Liver Volume Variation in Patients with Virus-Induced Cirrhosis: Findings on MDCT

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1 MDCT of Virus-Induced Cirrhosis Hepatobiliary Imaging Original Research Xiang-ping Zhou 1 Tao Lu 1 Yong-gang Wei 2 Xin-zu Chen 3 Zhou XP, Lu T, Wei YG, Chen XZ Keywords: Child-Pugh classification, cirrhosis, hepatitis, liver volume, MDCT DOI: /AJR Received January 21, 2007; accepted after revision March 28, Department of Radiology, West China Hospital, Sichuan University, 37 Guo Xue Xiang, Chengdu, Sichuan, , China. Address correspondence to T. Lu (elisa.lulu@gmail.com). 2 Department of Hepatobiliary Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China. 3 Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China. WEB This is a Web exclusive article. AJR 2007; 189:W153 W X/07/1893 W153 American Roentgen Ray Society Liver Volume Variation in Patients with Virus-Induced Cirrhosis: Findings on MDCT OBJECTIVE. The objective of our study was to establish a standard liver volume formula and explore the correlation between hepatic lobe variations in patients with virus-induced cirrhosis and the severity of disease by measuring the volume of the whole liver, the left lateral segment, and the caudate lobe using 16-MDCT. MATERIALS AND METHODS. The volume and per body surface area (BSA) volume of the whole liver, the left lateral segment, and the caudate lobe were calculated in 113 patients with normal livers and 101 patients with virus-induced cirrhosis who underwent volume CT. The proportion of the left lateral segment volume and the proportion of the caudate lobe volume to the total liver volume, the volume index, and the volume change ratio were also calculated, and these data were grouped by Child-Pugh classification and compared. The standard liver volume formula was constructed from body weight and body height or from BSA. RESULTS. There was a positive correlation between liver volume (LV) and body height, body weight (BW) [LV (cm 3 ) = BW (kg) ], and BSA [LV (cm 3 ) = BSA (m 2 ) ]. The total mean ± standard error (SE) liver volume of the control group was 1, ± cm 3. The mean volumes of the whole liver and of the left lateral segment were ± and ± cm 3, respectively, for Child-Pugh class C patients, which was significantly smaller than those values for Child-Pugh class A and B patients (p < 0.05). The mean volume of the caudate lobe was ± cm 3 for Child-Pugh class A patients, which is significantly larger than those values for Child-Pugh class B and C patients (p <0.05). CONCLUSION. CT-measured liver volume and standard liver volume formulas were helpful in evaluating liver volume variations. Enlargement of the left lateral segment was absolute in Child-Pugh class A and B patients, but was relative in Child-Pugh class C patients; enlargement of the caudate lobe was absolute in Child-Pugh class A patients, but was relative in Child-Pugh class B and C patients. irus-induced cirrhosis is predominant in Asia, with most cases re- V sulting from hepatitis B or C. Severe complications of liver cirrhosis include massive bleeding from the upper alimentary tract, hepatic encephalopathy, primary carcinoma of the liver, and so on. The goal of treating cirrhosis is to sustain or improve liver function and to prevent complications. A change in the volume of the liver could be used to predict liver reserve function in some respect [1]. The morphologic changes of the liver associated with the cirrhotic condition include atrophy of the quadrate lobe and the right lobe and hypertrophy of the left lateral segment and the caudate lobe. The causes of liver cirrhosis are viral infection, such as hepatitis B or C virus; alcohol abuse; primary sclerosing cholangitis; and other metabolic diseases, including Wilson s disease, primary biliary cirrhosis, and hemochromatosis. Several groups of researchers have shown that the morphologic variations of cirrhotic hepatic lobes differ depending on the cause of cirrhosis [2 4]. However, these reports mainly focused only on the hypertrophy of the caudate lobe, not the left lateral segment, and on cases of cirrhosis caused by primary sclerosing cholangitis or alcohol abuse. The availability of rapid volumetric scanning and 3D reconstruction techniques of MDCT has already provided a new method for precisely measuring liver volume before liver transplantation and liver resection. However, CT liver volume measurement in vivo has been limited mainly to healthy adults, and most of the previous studies of liver volume were performed on MR scanners [2, 4 6], which mea- W153

