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Developmental anomalies of the right hepatic lobe: systematic comparative analysis of radiological features

  • Li-Li Liang , Hao-Jie Li , Yao Hu , Anqin Li , Daoyu Hu and Zhen Li EMAIL logo
Published/Copyright: December 29, 2017
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Open Life Sciences
From the journal Open Life Sciences Volume 12 Issue 1

Abstract

Aim

To investigate the radiological characteristics of developmental anomalies of the right hepatic lobe and to systematically compare the efficiency of CT, MR and ultrasound (US) imaging in revealing characteristics of these disorders.

Methods

This retrospective study was approved by the institutional review board, and the requirement for informed consent was waived. CT, MR or US imaging and clinical data of 43 cases with developmental anomalies of the right hepatic lobe were independently reviewed by two experienced radiologists. Systematic comparative analysis of the CT, MR, and US imaging data indicating the main signs of right lobe aplasia or hypoplasia were obtained. Then, c2 tests were performed to compare the results, considering P<0.05 as the significance threshold.

Results

Agenesis of the right hepatic lobe was observed in two cases. The main imaging features were agenesis of the right lobe and the absence of the right branch of the portal vein and hepatic artery, although one patient exhibited right diaphragm agenesis and a diaphragmatic hernia. Aplasia or hypoplasia of the right hepatic lobe was observed in 41 patients, and among these patients, the main radiological characteristics were as follows: right lobe volume reduction and stenosis of the right portal vein (41 cases, 100%), ectopic gallbladder (39 cases, 95%), left lobe hypertrophy (39 cases, 95%), left portal vein thickening (37 cases, 90%), dextral displacement of the first hepatic portal (32 cases, 78%), caudate lobe hypertrophy (16 cases, 39%), cholelithiasis (12 cases, 29%), portal hypertension (14 cases, 34%), tumor complications (11 cases, 27%), liver abscess (2 cases, 5%), concurrent intrahepatic bile pneumatosis (5 cases, 12%), dysplasia of the right hepatic bile duct (2 cases, 5%), and Budd-Chiari syndrome (2 cases, 5%). Comparative analysis of the main signs of right lobe hypoplasia revealed no significant difference in overall diagnostic efficiency between CT, MRI and US (CT VS MR, X2 = 6.28, P = 0.985; CT VS US, X2 = 11.2, P = 0.797; US VS MR, X2 = 8.48, P = 0.903).

Conclusion

The main radiological characteristics of developmental anomalies of the right hepatic lobe were right lobe volume reduction, stenosis of the right portal vein, ectopic gallbladder, left lobe hypertrophy and dextral displacement of the first hepatic portal. By combining the data from imaging methods (CT, MRI, and US) with clinical data, developmental anomalies of the right hepatic lobe can be relatively accurately diagnosed. The results of this systematic comparative analysis may improve our understanding of this disease.

Keywords: Developmental anomalies; Right hepatic lobe; X-ray computed tomography; Magnetic Resonance Imaging; Ultrasound

1 Introduction

Developmental anomalies of the right hepatic lobe are relatively rare in the clinic. They are defined as a volume reduction or the absence of liver tissue of the right lobe without previous disease or surgery. Generally, these developmental abnormalities are associated with other anatomical alterations, such as hypertrophy of other liver segments, colonic interposition between the liver and the diaphragm, right diaphragmatic hernia, portal hypertension, or anomalous gallbladder positioning [1].

Developmental anomalies of the right hepatic lobe are typically incident findings revealed by ultrasound (US), computed tomography (CT), or magnetic resonance imaging (MRI) because no symptoms are evident. With the popularization of CT, MRI, US and other new imaging techniques, increasing developmental defects of the liver have been identified.

Surgical understanding of such anatomical anomalies is necessary for surgical planning, for appropriate interpretation of intraoperative surgical findings and for the design of postoperative therapy [2,3]. For example, developmental abnormalities associated with ectopic bile duct, hilar vessel or gallbladder in the right lobe of the liver could lead to injury to the gallbladder, bile duct and vascular during an operation [4,5]. Moreover, developmental abnormalities of the right lobe may predispose patients to the development of portal hypertension and esophageal varices, especially when the left lobe is not enlarged [6]. Knowledge of this diagnosis is much more important for the patients themselves because the risk for diseases related to this anatomical alteration is quite high. Thus, receiving a diagnosis of a developmental abnormality of the right liver lobe can remind those without evident clinical symptoms to undergo follow-up visits periodically [7].

According to Pages et al., morphological anomalies related to developmental defects can be categorized as follows: agenesis (absence of a lobe that is replaced by fibrous tissue); aplasia (one of the lobes is small and its structure is abnormal, along with few hepatic trabeculae, numerous bile ducts, and abnormal blood vessels); or hypoplasia (one of the lobes is small but is normal in structure) [8].

Unfortunately, at present, only sporadic cases of developmental anomalies of the right hepatic lobe have been reported, and systematic analyses of the imaging features of these cases have not been performed.

