DOI: 10.1148/radiol.2443061051
(Radiology 2007;244:845-851.)
© RSNA, 2007
Biliary Atresia: US Diagnosis1
Terry M. Humphrey, MHSC, DMU, DCR and
Mark D. Stringer, MS, FRCS, FRCPCH
1 From the Department of Radiology (T.M.H.) and Children's Liver & GI Unit (M.D.S.), St James's University Hospital, Beckett Street, Leeds LS9 7TF, England. Received June 17, 2006; revision requested August 21; revision received September 27; accepted November 1; final version accepted January 19, 2007.
Address correspondence to T.M.H. (e-mail: teresa.humphrey{at}leedsth.nhs.uk).
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ABSTRACT
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Purpose: To evaluate prospectively the sensitivity of ultrasonography (US) in the diagnosis of biliary atresia (BA), with surgery as the reference standard.
Materials and Methods: After institutional ethical approval and with informed parental consent, 90 consecutive fasting infants with conjugated hyperbilirubinemia underwent detailed US studies performed by a single operator with a 7.5-MHz curvilinear transducer and a 13.5-MHz linear-array transducer. The following features were prospectively recorded: gallbladder morphology, triangular cord sign, presence of a common bile duct, liver size and echotexture, splenic appearance, and vascular anatomy. The operator was blinded to results of other investigations. Sensitivity, specificity, and positive and negative predictive values were calculated for each US variable. BA and non-BA groups were compared by means of the Fisher exact test for categorical variables and an unpaired t test for continuous variables.
Results: Thirty infants (13 male, 17 female) had surgically confirmed BA, and 60 (35 male, 25 female) had other documented causes of neonatal jaundice; the mean ages at US assessment were 48.5 and 52.4 days, respectively (P > .5). Eight US features showed a significant difference between BA and non-BA groups (P < .001, Fisher exact test). The features with the greatest individual sensitivity and specificity, respectively, in the diagnosis of BA were triangular cord sign (73% and 100%), abnormal gallbladder wall (91% and 95%) and shape (70% and 100%), and an absent common bile duct (93% and 92%). The hepatic artery diameter was significantly larger in infants with BA than in those without BA (mean ± standard deviation, 2.2 mm ± 0.59 vs 1.6 mm ± 0.40, P < .001), but portal vein diameters were not significantly different. By means of all these US features, 88 of 90 infants were correctly classified as having or not having BA, for an overall accuracy of 98%.
Conclusion: BA can be distinguished with US from other causes of conjugated hyperbilirubinemia in 98% of infants if multiple US features are carefully evaluated.
© RSNA, 2007
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INTRODUCTION
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The evaluation of infants suspected of having biliary atresia (BA) is challenging because no single preoperative investigation enables the diagnosis to be made with certainty. Liver biochemistry assessment, biliary radionuclide excretion scanning, magnetic resonance cholangiography, endoscopic retrograde cholangiography, percutaneous needle liver biopsy, and laparoscopy can all be helpful, but their results are not individually diagnostic. The diagnosis of BA is usually suggested after results of several of these investigations (typically including liver biopsy) have been reviewed and the diagnosis is confirmed at laparotomy.
Numerous ultrasonographic (US) features have been described as useful pointers to the diagnosis of BA. Abnormalities in the shape and wall of the gallbladder have, for experienced operators, yielded sensitivities and specificities of more than 90% in the diagnosis of BA (1). The triangular cord (TC) sign, a focal area of increased echogenicity anterior to the bifurcation of the portal vein representing the fibrotic remnant of the extrahepatic biliary tree in BA, has been considered an important diagnostic feature by some (2,3). Other groups (4) have suggested that a combination of three gallbladder features—namely, length less than 19 mm, an irregular wall, and an indistinct mucosal lining (the so-called gallbladder ghost triad)—is diagnostic.
In addition to these US features, BA may be associated with other congenital structural anomalies that are detectable with US (5). For example, in the BA splenic malformation syndrome, as defined by Davenport et al (6), BA can be associated with polysplenia, situs inversus, an interrupted inferior vena cava, and other cardiovascular anomalies. Furthermore, infants with BA typically have a degree of hepatic fibrosis or cirrhosis, and the majority have some evidence of portal hypertension as early as 8 weeks of age (7); these pathologic changes may sometimes be evident at US. Finally, hypertrophy of the hepatic artery has been reported in infants with BA (8). The purpose of our study was to evaluate prospectively the sensitivity of US in the diagnosis of BA, with surgery as the reference standard.