2 sured the width or axial distance of the hepatic lobes but not the actual hepatic lobe volume. Our study focused solely on virus-induced (hepatitis B or C) cirrhosis because of its prevalence in Asia. We measured the volume of the whole liver (total liver volume), the left lateral segment, and the caudate lobe in both healthy and cirrhotic livers using 16-MDCT, and we explored the correlation between variations in liver volume and Child-Pugh classification for the purpose of evaluating liver reserve function more comprehensively and accurately. Materials and Methods Patient Population One hundred one patients with virus-induced cirrhosis who underwent serial abdominal CT at our institution between January 2006 and September 2006 were included in this study (77 men and 24 women; age range, years; mean age, 52 years; height range, m; weight range, kg). These patients had been referred for CT for further examination of an elevated level of α-fetoprotein; for evaluation of the severity of cirrhosis and portal hypertension; for assessment of suspected hepatic lesions seen on other imaging techniques; and for routine scanning before liver transplantation, splenectomy, or splenic artery embolization. There were 97 cases of hepatitis B virus and four cases of hepatitis C virus. All four patients with hepatitis C had histories of blood transfusion. All the patients were diagnosed by a viral antigen test and antibody titration. The diagnosis of cirrhosis was established by clinical evaluation, including liver function tests (n = 74), or by surgical biopsy (n = 27). Patients with hepatic space-occupying lesions, thrombosis in the portal vein system, hepatic duct dilatation, or a history of alcoholism were excluded. We were able to determine Child-Pugh classification from the available clinical records in all the cirrhotic patients: 39 cases were classified as Child- Pugh class A, 38 cases as Child-Pugh class B, and 24 cases as Child-Pugh class C. The control group consisted of 113 consecutive patients who underwent upper abdominal helical CT for conditions unrelated to the hepatobiliary system during the same period at our institution (66 men and 47 women; age range, years; mean age, 50 years; height range, m; weight range, kg). All patients had negative findings on hepatitis B and C surface antigen tests. Patients with conditions potentially affected by the biliary tree (e.g., pancreatic disease), with conditions associated with hemopoietic system disease (e.g., lymphoma and leukemia), and with a history of alcoholism were excluded. Imaging Parameters CT was performed using an MDCT scanner (Sensation 16, Siemens Medical Solutions) with a 0.5-second gantry rotation time. All patients received an injection of a standard dose of 100 ml of iopromide (300 mg I/mL, [Ultravist, Schering]) through a 21-gauge peripheral venous access (generally an antecubital vein) at a flow rate of ml/s. A standard delay of 25 and 70 seconds, respectively, for the arterial and venous phases was applied in all patients. The bolus-injection technique was used to administer contrast material with an automated injector (Vistron CT, Medrad) and was carefully monitored by a nurse. All patients underwent scanning in the supine position during a single breath. The CT examination was performed with a triphasic helical CT protocol that included unenhanced scanning of the upper abdomen from the dome of the diaphragm to include the entire liver ( mm collimation, 7-mm thickness, 7-mm reconstruction interval, 12 mm per rotation, table speed, mas, and 120 kvp). The described imaging technique represents a routine abdominal CT scanning protocol at our institution. Liver Volume Measurement After scanning, portal vein phase 5-mm reconstruction images obtained from the raw data were imported into a volume-measuring program (Volmode VB28B-W, version , Syngo) on an interactive workstation (Leonardo, Siemens). The computer mouse was used to outline the profile of the liver excluding the inferior vena cava and gallbladder on each slice, and the enclosed area was measured. Multiplication of each slice area and the used slice thickness were then calculated automatically. The umbilical portion of the left portal vein and the falciform ligament were used as landmarks on CT images to indicate the borders of the left lateral segment, and the inferior vena cava and the right branch of the portal vein