The aim of our prospective study was to investigate the clinical and imaging characteristics of developmental defects of the right hepatic lobe and to perform a systematic analysis of the imaging features of this disease.

2 Materials and Methods

2.1 Patients

CT, MR or US imaging and clinical data of 49 cases with developmental defects of the right hepatic lobe from March 2010 to June 2014 were reviewed. Two cases were excluded from the study due to hepatitis B infection, as demonstrated by biochemical examination. An additional four cases were excluded due to long-term alcohol abuse. The remaining 43 cases (20 men, 23 women; age range, 7-83 years; mean age, 59.9 years) undergoing a clinical inspection that excluded hepatitis virus infection, alcohol and drug abuse and liver operation history were enrolled in this study (Table 1). In fifteen cases, developmental abnormalities were identified based on physical examination (no abdominal dysfunction, accompanied by other diseases such as tumor; trauma patients were included in this category). Ten cases presented with abdominal discomfort and loss of appetite. Fifteen cases exhibited icterus. Abdominal pain, chills, and fever were found in 3 cases. All patients underwent CT, twenty-two patients underwent MRI, thirty patients underwent US, and nine patients underwent surgery that confirmed the diagnosis.

Table 1

Clinical and Biochemical Findings in 43 Patients

CategoryData
Mean age(y)[*]59.86±15.59(7-83)
Gender
men20
women23
The main clinical symptoms
No clinical symptom15
abdominal discomfort10
Icterus15
chills, fever3
Biochemical Findings
Abnormal liver function14
high bilirubin14
Abnormal of tumor markers
CA19916
AFP0
CT43
MRI22
US30

Ethical approval

The research related to human use has been complied with all the relevant national regulations, institutional policies and in accordance the tenets of the Helsinki Declaration, and has been approved by the authors’ institutional review board or equivalent committee. This retrospective study was approved by the institutional review board, and the requirement for informed consent was waived.

2.2 CT Imaging Technique

All examinations were performed using a 64-MDCT scanner (LightSpeed VCT 64, GE Healthcare). CT was performed after administration of 80–100 mL (1.5 mL/kg body weight) of nonionic iodinated contrast medium (iopromide 370 mg I/mL; Ultravist, Shanghai Bracco Sine Pharmaceutical). Arterial phase, venous phase and delayed scans were performed 25 s, 50 s and 3-5 min after injection, respectively. Images were acquired using the following protocol: 120–140 kV, 350 mA, pitch of 0.8, collimation of 1.375 mm, slice thickness of 5.0 mm, reconstruction interval of 0.625 mm, matrix of 512 × 512, and scan time of 6–8 seconds. The original images were reconstructed with a slice thickness of 0.625 mm and a slice interval of 0.625 mm in all 43 patients. The primary methods of image processing were maximum intensity projection (MIP), multiplanar reconstruction (MPR), and volume rendering (VR).

2.3 MRI Technique

Fifteen patients underwent examination using a 1.5-T superconductive unit at an amplitude of 33 mT/m, a slew rate of 80 (mT • m-1) msec-1 (Excite HD; GE Healthcare, Waukesha, WI, USA), and eight patients underwent MRCP. An additional seven patients underwent MRI in the supine position using a 3.0-T MR scanner (Discovery 750, GE Medical Systems, Milwaukee, WI, USA) equipped with a 32-channel phased-array coil. The imaging parameters were as follows: 1.5-T MRI: axial T2 (TR, 2500 ms; TE, 80 ms; NEX, 3; matrix, 192 × 256; FOV, 40 × 40 cm2; section thickness, 5 mm; and spacing, 1 mm), axial T1 (TR, 180 ms; TE, 4.6/2.3 ms; flip angle, 80°; NEX, 1; matrix, 192 × 256; FOV, 40 × 40 cm2; section thickness, 5 mm; and spacing, 1 mm), coronal T2 (TR, 2500 ms; TE, 80 ms; NEX, 2; matrix, 192 × 256; FOV, 40 × 40 cm2; section thickness, 4 mm; and spacing, 0.5 mm), and MRCP (TR, 2050 ms; TE, 900 ms; matrix, 256 × 256; FOV, 20 × 20 cm2; and thickness, 50 mm);

3.0-T MRI: axial T2 (TR, 7500 ms; TE, 45 ms; NEX, 3; matrix, 256 × 256; FOV, 40 × 40 cm2; section thickness, 5 mm; and spacing, 1 mm) and axial T1 (TR, 300 ms; TE, 15/7.5 ms; NEX, 1; matrix, 192 × 256; FOV, 40 × 40 cm2; section thickness, 5 mm; and spacing, 1 mm).

2.4 US Examinations

US examinations were performed by two radiologists (Y.C., with 10 years of experience; X.Y., with 4 years of experience) using a scanner (Philips iU22; Philips Medical Systems, Best, the Netherlands) equipped with 4-MHz and 5–7-MHz electronic convex transducers.