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MATERIALS AND METHODS
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Study Group
Between February 2002 and November 2005, consecutive infants with conjugated hyperbilirubinemia of unknown cause were prospectively evaluated at our supraregional unit, which is one of three pediatric liver units in the United Kingdom. The study was approved by our Institutional Clinical Research Ethics Committee, and informed parental consent was obtained. Infants with conjugated hyperbilirubinemia of unknown cause undergo a series of investigations to establish the diagnosis. In those suspected of having BA, the investigations include a detailed biochemical and metabolic workup, an abdominal US scan, a radioisotope biliary excretion scan, and a percutaneous needle biopsy of the liver. In all cases of BA, the diagnosis was confirmed at laparotomy, the reference standard.
US Imaging
All infants underwent a detailed abdominal US examination performed by a single operator (T.M.H., with 10 years of experience with pediatric US) who was blinded to the results of other investigations, such as hepatobiliary scintigraphy, liver function testing, and histologic findings after liver biopsy. The equipment used was a US system (Sonoline Elegra; Siemens, Washington, DC) with a 7.5-MHz multifrequency curvilinear transducer and a 13.5-MHz multifrequency linear-array transducer. Infants were not fed for 4 hours before their examinations because it was thought that the gallbladder could be assessed more easily when it was not contracted. None of the infants were sedated.
The gallbladder was interrogated with the 13.5-MHz linear-array transducer to assess its shape and the regularity of its wall. An irregular wall and a distortion of the gallbladder's usual shape were considered abnormal (Fig 1). In some instances, irregularity of the gallbladder wall may be subtle (Fig 1c), and it is therefore important that the gallbladder is examined with a high-frequency probe. The gallbladder length was measured. The high-frequency transducer was also used to look for the TC sign; when present, this sign can be found by scanning in a transverse oblique plane and identifying a focal area of increased echogenicity anterior to the bifurcation of the portal vein (Fig 2). If the common bile duct (CBD) was visible, its caliber was recorded. Color Doppler flow imaging was used to help identify the CBD. Liver size and echotexture were assessed; the liver was considered to be enlarged if the right lobe extended below the right kidney (9). Features of portal hypertension, such as ascites, reversed blood flow in the portal vein, portal vein caliber, splenic varices, and splenomegaly, were recorded, and the caliber of the hepatic artery was noted. Splenomegaly was defined as when the spleen had a length of more than 6 cm (10). Any features suggestive of the BA splenic malformation syndrome (6), such as polysplenia and an interrupted retrohepatic vena cava, were also noted.
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Figure 1a: Longitudinal sonograms obtained with 13.5-MHz transducer. (a) Normal gallbladder (arrow) in 5-week-old infant without BA has normal shape and regular wall. Calipers and dotted line indicate gallbladder length measurement. Bowel (arrowhead) is seen posterior to the gallbladder. (b) Small, abnormal gallbladder (arrow) in 8-week-old infant with BA has irregular wall and abnormal shape. (c) Abnormal gallbladder (arrow) in 10-week-old infant with BA. Note the more subtle irregularity of the wall (arrowheads) of this 21-mm-long gallbladder.
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Figure 1b: Longitudinal sonograms obtained with 13.5-MHz transducer. (a) Normal gallbladder (arrow) in 5-week-old infant without BA has normal shape and regular wall. Calipers and dotted line indicate gallbladder length measurement. Bowel (arrowhead) is seen posterior to the gallbladder. (b) Small, abnormal gallbladder (arrow) in 8-week-old infant with BA has irregular wall and abnormal shape. (c) Abnormal gallbladder (arrow) in 10-week-old infant with BA. Note the more subtle irregularity of the wall (arrowheads) of this 21-mm-long gallbladder.
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Figure 1c: Longitudinal sonograms obtained with 13.5-MHz transducer. (a) Normal gallbladder (arrow) in 5-week-old infant without BA has normal shape and regular wall. Calipers and dotted line indicate gallbladder length measurement. Bowel (arrowhead) is seen posterior to the gallbladder. (b) Small, abnormal gallbladder (arrow) in 8-week-old infant with BA has irregular wall and abnormal shape. (c) Abnormal gallbladder (arrow) in 10-week-old infant with BA. Note the more subtle irregularity of the wall (arrowheads) of this 21-mm-long gallbladder.