were used to determine the borders of the caudate lobe. Body weight (BW) and body height (BH) recorded at the time of the CT examination were used to calculate body surface area (BSA): BSA = [ BH (cm) BW (kg)] [7]. To allow for differences among individuals, the per-bsa volume of the whole liver, the left lateral segment, and the caudate lobe were calculated. The proportion of the left lateral segment (LLS) and caudate lobe (CL) volume to the total liver volume (TLV) were also calculated (LLS / TLV, CL / TLV, respectively). The standard liver volume formula was deduced on the basis of body weight and body height or BSA, so a formula liver volume (FLV) could be obtained for every patient in the case group to compare with the CT-measured liver volume (CTLV). The volume index (VI = FLV / CTLV) and volume change ratio (VCR = [(CTLV FLV) / CTLV 100%]) were calculated. Statistical Analysis Results were expressed as means ± standard error (SE). The Student-Newman-Keuls test of oneway analysis of variance was used for multiple comparisons. A p value of less than 0.05 was considered statistically significant. Linear regression analysis was used to predict total liver volume using body indexes. Statistical analysis was performed on a computer using an SPSS statistics software package (version 12.0, SPSS). Results Liver volume (LV) positively correlated with BSA: LV (cm 3 ) = BSA (m 2 ) (r 2 = 0.388, p < 0.05). Figure 1 shows the correlation between liver volume and BSA. At the same time, liver volume positively correlated with body height and body weight. The multiple linear stepwise regression model showed that body weight (BW) correlated with liver volume more closely than body height: LV (cm 3 ) = BW (kg) (r 2 = 0.373, p < 0.05), as shown in Figures 2 and 3. The formula liver volumes calculated from BSA for the study group patients with Child- Pugh class A, B, or C cirrhosis compared with those of the healthy control subjects did not show a statistically significant difference (p > 0.05). The volume index of Child-Pugh class C patients was 0.66 ± 0.18, which is significantly lower than the volume index of Child-Pugh class A and B patients (p < 0.05). The volume change ratio of Child-Pugh class C patients was 33.72% ± 18.05%, which is significantly higher than the volume change ratio of Child-Pugh class A and B patients (p < 0.05) (Table 1). The total liver volume of the control group was 1, ± cm 3. The volume of the left lateral segment was ± cm 3 and the volume of the caudate lobe was ± cm 3. The proportion of the left lateral segment volume and the proportion of the caudate lobe volume to the total liver volume were 16.63% ± 4.40% and 2.25% ± 0.76%, respectively (Tables 2 and 3). The total liver volume and per-bsa total liver volume were significantly smaller in cirrhotic patients than in healthy control subjects (p < 0.05), whereas there was not a statistically significant difference between those values for Child-Pugh class A and B patients (p > 0.05). In Child-Pugh class C patients, the W154

3 MDCT of Virus-Induced Cirrhosis 1,800 Fig. 1 Scatterplot shows correlation between liver volume and body surface area. Total Liver Volume (cm 3 ) Total Liver Volume (cm 3 ) 1,600 1,400 1,200 1, ,800 1,600 1,400 1,200 1, Body Surface Area (m 2 ) Body Weight (kg) Fig. 2 Scatterplot shows correlation between liver volume and body weight. total liver volume was the smallest. The left lateral segment volume of Child-Pugh class A and B patients was significantly larger than those of healthy control subjects and Child- Pugh class C patients (p < 0.05), whereas there was not a statistically significant difference in the volume or per-bsa volume of the left lateral segment between healthy control subjects and Child-Pugh class C patients and between Child-Pugh class A and B patients 90 Total Liver Volume (cm 3 ) 1,800 1,600 1,400 1,200 1, Body Height (m) Fig. 3 Scatterplot shows correlation between liver volume and body height. 180 (p > 0.05). The volume and per-bsa volume of the caudate lobe were significantly larger in Child-Pugh class A patients than in healthy control subjects and Child-Pugh class B and C patients (p < 0.05), while the differences in these values between healthy control subjects and Child-Pugh class B and C patients were not statistically significant (Table 2). The data in Tables 1 3 show that the total liver volume was significantly smaller in cirrhotic patients than in healthy control subjects. The total liver volume in Child-Pugh class C patients was the smallest, so the volume index was the lowest and the volume change ratio was the highest in that group. The absolute volume of the left lateral segment was significantly larger in Child-Pugh class A and B patients than in Child-Pugh class C patients and healthy control subjects, whereas there was not a difference between healthy control subjects W155