2.5 Image Analyses

MIP was used to display the portal vein, the hepatic artery, the hepatic vein, and the inferior vena cava. MPR was used for multi-azimuth observation of liver lesions, and VR was applied to improve the visualization of the images. The developmental defects of the right hepatic lobe and their complications were assessed based on consensus between two radiologists (L.L., with 5 years of experience; Z.L., with 14 years of experience). The two radiologists assessed and recorded the main signs of right lobe aplasia or hypoplasia. A final result was assigned when the two radiologists reached the same diagnosis. If discrepancies were noted, the radiologists consulted with one another and observed the image together.

2.6 Statistical Assessment

Using SPSS19.0 software, comparative analysis of the main signs of right lobe aplasia or hypoplasia based on the CT, MR, and US imaging findings were analyzed using the c2 test, and P values less than 0.05 indicated statistical significance.

3 Results

Diagnoses were confirmed by surgery in nine patients: abscesses were verified by operation in two patients, cholangiocarcinoma was demonstrated by PTCD in six patients, and poorly differentiated hepatocellular carcinoma of the right lobe of the liver was established by pathology in one patient.

3.1 Agenesis of the Right Hepatic Lobe

Agenesis of the right hepatic lobe, a rare congenital anomaly, was observed in two cases in our study. Chou et al. described the criteria for the diagnosis of agenesis of the right hepatic lobe on CT as the absence of the right hepatic vein, the right portal vein and its branches and dilation of the right intrahepatic ducts [10]. We emphasized the importance of visibility of the right portal vein and its branches in the identification of agenesis and differentiation of this disorder from aplasia or hypoplasia of the right lobe of the liver.

The absence of the right portal vein was observed in both cases. Simultaneously, the left portal vein exhibited compensatory thickening. One patient had an anomalously positioned gallbladder (Figure 1). The other patient lacked the right diaphragm and exhibited a right diaphragmatic hernia. As a consequence, the gallbladder and a portion of the intestine were in the thoracic cavity. Moreover, hypertrophy of the caudate lobe and the left lobe and the absence of the right hepatic artery were observed in this patient (Figure 2).

Figure 1 Images of a 46-year-old man who was diagnosed with agenesis of the right hepatic lobe. (A) Axial contrast-enhanced CT in the portal venous phase displays ectopic gallbladder. (B) MIP reconstruction of a coronal CT image shows the lack of the right branch of the portal vein and compensatory thickening of the left portal vein (arrow).
Figure 1

Images of a 46-year-old man who was diagnosed with agenesis of the right hepatic lobe. (A) Axial contrast-enhanced CT in the portal venous phase displays ectopic gallbladder. (B) MIP reconstruction of a coronal CT image shows the lack of the right branch of the portal vein and compensatory thickening of the left portal vein (arrow).

Figure 2 Images of a 31-year-old man who was diagnosed with agenesis of the right hepatic lobe in association with the absence of the right diaphragm and a right diaphragmatic hernia. (A, B) Coronal contrast-enhanced CT shows the absence of the right diaphragm and an upward shift of the pancreas (arrow A). The gallbladder herniated into the thoracic cavity (arrow B). (C, D) MIP vascular reconstruction of the CT data reveals the absence of the right branch of the portal vein and hepatic artery. (E) An axial CT scan shows hypertrophy of the caudate lobe (star). (F) US examination shows hypertrophy of the left lobe and abnormal broadening of the left portal vein.
Figure 2

Images of a 31-year-old man who was diagnosed with agenesis of the right hepatic lobe in association with the absence of the right diaphragm and a right diaphragmatic hernia. (A, B) Coronal contrast-enhanced CT shows the absence of the right diaphragm and an upward shift of the pancreas (arrow A). The gallbladder herniated into the thoracic cavity (arrow B). (C, D) MIP vascular reconstruction of the CT data reveals the absence of the right branch of the portal vein and hepatic artery. (E) An axial CT scan shows hypertrophy of the caudate lobe (star). (F) US examination shows hypertrophy of the left lobe and abnormal broadening of the left portal vein.

3.2 Aplasia or Hypoplasia of the Right Hepatic Lobe

Forty-one patients with aplasia or hypoplasia of the right hepatic lobe were found in our study. The main imaging findings are presented in Table 2.

Table 2

CT, MRI, and US findings related to aplasia or hypoplasia of the right hepatic lobe

Imaging manifestationsCT (n=41 )MRI (n=22 )US (n=29 )
Right lobe volume reduction41 (100%)22 (100%)20 (69%)
Left lobe hypertrophy39 (95.1%)18 (81.8%)13 (44.8%)
Caudate lobe hypertrophy16 (39%)4 (18.2%)3 (10.3%)
Ectopic gallbladder39 (95.1%)15 (68.2%)20 (69%)
Posterolateral interposition of the hepatic flexure of the colon10 (24.4%)3 (13.6%)1 (3.4%)
Stenosis of the right portal vein41 (100%)10 (45.5%)16 (55.2%)
Left portal vein thickening18 (43.9%)8 (36.4%)15 (51.7%)
Hepatic venous dysplasia1 (2.4%)0 (0%)1 (3.4%)
Dextral displacement of the first hepatic portal32 (78%)16 (72.7%)21 (72.4%)
Cholecystitis10 (24.4%)6 (27.3%)7 (24.1%)
Cholecystolithiasis5 (12.2%)4 (18.2%)4 (13.8%)
Calculi in the bile duct13 (31.7%)6 (27.3%)10 (34.5%)
Portal hypertension14 (34.1%)5 (22.7%)4 (13.8%)
Liver infection2 (4.9%)1 (4.5%)0 (0%)
Biliary tract neoplasm11 (26.8%)4 (18.2%)4 (13.8%)
Bile pneumatosis5 (12.2%)0 (0%)0 (0%)
Dysplasia of the right hepatic bile duct2 (4.9%)1 (4.5%)1 (3.4%)
Budd-Chiari syndrome2(4.9%)0 (0%)2 (6.9%)

