation of hepatic arterial and portal venous phases of enhancement on dual-phase helical CT. We believe that an injection rate of 4 mL/s is optimal for the better separation of hepatic arterial and portal venous phases, although the separation might be easier owing to the short acquisition time of MDCT, if a lower injection rate were used.
Some limitations of our study should be mentioned. First, our study population included patients with or without chronic liver damage, although HCCs commonly arise in livers with chronic liver damage. In our subanalysis of 30 patients with HCCs, most of whom also had chronic liver damage, the liver parenchyma most intensely enhanced (51-59 H) at 45-55 seconds, although the enhancement was somewhat weaker with livers in the 30-patient subgroup than with livers overall (59-63 H). Based on these results, we infer that the optimal scan delay for portal venous phase imaging, aiming for HCC detection by revealing tumor washout, may not differ much between livers with and without chronic liver damage. However, severe chronic liver damage causing portal hypertension may well affect the intensity and timing of maximal liver parenchymal enhancement.
Second, although a trend to significance was shown in the time-density curves (36 for HCC) and the quantitative and qualitative assessments showed agreement, the lack of statistical significance was probably because of the insufficient size of the population of patients with HCC. In the current study, we assessed optimization for the detection of hypervascular HCCs, but not for hypovascular hepatic tumors such as metastases. Portal venous phase imaging, in which the liver is most intensely enhanced and the greatest tumor-to-liver contrast is achieved, should be investigated in a future work.
In conclusion, optimal enhancement of the hepatic arterial and portal venous phases is achieved when images are obtained from scans initiated at 10-15 and 45-55 seconds after the arrival of contrast material in the lower thoracic aorta. This imaging delay should apply when the given iodine concentration (300 mg I/mL, 2 mL/kg of body weight) is injected IV at a rate of 4 mL/s and a threshold of 50 H is used for a bolus-tracking program.
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1.5 cm) malignant hepatic neoplasms.
AJR 1995; 164:879
-884
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