4 TABLE 1: Correlation Between Cirrhotic Liver Volume Variation and Liver Function Child-Pugh Classification No. of Patients FLV (cm 3 ) CTLV (cm 3 ) Volume Index a and Child-Pugh class C patients. However, the ratio of the left lateral segment to total liver volume (LLS/TLV) was significantly higher in the cirrhotic patients than in healthy control subjects; this finding indicates that the enlargement of the left lateral segment was absolute in Child-Pugh class A and B patients, but was relative in Child-Pugh class C patients. The absolute volume of the caudate lobe was significantly larger in Child-Pugh class A patients than in healthy control subjects and Child- Pugh class B and C patients. However, the ratio of the caudate lobe to total liver volume (CL/TLV) was again significantly higher in all classes of cirrhotic patients. These findings indicate that the caudate lobe hypertrophied absolutely in Child-Pugh class A patients but relatively in Child-Pugh class B and C patients. Figures 4 7 show CT images of a healthy patient and patients with cirrhosis. Volume Change Ratio b A 39 1, ± , ± ± ± B 38 1, ± , ± ± ± C 24 1, ± ± c 0.66 ± 0.18 c ± c Note FLV = formula liver volume, CTLV = CT-measured liver volume. Data are mean ± standard error. a CTLV / FLV. b [(FLV CTLV) / FLV 100%]. c Compared with Child-Pugh classes A and B (p < 0.05). TABLE 2: Comparison of Hepatic Lobe Between Patients with Cirrhosis and Healthy Control Subjects Study Group No. of Patients TLV (cm 3 ) TLV/BSA (cm 3 /m 2 ) LLS (cm 3 ) LLS/BSA (cm 3 /m 2 ) CL (cm 3 ) CL/BSA (cm 3 /m 2 ) Control group 113 1, ± ± ± ± ± ± 6.23 Cirrhotic patients A a 39 1, ± ± ± ± ± ± B a 38 1, ± ± ± ± ± ± 8.64 C a ± ± ± ± ± ± 5.98 Note TLV = total liver volume = TLV/BSA, per body surface area total liver volume, LLS = left lateral segment volume, LLS/BSA = per body surface area volume of the left lateral segment, CL = caudate lobe volume, CL/BSA = per body surface area volume of the caudate lobe. Data are mean ± standard error. a Child-Pugh class. TABLE 3: Comparison of Hepatic Lobe Volume to the Total Liver Volume Between Patients with Cirrhosis and Healthy Control Subjects Study Group No. of Patients LLS/TLV (%) CL/TLV (%) Control group ± 4.40 a 2.25 ± 0.76 a Cirrhotic patients A b ± ± 1.49 B b ± ± 1.42 C b ± ± 1.45 Note LLS/TLV, the percentage of the left lateral segment volume to the total liver volume; CL/BSAP, the percentage of the caudate lobe volume to the total liver volume. Data are mean ± standard error. a Compared with cirrhotic patients (p < 0.05). b Child-Pugh class. Discussion Heymsfield and associates [8] first measured the volume of a cadaver s liver using CT in 1979; they showed that the discrepancy between the volume measured using CT and that measured using the water replacement method was within 5%. In 1981, Moss et al. [9] reported that they also measured liver volume using CT and confirmed the conclusion of Heymsfield et al. Many different researchers have reported that the difference between CTmeasured liver volume and the actual liver volume is minor [8, 10, 11]. Previous studies have shown that sources of error in CT volume calculation include partial volume effect, respiratory phase motion, and interobserver variation [8, 12]. However, because of its faster speed of data collecting and image processing, thinner slice thickness, and fewer of artifacts from respiratory motion, MDCT provides more accurate 3D reconstruction images and finer anatomic images can be obtained even in patients with significant ascites. Joyeux et al. [13] measured 50 healthy livers using CT and obtained a mean total liver volume of 1,497 cm 3 ; Li et al. [14] found that the mean total liver volume of healthy Chinese W156