3.2.1 CT

Right lobe volume reduction and right portal vein stenosis were observed in 41 patients (Figures 3-8).

Figure 3 Images of a 70-year-old woman with abdominal pain and jaundice who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with common bile duct stones and bile pneumatosis. (A) Coronal CT reconstruction shows dilatation of the common bile duct and calculi of high density (arrow). (B) Axial contrast-enhanced CT in the portal venous phase displays stenosis of the right portal vein (triangle). Gas density (arrow) was observed in the bile duct. (C) Coronal T2-weighted MR image shows a low-signal filling defect in the bile duct(arrow). (D) Axial T2-weighted MR image shows ectopic gallbladder and gallbladder wall thickening, suggesting inflammation of the gallbladder(arrow) . (E) MRCP shows dilatation of the bile duct and a clearly detectable bile duct stone. (F) US shows dilatation of the bile duct and strong echoes with acoustic shadows in the bile duct.
Figure 3

Images of a 70-year-old woman with abdominal pain and jaundice who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with common bile duct stones and bile pneumatosis. (A) Coronal CT reconstruction shows dilatation of the common bile duct and calculi of high density (arrow). (B) Axial contrast-enhanced CT in the portal venous phase displays stenosis of the right portal vein (triangle). Gas density (arrow) was observed in the bile duct. (C) Coronal T2-weighted MR image shows a low-signal filling defect in the bile duct(arrow). (D) Axial T2-weighted MR image shows ectopic gallbladder and gallbladder wall thickening, suggesting inflammation of the gallbladder(arrow) . (E) MRCP shows dilatation of the bile duct and a clearly detectable bile duct stone. (F) US shows dilatation of the bile duct and strong echoes with acoustic shadows in the bile duct.

Figure 4 Images of a 61-year-old woman with abdominal pain and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with common bile duct and gallbladder stones. (A, B) Coronal contrast-enhanced CT in the arterial phase shows ectopic gallbladder, cystic duct tortuosity, and stones in the gallbladder (arrow A) and the bile duct (arrow B). (C) MIP reconstruction of a CT image shows stenosis of the right portal vein.
Figure 4

Images of a 61-year-old woman with abdominal pain and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with common bile duct and gallbladder stones. (A, B) Coronal contrast-enhanced CT in the arterial phase shows ectopic gallbladder, cystic duct tortuosity, and stones in the gallbladder (arrow A) and the bile duct (arrow B). (C) MIP reconstruction of a CT image shows stenosis of the right portal vein.

Figure 5 Images of a 40-year-old man who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with dysplasia of the right hepatic bile duct. Enhanced and unenhanced CT images display right lobe volume reduction and multiple hypodense lesions (dysplasia of the bile duct).
Figure 5

Images of a 40-year-old man who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with dysplasia of the right hepatic bile duct. Enhanced and unenhanced CT images display right lobe volume reduction and multiple hypodense lesions (dysplasia of the bile duct).

Figure 6 Images of a 42-year-old man with chills and fever who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with a liver abscess. (A, B) Coronal contrast-enhanced CT shows the left hepatic lobe with circular, mildly enhanced heterogeneous density (triangle), along with left intrahepatic duct stones (arrow). (C, D) Coronal and axial T2-weighted MR images show a blade-shaped shadow with slightly high density and calculi in the bile duct of the left hepatic lobe. (E) Axial T2-weighted MR image shows retroperitoneal lymph node enlargement (arrow). (F) MRCP shows ectopic gallbladder and partial truncation of the bile duct.
Figure 6

Images of a 42-year-old man with chills and fever who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with a liver abscess. (A, B) Coronal contrast-enhanced CT shows the left hepatic lobe with circular, mildly enhanced heterogeneous density (triangle), along with left intrahepatic duct stones (arrow). (C, D) Coronal and axial T2-weighted MR images show a blade-shaped shadow with slightly high density and calculi in the bile duct of the left hepatic lobe. (E) Axial T2-weighted MR image shows retroperitoneal lymph node enlargement (arrow). (F) MRCP shows ectopic gallbladder and partial truncation of the bile duct.