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Figure 2a: TC sign. (a) Transverse sonogram shows TC sign (arrow) in 7-week-old infant with BA. Area of increased echogenicity (as indicated by calipers) is seen anterior to bifurcation of portal vein (arrowheads). (b) Sagittal sonogram in 10-week-old infant with BA shows TC sign (arrow) superior to portal vein (arrowhead).
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Figure 2b: TC sign. (a) Transverse sonogram shows TC sign (arrow) in 7-week-old infant with BA. Area of increased echogenicity (as indicated by calipers) is seen anterior to bifurcation of portal vein (arrowheads). (b) Sagittal sonogram in 10-week-old infant with BA shows TC sign (arrow) superior to portal vein (arrowhead).
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Statistical Analysis
Sensitivity, specificity, and positive and negative predictive values were calculated for each US variable. The Fisher exact test was used to determine whether the frequency of each variable differed significantly between the BA and non-BA groups. An unpaired t test was used to compare normally distributed continuous variables, such as portal vein and hepatic artery diameters. The Bonferroni method was used to adjust for multiple comparisons. Statistically significant differences were defined as those with P values less than .05, and analyses were performed with statistical software (SPSS, version 12; SPSS, Chicago, Ill).
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RESULTS
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A total of 90 infants were evaluated—30 with BA and 60 with other causes of conjugated hyperbilirubinemia (Fig 3). Clinical characteristics were compared for the two patient groups at the time of US scanning; there was no significant difference (P > .5) in age between the groups (Table 1).
BA Group
In all infants with BA (n = 30), the diagnosis was confirmed at surgery and at subsequent histologic examination; 29 infants had type 3 BA (no residual patent extrahepatic bile ducts), and one infant had type 1 BA (CBD atresia). Four had features of the BA splenic malformation syndrome (6) (see below). Preoperative evaluation included a radioisotope (technetium 99m [99mTc] HIDA) biliary excretion scan in 29 infants, which showed no excretion in all 29, and percutaneous needle liver biopsy in 21 infants. One patient in this group died of congenital heart disease. All others were still being followed up at a median age of 14 months (range, 2–46 months); 18 were free of jaundice and were well after a Kasai portoenterostomy, and 11 had undergone successful transplantation.
Non-BA Group
A wide variety of diagnoses accounted for conjugated hyperbilirubinemia in this group of infants (n = 60) (Table 2). A radioisotope (99mTc HIDA) biliary excretion scan was performed in 53 infants (no excretion was found in 23 infants), and a percutaneous needle liver biopsy was performed in 27. Five infants in this group eventually required laparotomy, surgical cholangiography, and wedge liver biopsy to exclude BA definitively. Five infants underwent follow-up elsewhere, and the other 55 were followed up locally for a median of 16 months (range, 3–44 months). In 44 of 55 infants, jaundice completely resolved (as was confirmed with biochemical testing). Six infants had persistent jaundice (two each had progressive familial intrahepatic cholestasis, Alagille syndrome, and cystic fibrosis), four infants with complex multisystem disorders died, and one infant with neonatal sclerosing cholangitis underwent successful liver transplantation. This group of patients had a wide spectrum of disorders, and detailed follow-up confirmed that none had BA.
US Findings
There was a significant difference in the frequency of each US feature between the BA and non-BA groups (Table 3). In two comparisons, detection of the gallbladder and polysplenia, differences just failed to reach statistical significance after adjustment for multiple comparisons. When all US features were used, 88 of 90 infants were correctly classified into the BA or non-BA group, for an overall accuracy of 98% (Table 4). Two infants were incorrectly classified as having BA; one infant with histologic features of biliary hypoplasia had a sonographically abnormal gallbladder wall and no visible CBD, and one premature, growth-retarded infant with neonatal hepatitis syndrome had no detectable gallbladder or CBD at US.
The mean gallbladder length was significantly smaller in infants with BA (mean ± standard deviation, 18.8 mm ± 7.9 [n = 23]) than in those without BA (25.9 mm ± 6.9 [n = 58], P < .001) (Fig 4). The mean hepatic artery diameter was significantly larger in the BA group than in the non-BA group (2.2 mm ± 0.59 vs 1.6 mm ± 0.40, respectively; P < .001) (Fig 5). In contrast, portal vein diameters were not significantly different between the two groups (BA group, 4.1 mm ± 0.58 [n = 29]; non-BA group, 4.1 mm ± 0.59 [n = 60]; P > .5), and there were no infants with reversed blood flow in the portal vein, an occluded portal vein, or splenic varices. Only one infant, a boy with BA, had an abnormal, coarse liver echotexture.