5 MDCT of Virus-Induced Cirrhosis Fig. 4 CT image obtained in 34-year-old woman from control group shows normal liver. Fig. 6 CT image obtained in 32-year-old man with Child-Pugh class B liver cirrhosis shows hypertrophy of left lateral segment (arrow). adults was 1,250 ± 141 cm 3, which is close to the mean total liver volume of the control group in our study (1, ± cm 3 ) if considering differences in measuring methods and race. In our study, the volume of the left lateral segment and the volume of the caudate lobe were ± and ± cm 3, respectively, and the left lateral segment to total liver volume ratio (LLS/TLV) and caudate lobe to total liver volume ratio (CL/TLV) were 16.63% ± 4.40% and 2.25% ± 0.76%, respectively. Leelaudomlipi et al. [15] measured the volume of 155 hepatic lobes and calculated their proportion to the total liver volume using CT. They reported that the average volumes of the left lateral segment and caudate lobe were 220 ± 57 and 25 ± 7 cm 3, respectively, and accounted for 17% ± 4% and 2% ± 1% of total liver volume, respectively. Abdalla et al. [16] found left lateral segment volume was 242 ± 79 cm 3, or 16% of the total liver volume. These results generally resemble ours, which supports the accuracy and reliability of our measuring method. Fig. 5 CT image obtained in 42-year-old man with Child-Pugh class A liver cirrhosis shows hypertrophy of left lateral segment and caudate lobe (arrows). Fig. 7 CT image obtained in 61-year-old man with Child-Pugh class C liver cirrhosis shows severe atrophy of whole liver. The standard liver volume formula has already been widely and intensively investigated, and together with the CT-measured liver volume, they have been applied to match donor recipient pairs before liver transplantation, to decide the minimum hepatic volume of the donor to select the most appropriate surgical procedure, and to ensure liver function is normal in both donors and recipients after transplantation. The standard LV calculations used for our study can be easily applied in the clinic: LV (cm 3 ) = BSA W157

6 (m 2 ) or LV (cm 3 )=12.90 BW (kg) We can calculate normal standard liver volume for an adult from body height and body weight or from BSA immediately and then compare that value with the CT-measured liver volume in a patient with a pathologic condition. Moreover, we can quantitatively evaluate hepatic volume variation, which could be a helpful supplement for evaluating liver reserve function, selecting an appropriate treatment, and determining the prognosis. The mean total liver volumes of Child-Pugh class A, B, and C patients were 1, ± , 1, ± , and ± cm 3, respectively, all of which are significantly smaller than those of the healthy control subjects. The total liver volumes of Child-Pugh class C patients were significantly smaller than those of Child-Pugh class A and B patients. At the same time, from the volume index and volume change ratio, we can see that the liver of Child-Pugh class C patients not only shrank in size in general, but also varied the most in volume (33.72%), a significantly higher volume change than seen in Child-Pugh class A and B patients. All of these data directly reflect the deduction that the lower amount of liver cells in Child-Pugh class C patients led to the disturbance of the pathophysiologic state and the worst clinical manifestations of the condition. The shape and volume of the left lateral segment vary to some degree even in healthy adults; however, even with this consideration in mind, the absolute volume of the left lateral segment was significantly larger in Child- Pugh class A and B patients, but not in Child- Pugh class C patients, than in healthy control subjects. The left lateral segment to total liver volume ratio (LLS/TLV) was higher among the cirrhotic group than healthy control subjects; thus, enlargement of the left lateral segment in virus-induced cirrhosis patients was absolute in Child-Pugh class A and B patients, so the absolute volume of the left lateral segment and its proportion to the total liver volume were all higher than those values in the control group. On the other hand, in Child-Pugh class C patients, because of the shrinkage of the whole liver, enlargement of the left lateral segment was relative. Due to the redistribution of intrahepatic blood during the early stages of cirrhosis (Child-Pugh class A and B), the total liver volume has already atrophied and the left lateral segment instead swells to compensate for the atrophy and allow seemingly normal liver function. As the disease progresses to the late stage (Child-Pugh class C), the total liver volume has atrophied even more, and that change inevitably influences the left lateral segment so that it is unable to sustain the need for compensation; thus, the actual volume could not be significantly larger, but relatively larger. The volume of the caudate lobe