Figure 7 Images of a 62-year-old woman with abdominal pain and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with cholangiocarcinoma. (A) US shows mild dilatation and wall thickening of the common bile duct. (B) MIP reconstruction of an axial CT image shows stenosis of the right portal vein (arrow). (C, D) Axial and coronal contrast-enhanced CT in the portal venous phase display irregular thickening and enhancement of the bile duct wall (arrow). (E) Coronal T2-weighted MR image shows slightly high signal intensity in the bile duct area. (F) MRCP shows hilar bile duct truncation and intrahepatic bile duct dilatation.
Figure 7

Images of a 62-year-old woman with abdominal pain and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with cholangiocarcinoma. (A) US shows mild dilatation and wall thickening of the common bile duct. (B) MIP reconstruction of an axial CT image shows stenosis of the right portal vein (arrow). (C, D) Axial and coronal contrast-enhanced CT in the portal venous phase display irregular thickening and enhancement of the bile duct wall (arrow). (E) Coronal T2-weighted MR image shows slightly high signal intensity in the bile duct area. (F) MRCP shows hilar bile duct truncation and intrahepatic bile duct dilatation.

Figure 8 Images of a 61-year-old woman with abdominal distention and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with portal hypertension. (A) Axial contrast-enhanced CT in the portal venous phase displays right lobe volume reduction, increased left lobe volume and splenomegaly. (B) Sagittal contrast-enhanced CT in the arterial phase shows retrohepatic gallbladder and a gallstone (triangle). (C) Axial T2-weighted MR image shows ectopic gallbladder, a gallstone (thick arrows) and a small amount of pleural effusion.
Figure 8

Images of a 61-year-old woman with abdominal distention and nausea who was diagnosed with aplasia or hypoplasia of the right hepatic lobe in association with portal hypertension. (A) Axial contrast-enhanced CT in the portal venous phase displays right lobe volume reduction, increased left lobe volume and splenomegaly. (B) Sagittal contrast-enhanced CT in the arterial phase shows retrohepatic gallbladder and a gallstone (triangle). (C) Axial T2-weighted MR image shows ectopic gallbladder, a gallstone (thick arrows) and a small amount of pleural effusion.

Left lobe volume was increased in 39 cases, and caudate lobe volume was increased in 16 cases. Two cases exhibited left lobe volume reduction, and one case exhibited caudate lobe atrophy. Ectopic gallbladder was found in 39 patients, who showed retrohepatic gallbladder or transverse gallbladder (Figures 3-7). Thirteen cases were complicated with bile duct stones (Figures 3A, 4B, and 6A), and five cases were complicated with gallbladder stones; these stones displayed high density in the bile duct or gallbladder without contrast enhancement (Figures 4A, and 8B). Fourteen patients were complicated with portal hypertension, as demonstrated by a tortuous portal vein, a varicose vein, splenomegaly or ascites surrounding the liver (Figure 8). In 5 cases, bile pneumatosis was detected as air density along the bile duct (Figures 3B and 4A). Two abscesses that were confirmed by operation were identified as heterogeneous density of a fuzzy boundary and heterogeneous contrast enhancement (Figure 6A, B). Another eleven patients were diagnosed with cholangiocarcinoma, as revealed by slight hypodensity with inhomogeneous contrast enhancement at the hilus (Figure 7C, D). Moreover, dysplasia of the right hepatic bile duct was detected in 2 patients based on multiple areas of low density in the right hepatic lobe (Figure 5). Budd-Chiari syndrome was found in 2 cases.

3.2.2 MRI

Twenty-two patients underwent MRI or MRCP examination. Right lobe volume reduction was found in all twenty-two patients. Left lobe volume was increased in eighteen cases, and caudate lobe volume was increased in 4 cases. Ectopic gallbladder was found in 15 patients (Figures 3D, 6E, and 7E). Seven patients were complicated with cholelithiasis, as demonstrated by a low signal filling defect in the bile duct or the gallbladder (Figure 3C). Five patients were complicated with portal hypertension, and one patient was complicated with a tumor; these complications were identified by slightly long T2 signal intensity together with intrahepatic bile duct dilatation at the hilus hepatis (Figure 7E). Furthermore, one patient exhibited a liver abscess, as demonstrated by slightly long T2 signal intensity with a fuzzy boundary in the left hepatic lobe (Figure 6D).

3.2.3 US

A total of 29 patients underwent US examination. Right lobe volume reduction was found in 20 patients. Left lobe volume was increased in 13 cases, and caudate lobe volume was increased in 3 cases. Right portal vein stenosis was observed in 16 patients. Ten patients were complicated with bile duct stones, and four patients were complicated with gallbladder stones; these stones were detected as strong echoes with acoustic shadows in the gallbladder or the bile duct (Figure 3F). Ectopic gallbladder was found in twenty patients. A tumor at the hilus hepatis was found in 4 cases based on uneven thickening of the bile duct wall (Figure 7A). Budd-Chiari syndrome was found in 2 cases.

3.3 Comparative Analysis of Imaging Findings of Aplasia or Hypoplasia of the Right Hepatic Lobe

In our study, twenty-two patients underwent both CT and MRI, Twenty-nine underwent both CT and US, and nineteen underwent both MRI and US. We performed comparative analysis of the imaging findings of aplasia or hypoplasia of the right hepatic lobe (Tables 3, 4, and 5, c2 test).