In two infants with BA, the CBD was considered to be visible at US. One of these infants was found at surgery to have a patent distal CBD in continuity with the gallbladder but no patent proximal extrahepatic bile ducts (type 3 BA). Of the four infants with the BA splenic malformation syndrome, three had polysplenia and an interrupted retrohepatic vena cava at US. The fourth had an absent portal vein, and at laparotomy he was found to have a congenital portocaval fistula and a segmented spleen. One other infant had an interrupted vena cava and BA but no other anomalies at laparotomy.
Three infants in the non-BA group had cystic fibrosis; two of these infants had a small gallbladder (<19 mm long) and two had an irregular, thickened gallbladder wall (Fig 6). In two infants in the non-BA group, the gallbladder could not be identified with US. One infant with no other US evidence of BA had inspissated bile plug syndrome with agenesis of the gallbladder that was subsequently confirmed at laparotomy. The other also had an absent CBD and was one of the two infants with incorrectly classified disease described above.
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Figure 6: Longitudinal sonogram of abnormal irregular gallbladder wall (arrow) in 6-week-old infant with cystic fibrosis and conjugated hyperbilirubinemia. This infant did not have BA.
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DISCUSSION
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Several groups have previously attempted to diagnose BA by means of a limited number of specific US features. Using a 7.5-MHz probe in jaundiced infants, Farrant et al (1) determined that an absent gallbladder or one with an irregular wall or abnormal shape had a sensitivity, specificity, and accuracy of 90%, 92.4%, and 91.9%, respectively, in the diagnosis of BA. Diagnostic accuracy improved to 95.6% in a subsequent study (11) of 158 infants (35 of whom had BA) when a 13-MHz linear-array probe was used. Patients were not fasting, and the presence of a TC sign was not recorded. Tan Kendrick et al (4) used the gallbladder ghost triad (gallbladder length < 19 mm, lack of a smooth mucosal lining with an indistinct wall, and irregular or lobular contour) in the diagnosis of BA. US examinations were performed with a 5–12-MHz linear-array transducer in fasting infants. The gallbladder ghost triad was present in 30 of 31 infants with BA, with no false-positive findings.
Choi et al (3) evaluated the TC sign in 41 infants and concluded that it was a sensitive marker of BA. BA was confirmed in 12 of 13 jaundiced infants with a positive sign, but one of the 28 infants with an absent TC sign was mistakenly considered to have neonatal hepatitis and was later found to have BA. Whereas some authors (12,13) have promoted the TC sign as a sensitive and specific US marker of BA, others (4,14,15) have been more cautious. Thus, Park et al (14) found that the TC sign had a sensitivity of 84% and a specificity of 98% in their series of 79 infants, 25 of whom had BA, and Tan Kendrick et al (4) identified an identical sensitivity in 31 infants with BA.
Other US features of BA have been evaluated. Azuma et al (16) recorded the presence or absence of the CBD in 30 infants, as seen with a 5- or 7-MHz probe. In the 23 infants with confirmed BA, nonvisualization of the CBD had a sensitivity of 83% but a specificity of only 71%. False-negative results are inevitable when the presence or absence of the CBD is used as a criterion for diagnosing BA, because a patent distal CBD in continuity with the gallbladder can be found in 10%–20% of affected infants with type 3 BA (17). Ho et al (8) noted that the hepatic artery in children with BA appeared hypertrophied, and others (4) have also commented on the prominence of the hepatic artery in infants with BA.
After a detailed review of previous reports, we evaluated these and other US features prospectively in a consecutive series of infants suspected of having BA to determine the accuracy of abdominal US in diagnosis. Although the frequency of each US feature was significantly different between the BA and non-BA groups, the variable sensitivity and specificity of individual features noted in the literature were confirmed. Using the criteria proposed by Farrant et al (11) (irregular gallbladder wall and shape), we obtained an overall diagnostic accuracy of 95%. We agree with Tan Kendrick et al (4) that the TC sign is a highly specific but less sensitive marker of BA, but we could not confirm the accuracy of their gallbladder ghost triad. Indeed, gallbladder length was 19 mm or greater in nine of 23 infants (39%) with BA in our series.