was significantly larger in Child-Pugh class A patients than in Child-Pugh class B and C patients, whereas there was not a difference between the Child-Pugh class B and C patients and the control group. However, the caudate lobe to total liver volume ratio (CL/TLV) was generally higher in all the classes of the cirrhotic group, so we can conclude that enlargement of the caudate lobe is absolute in patients with Child- Pugh class A cirrhosis but is relative in those with Child-Pugh class B and C cirrhosis. The causes of caudate lobe hypertrophy are unclear but are thought to be linked to alterations in portal blood flow. Hepatic fibrosis causes attenuation of the intrahepatic portal and hepatic venous branches, and the hepatic vascular bed is reduced [17]. Impaired drainage of blood from the liver, caused by compression of hepatic venous tributaries by regenerating nodules or fibrosis, increases the resistance to portal flow [18]. The caudate lobe is probably supplied by the posterior branch of the right portal vein, which has a shorter intrahepatic course, and the hepatic venous drainage of this region is preserved; all these factors prevent this region of the liver from atrophying significantly [4, 19, 20]. Therefore, in Child- Pugh class A patients, the whole liver atrophies and the caudate lobe swells to compensate liver function as the left lateral segment. In Child- Pugh class B and C patients, the ever-aggravating liver fibrosis violates the whole liver gradually and the caudate lobe begins to shrink to its normal size; however, the caudate lobe shrinks to a lesser degree than the right lobe and the quadrate lobe [3], so the proportion of the caudate lobe to the whole liver is still higher in Child-Pugh class B and C patients than in the control group. Okazaki et al. [2] compared alcoholic and virus-induced cirrhosis and found that enlargement of the caudate lobe was more frequently seen in patients with alcoholic cirrhosis. Dodd et al. [3] reported that the caudate lobe was the most frequently seen region of hypertrophy in patients with end-stage cirrhosis caused by primary sclerosing cholangitis. All the patients enrolled in our study had virus-induced cirrhosis. We found significant hypertrophy of the caudate lobe in Child- Pugh class A patients that differed distinctly from Child-Pugh class B and C patients. This difference is notable especially for Child- Pugh class B cases because there were not statistical differences in the other indexes we used. Meanwhile, the significant hypertrophy of the left lateral segment could be used to differentiate Child-Pugh class B from Child- Pugh class C. The volume variations of the left lateral segment and of the caudate lobe were part of the continuously developing process of the cirrhotic condition: They initially hypertrophied and then gradually atrophied to resemble their normal size. Therefore, we can conclude that the atrophy mainly happened to the right lobe and the quadrate lobe and became more obvious with the elevating of the Child-Pugh classification. Even in Child- Pugh class C patients, the left lateral segment and caudate lobe did not atrophy, although the whole liver atrophied dramatically. In Child-Pugh class A cirrhosis, both the left lateral segment and the caudate lobe played a role in compensating to allow better liver function; in Child-Pugh class B cirrhosis, only the left lateral segment compensated; in Child- Pugh class C cirrhosis, neither did, and an obstinate decompensation emerged. It seems that the volume of the left lateral segment and the caudate lobe could be used to predict liver function to some extent: the bigger, the better. The five indexes (total bilirubin, albumin, prothrombin time, grade of ascites, and hepatic encephalopathy) that compose the Child-Pugh classification are always influenced by clinical interventions and thus can fluctuate dramatically in a short time, whereas volume is a more stable index and cannot be easily influenced. Liver volume is already considered to be an index of liver function that is as important as the Child-Pugh classification. Liver volume can reflect not only the amount of liver cells but also the hepatic demands. Together with determining the indocyanine green retention rate after 15 minutes, measuring liver volume has been recommended to evaluate liver reserve function in the setting of acute and chronic liver disease, liver transplantation, and liver resection. There are a few limitations in our study. The main limitation is the lack of pathologic confirmation of cirrhosis in 74 patients because liver biopsy was obviated on the basis of a clinical diagnosis of cirrhosis. In clinical practice, the evaluation of extrahepatic conditions, such as varices and ascites, is more helpful for internal medical treatment than for evaluation of the severity of fibrosis and activity of hepatitis in cirrhotic livers. The sec- W158