Table 3

Comparative analysis of CT and MRI imaging findings of aplasia or hypoplasia of the right hepatic lobe

Imaging manifestationsCT(n=22)MRI(n=22)
Right lobe volume reduction22 (100%)22 (100%)
Left lobe hypertrophy20 (90.9%)18 (81.8%)
Caudate lobe hypertrophy10 (45.5%)4 (18.2%)
Ectopic gallbladder20 (90.9%)15 (68.2%)
Posterolateral interposition of the hepatic flexure of the colon4 (18.2%)3 (13.6%)
Stenosis of the right portal vein22 (100%)10 (45.5%)
Left portal vein thickening10 (45.5%)8 (36.4%)
Hepatic venous dysplasia1 (4.5%)0 (0%)
Dextral displacement of the first hepatic portal21 (95.5%)16 (72.7%)
Cholecystitis8 (36.4%)6 (27.3%)
Cholecystolithiasis5 (22.7%)4 (18.2%)
Calculi in the bile duct11 (50.0%)6 (27.3%)
Portal hypertension8 (36.4%)5 (22.7%)
Liver infection2 (9.1%)1 (4.5%)
Biliary tract neoplasm5 (22.7%)4 (18.2%)
Bile pneumatosis2 (9.1%)0 (0%)
Dysplasia of the right hepatic bile duct1 (4.5%)1 (4.5%)
Budd-Chiari syndrome1(4.5%)0 (0%)

Table 4

Comparative analysis of CT and US imaging findings of aplasia or hypoplasia of the right hepatic lobe

CT (n=29)US (n=29)
Right lobe volume reduction29 (100%)20 (69%)
Left lobe hypertrophy27 (93.1%)13 (44.8%)
Caudate lobe hypertrophy13 (44.8%)3 (10.3%)
Ectopic gallbladder28 (96.6%)20 (69%)
Posterolateral interposition of the hepatic flexure of the colon5 (17.2%)1 (3.4%)
Stenosis of the right portal vein29 (100%)16 (55.2%)
Left portal vein thickening16 (72.7%)15 (51.7%)
Hepatic venous dysplasia1 (4.5%)1 (3.4%)
Dextral displacement of the first hepatic portal24 (82.8%)21 (72.4%)
Cholecystitis9 (31.0%)7 (24.1%)
Cholecystolithiasis5 (12.2%)4 (13.8%)
Calculi in the bile duct12 (41.4%)10 (34.5%)
Portal hypertension11 (37.9%)4 (13.8%)
Liver infection1 (3.4%)0 (0%)
Biliary tract neoplasm9 (31.0%)4 (13.8%)
Bile pneumatosis5 (17.2%)0 (0%)
Dysplasia of the right hepatic bile duct1 (3.4%)1 (3.4%)
Budd-Chiari syndrome2(6.9%)2 (6.9%)

Table 5

Comparative analysis of MRI and US imaging findings of aplasia or hypoplasia of the right hepatic lobe

Imaging manifestationsMRI (n=19)US (n=19)
Right lobe volume reduction19 (100%)13 (68.4%)
Left lobe hypertrophy16 (84.2%)9 (47.4%)
Caudate lobe hypertrophy4 (21.1%)2 (10.5%)
Ectopic gallbladder14 (73.7%)12 (63.2%)
Posterolateral interposition of the hepatic flexure of the colon3 (15.8%)0 (0.0%)
Stenosis of the right portal vein9 (47.4%)9 (47.4%)
Left portal vein thickening7 (36.8%)8 (42.1%)
Hepatic venous dysplasia0 (0%)1 (5.3%)
Dextral displacement of the first hepatic portal14 (73.7%)16 (84.2%)
Cholecystitis5 (26.3%)6 (31.6%)
Cholecystolithiasis5 (26.3%)4 (21.1%)
Calculi in the bile duct5 (26.3%)8 (42.1%)
Portal hypertension5 (26.3%)3 (15.8%)
Liver infection1 (5.3%)0 (0%)
Biliary tract neoplasm4 (21.1%)3 (15.8%)
Bile pneumatosis0 (0%)0 (0%)
Dysplasia of the right hepatic bile duct1 (5.3%)1 (5.3%)
Budd-Chiari syndrome0 (0%)1 (5.3%)

  1. CT VS MRI: X2=6.28, P=0.985; CT VS US: X2=11.2, P=0.797; US VS MRI: X2=8.48, P=0.903.

There were differences in the detection of certain signs between CT, MRI and US. CT and MRI were superior to US for the identification of some signs, as is shown in Table 3. However, no significant difference in the overall efficiency of right lobe hypoplasia diagnosis between CT, MRI, and US based on our statistical analysis (P>0.05).