In our study, visualization of the CBD was associated with a sensitivity and specificity of more than 90%, but the reliability of this feature is limited for several reasons. The normal caliber of the CBD in an infant is 0.74 mm ± 0.4 (18), which makes detection technically challenging. Moreover, confirming that a feature is absent is often more demanding than ascertaining its presence. Finally, a patent distal CBD may be present in some infants with BA and proximal extrahepatic bile duct occlusion.
We have shown for the first time, to our knowledge, that the caliber of the hepatic artery is significantly larger in infants with BA, but the degree of overlap with the non-BA group and the potential likelihood of intraoperator variability mean that individual measurements are not particularly discriminative. However, a prominent hepatic artery can be regarded as a supporting feature for the diagnosis of BA. Why the extrahepatic artery is larger in BA is unknown, but the increased size may be secondary to increased arterial resistance from hypertrophy of the media of intrahepatic arteries, which has been observed specifically in BA (19). Portal vein diameters were not significantly different between infants with BA and those with other causes of conjugated hyperbilirubinemia, indicating that the narrow portal vein commonly seen in infants with BA at liver transplantation (20) is acquired rather than congenital.
An enlarged liver and splenomegaly were both found to be individually statistically significant features in infants with BA. However, these are relatively nonspecific findings, and a diagnosis of BA could not be made solely on their basis. As with hepatic artery caliber, the presence of these "soft markers" can support the diagnosis of BA.
A possible limitation of our study was that all US examinations were performed by a single operator. Operator experience is a critical component in the detection and interpretation of US findings, and similar results may be achieved only if infants with conjugated hyperbilirubinemia are assessed by dedicated experienced personnel in a referral center that deals with similarly large numbers of infants with conjugated hyperbilirubinemia. We have not yet attempted to determine the interobserver variability of our findings in the US evaluation of BA.
The key conclusion of our study is that with use of a combination of all US features, 88 of 90 infants were correctly classified in the BA or non-BA group, for an overall accuracy of 98%. Importantly, no infant with BA was incorrectly classified in the non-BA group. Our study suggests that in most patients BA can be accurately diagnosed by means of US, avoiding the need for potentially harmful and expensive additional diagnostic procedures in this group of patients. If a TC sign is clearly visualized, the patient can proceed to minilaparotomy and surgical cholangiography. The likelihood of seeing a TC sign in a jaundiced infant who does not have BA is extremely small; in a total of seven published series (3,4,12–15,21) comprising 416 infants with conjugated jaundice, only three (0.7%) had a false-positive TC sign. In four of these series, no false-positive TC sign was recorded, which concurs with our experience to date.
An abnormal gallbladder is also an important positive pointer to BA, but this is less reliable as an isolated finding in the absence of other US features of BA, as we also observed it in infants with jaundice associated with cystic fibrosis.
Infants with no US evidence of BA will still require further investigation to establish the cause of their conjugated hyperbilirubinemia. An accurate diagnosis of BA is possible if multiple US features are carefully analyzed by an experienced operator.
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ADVANCES IN KNOWLEDGE
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- An accuracy of 98% can be achieved in the US diagnosis of biliary atresia (BA).
- We have shown for the first time, to our knowledge, that the caliber of the hepatic artery is significantly increased in infants with BA compared with the caliber in infants with other causes of conjugated jaundice.
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IMPLICATION FOR PATIENT CARE
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- Accurate diagnosis of biliary atresia with US may reduce the need for invasive procedures such as percutaneous needle liver biopsy.
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ACKNOWLEDGMENTS
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We thank Vicki Allgar, PhD, for her assistance with the statistical analysis.
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FOOTNOTES
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Abbreviations: BA = biliary atresia • CBD = common bile duct • TC = triangular cord
Authors stated no financial relationship to disclose.
Author contributions:Guarantors of integrity of entire study, T.M.H., M.D.S.; study concepts/study design or data acquisition or data analysis/interpretation, T.M.H., M.D.S.; manuscript drafting or manuscript revision for important intellectual content, T.M.H., M.D.S.; manuscript final version approval, T.M.H., M.D.S.; literature research, T.M.H., M.D.S.; clinical studies, T.M.H., M.D.S.; statistical analysis, T.M.H., M.D.S.; and manuscript editing, T.M.H., M.D.S.
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A. Giannattasio, F. Cirillo, D. Liccardo, M. Russo, G. Vallone, R. Iorio, T. M. Humphrey, and M. D. Stringer
Diagnostic Role of US for Biliary Atresia
Radiology,
June 1, 2008;
247(3):
912 - 913.
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ABSTRACT
INTRODUCTION