7 MDCT of Virus-Induced Cirrhosis ond limitation is that cirrhosis in all patients was secondary to viral hepatitis B or C. Patients with cirrhosis secondary to other causes were excluded from our study population. Hepatic lobe variation may differ on the basis of the cause of cirrhosis, so further study is still needed. Finally, the investigators who performed most of the previous studies evaluating cirrhosis preferred to use an MR scanner because it may offer a more extensive and comprehensive evaluation of cirrhosis and because volume measurements on MRI can be as accurate as those made using CT. Therefore, further study is also needed to compare CT and MRI volume measurements. In conclusion, due to the most obvious shrinkage of the whole liver seen in patients with Child-Pugh class C cirrhosis, its volume change was also the greatest. Enlargement of the left lateral segment was absolute in Child- Pugh class A and B patients, but was relative in Child-Pugh class C patients, and enlargement of the caudate lobe was absolute in Child-Pugh class A patients, but was relative in Child-Pugh class B and C patients. References 1. Kubota K, Makuuchi M, Kusaka K, et al. Measurement of liver volume and hepatic functional reserve as a guide to decision-making in resectional surgery for hepatic tumors. Hepatology 1997; 26: Okazaki H, Ito K, Fujita T, Koike S, Takano K, Matsunaga N. Discrimination of alcoholic from virusinduced cirrhosis on MR imaging. AJR 2001; 175: Dodd GD III, Baron RL, Oliver JH III, Federle MP. End-stage primary sclerosing cholangitis: CT findings of hepatic morphology in 36 patients. Radiology 1999; 211: Awaya H, Mitchell DG, Kamishima T, Holland G, Ito K, Matsumoto T. Cirrhosis: modified caudate right lobe ratio. Radiology 2002; 224: Ito K, Mitchell DG, Hann HW, et al. Viral-induced cirrhosis: grading of severity using MR imaging. AJR 1999; 173: Saygili OB, Tarhan NC, Yildirim T, Serin E, Ozer B, Agildere AM. Value of CT and MRI for assessing severity of liver cirrhosis secondary to viral hepatitis. Eur J Radiol 2005; 54: Hu YM, Wu XL, Hu ZH, et al. Study of formula calculating body surface areas of the Chinese adults [in Chinese]. Sheng Li Xue Bao 1999; 51: Heymsfield SB, Fulenwider T, Nordlinger B, Barlow R, Sones P, Kutner M. Accurate measurement of liver, kidney, and spleen volume and mass by computerized axial tomography. Ann Intern Med 1979; 90: Moss AA, Friedman MA, Brito AC. Determination of liver and spleen volume by CT: an experimental study in dogs. J Comput Assist Tomogr 1981; 5: Nawarantne S, Fabiny R, Brien JE, et al. Accuracy of volume measurement using helical CT. J Comput Assist Tomogr 1997; 21: Sakanoto S, Uemoto S, Urynkara K, et al. Graft size assessment and analysis of donors for living donor liver transplantation using right lobe. Transplantation 2002; 71: Higashiyama H, Yamaguchi T, Mori K, Nakano Y, Yokoyama T, Takeuchi T. Graft size assessment by preoperative CT in living related partial liver transplantation. Br J Surg 1993; 80: Joyeux H, Berticelli J, Chemouny S, Masson B, Borianne P. Semi-automatic measurements of hepatic lobes: application to study of liver volumes analysis of 50 computed tomography of normal liver [in French]. Ann Chir 2003; 128: Li YM, Lv F, Ji H, Bai ZL, Lei TJ. A study on the correlation between hepatic volume and liver functional reserve [in Chinese]. Chin J Gen Surg 2003; 18: Leelaudomlipi S, Sugawara Y, Kaneko J, Matsui Y, Ohkubo T, Makuuchi M. Volumetric analysis of liver segments in 155 living donors. Liver Transpl 2002; 8: Abdalla EK, Denys A, Chevalier P, Nemr RA, Vauthey JN. Total and segmental liver volume variations: implications for surgery. Surgery 2004; 135: McIndoe AH. Vascular lesions of portal cirrhosis. Arch Pathol Lab Med 1928; 5: Popper H. Pathologic aspects of cirrhosis: a review. Am J Pathol 1977; 87: Mizumoto R, Kawarada Y, Suzuki H. Surgical treatment of hilar carcinoma of the bile duct. Surg Gynecol Obstet 1986; 162: Doehner GA, Ruzicka FF, Hoffman G, Rousselot M. The portal venous system: its roentgen anatomy. Radiology 1955; 64: W159