4 Discussion

Developmental anomalies of the right hepatic lobe are rare findings. Most studies of these disorders are case reports, and systematic analyses of their imaging features are lacking [2,3,4,5,6,7,8,9]. These abnormalities were first reported in 1870 by Heller to correspond to developmental defects during embryogenesis. The development of the human liver begins during the third to fourth week of gestation. Epithelial hyperplasia at the end of the ventral wall of the foregut forms an outwardly projecting saccular protuberance termed the hepatic diverticulum. The head of the hepatic diverticulum grows rapidly in association with epithelial cell proliferation. Cell cords form and then branch and anastomose to form liver cell plates. The tail of the hepatic diverticulum develops into the gallbladder and the bile duct. Developmental anomalies of the right lobe of the liver are considered to be caused by a failure of the right portal vein to develop or by an error in mutual induction between the primitive diaphragm and the endodermal diverticulum, representing the primitive liver [10].

The mean age of the 43 patients was 59.9 years, ranging from 7 to 83 years; this result indicated that this anomaly is typically latent. This finding is in line with the findings of previous studies [5]. Thus, developmental anomalies of the right lobe can be found at any age.

In our study, 35% of the patients presented with no evident symptoms, and anomalies were found via routine examination, in some cases during an examination for a different cause. Ten (23%) of the patients presented with abdominal discomfort. Moreover, fifteen cases (35%) appeared with jaundice, and three (7%) appeared with chills and fever. One patient exhibited the absence of the right diaphragm and a right diaphragmatic hernia; this patient reported the symptom of chest tightness. Abnormality of liver functions was noted in only 14 patients, and this complication appeared not to be associated with the liver disorder itself but rather with complications of cholecystolithiasis, cholecystitis or a biliary tract neoplasm. These observations indicated that the abnormal hepatic morphology had not induced liver injury, as this abnormality typically remained latent. None of the 43 patients were infected with hepatitis, as demonstrated by an AFP level in the normal range. Increases in CA199 expression were found in 16 cases, 11 of which were complicated with a tumor and 5 with gallbladder or bile duct stones. None of these right hepatic lobe agenesis patients displayed abnormal laboratory results.

4.1 Radiological Features of Agenesis of the Right Hepatic Lobe

Agenesis of the right hepatic lobe is a rare diagnosis and is generally diagnosed incidentally based on imaging, such as US, CT, and MR. Detection of the lack of the right hepatic vein, the right portal vein, and its associated branches and dilation of the right hepatic duct are essential criteria for a radiological diagnosis [9]. The characteristics of 2 cases of agenesis of the right hepatic lobe in our study were the absence of the right lobe of the liver, ectopic gallbladder, hypertrophy of the left lobe and the absence of the right portal vein. One patient exhibited a diaphragmatic hernia and gallbladder herniation into the thoracic cavity.

4.2 Radiological Features of Aplasia or Hypoplasia of the Right Hepatic Lobe

Combining the previous literature [2,3,4,5,6,7,8,9,10,11] with the imaging findings of the 41 patients with aplasia or hypoplasia of the right hepatic lobe examined in our study, we summarize the main imaging features of aplasia or hypoplasia of the right hepatic lobe as follows. 1. The right lobe volume is reduced to varying degrees, in some cases accompanied by left hepatic lobe or caudate lobe hypertrophy. The right lobe volume was reduced in all 41 cases, and the volume of the left hepatic lobe or the caudate lobe was occasionally reduced. The left lobe or caudate lobe volume was reduced in 2 cases and 1 case, respectively. The reason for the lack of compensatory hypertrophy of the left lobe is uncertain, but it has been suggested that the process responsible for agenesis of the right lobe also involves the left lobe, although to a lesser degree [12]. 2. Retrohepatic or transverse gallbladder is observed. The gallbladder is compressed downward and dorsally, and its axis is displaced form a right-anterior to a right-posterior orientation. The gallbladder volume was significantly reduced in an additional two cases, and the remaining gallbladder exhibited a cord-like structure, which may be attributable to developmental abnormalities of the gallbladder.

3. Posterolateral interposition of the hepatic flexure of the colon is detected. 4. The vascular system exhibits an abnormality in which the right portal veins are stenotic and some of these veins display a cord-like morphology. This is the most important characteristic for the diagnosis of dysplasia of the right lobe, as all patients exhibited this feature. Left portal vein thickening was found in 37 cases (86%). Right hepatic artery branch thinning was observed in some patients. Hepatic vein and inferior vena cava hypoplasia could also be found. A reduced size of the hepatic inferior vena cava and compensatory widening of the azygos vein, the hemiazygos vein and the collateral circulation were found in 1 patient. 5. Dextral displacement of the first hepatic portal is detected. A portion of the common bile ducts parallel the right portal vein.

The main complications of these anomalies are as follows. 1. Cholecystitis and cholecystolithiasis were found in 10 cases (24%) and 5 cases (12%), respectively, in our study. The reason for cholecystitis or cholecystolithiasis may be that the abnormal hepatic anatomy and the resultant displacement of the gallbladder produces compression or torsion of the cystic duct, leading to bile stasis in the gallbladder and, ultimately, calculus formation [2]. 2. Choledocholithiasis may be found in association with dilated intrahepatic ducts. The etiology of choledocholithiasis may be associated with abnormal development of the gallbladder, resulting in an elongated tortuous cystic duct and a relatively low position of the common bile duct. These positional changes may cause the cystic duct and the common bile duct to be in parallel, squeezing the common bile duct. Cystic duct stones coupled with repeated inflammation caused by inflammatory factors in the hepatobiliary triangleresulted in poor drainage and stricture of bile duct, which is essential for the development of choledocholithiasis. Congenital bile duct abnormalities, which might also cause choledocholithiasis, were found in 2 patients. It was reported that approximately half of the cases of developmental abnormalities of the right lobe were complicated with gallstones or bile duct stones [13,14]. The results of this study were similar to those of previous studies. 3. Portal hypertension was found in seven patients of our cohort. The probable etiology of portal hypertension appears to be a reduction in the number of intrahepatic branches of the portal vein that is not compensated by increased density of the left lobe vasculature [15,16]. An imbalance between portal inflow and the capacity of the portal bed could be an alternative cause of portal hypertension. Possible vascular resistance in the right portal branches might also cause portal hypertension [12]. 4. Liver infection was detected as liver abscess in two patients. In one case, the abscess was in the left hepatic lobe, and in the other case, the abscess was in the right lobe, which exhibited hypoplasia. Liver infection may be associated with repeated stimulation of bile duct stones, cholestasis and congenital abnormalities of the biliary tract. 5. Biliary tract cholangiocarcinoma was in the hilus in ten cases and in the right lobe in on case. The relationship between aplasia or hypoplasia of the right hepatic lobe and malignant biliary tumors remains to be determined. One explanation for this relationship may be that right hepatic lobe hypoplasia may occur in association with compensatory left hepatic lobe hypertrophy as a consequence of portal vein obstruction due to hilar cholangiocarcinoma [2]. 6. Bile pneumatosis was found in 4 cases (9.7%) of our cohort. This complication might be related to dysfunction of the sphincter of Oddi and congenital dysplasia of the intrahepatic bile duct. There was no previous report of bile pneumatosis in patients with developmental abnormalities of the right hepatic lobe. 7. We observed other complications, such as Budd-Chiari syndrome and idiopathic retroperitoneal fibrosis or absence of the inferior vena cava [17]. Budd-Chiari syndrome was found in 2 cases. Idiopathic retroperitoneal fibrosis was reported by Hisatomi et al. in 2004 [12]. Pulmonary system alterations and the modification of intestinal rotation may also occur.

The differential diagnosis of the lack of the right hepatic lobe includes severe right hepatic lobe atrophy secondary to liver cirrhosis, cholangiocarcinoma, and prior surgical resection.

In our study, ten of the twenty-eight patients underwent CT, MRI and US. We performed comparative analysis of these images for the detection of aplasia or hypoplasia of the right hepatic lobe (Table 3). Some differences in the detection of certain signs were observed between CT, MRI and US; CT and MRI were superior to US in revealing certain signs (Table 3). However, there was no significant difference in the overall efficiency of right lobe hypoplasia diagnosis between CT, MRI, and US based on statistical analysis (CT VS MRI: X2=6.28, P=0.985; CT VS US: X2=11.2, P=0.797; US VS MRI:X2=8.48, P=0.903).

There were several limitations to our study. First, the sample size is relatively small. This limitation might lead to biased results. Second, limited histopathologic data was available for further understanding and substantiating the interpretation of developmental anomalies of the right hepatic lobe. Most patients with the right lobe hypoplasia exhibited no clinical symptoms or had surgical indications; as a result, pathological confirmation of these anomalies was difficult. Third, only 10 of the 28 patients underwent CT, MRI and US. Thus, the results of comparative analysis of aplasia or hypoplasia of the right hepatic lobe may be biased.

5 Conclusion

Developmental anomalies of the right hepatic lobe are relatively rare in the clinic, and there is no evident clinical hallmark of these disorders. There was no difference in the efficiency of CT, MRI and US in revealing characteristics of developmental anomalies of the right hepatic lobe.

  1. Author contributions: Zhen Li contributed to conception and design, Li-Li Liang was responsible for acquired data, Hao-Jie Li and Yao Hu contributed to analysis of data and Anqin Li contributed to interpretation of data; the article was written and edited by Li-Li Liang and Zhen Li and all authors revised and approved the final version.

    Supported by the National Natural Science Foundation of China (grants 81271529), the Hubei Provincial Natural Science Foundation of China (grants 2014CFB298), Health and Family Planning Commission Foundation of the Hubei Provincial (grants WJ2015MB066).

Acknowledgments

We thank Ruobing Liu, Yaqi Shen, Xuemei Hu, and Xiaojuan Li, whose important contributions to this study were indispensable to its success.

  1. Conflict of interest: Authors state no conflict of interest

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Received: 2017-6-16
Accepted: 2017-11-2
Published Online: 2017-12-29

© 2017 Li-Li Liang et al.

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

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https://doi.org/10.1515/biol-2017-0058
Keywords for this article
Developmental anomalies; Right hepatic lobe; X-ray computed tomography; Magnetic Resonance Imaging; Ultrasound
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