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C
Mo Malaki
C
Kamarjit Mangat
C
Abstract
Several imaging modalities are used to investigate the liver and biliary
tract. The commonest is ultrasound, which is safe, cheap and readily
available. It is often used as a screening modality. Computed tomography
or magnetic resonance imaging or both are often the next modalities of
choice, and are used to explore any unusual findings detected on ultrasound. Fluoroscopic imaging procedures, such as percutaneous cholangiography and endoscopic retrograde cholangiopancreatography, are often
used when intervention is required, usually for therapeutic reasons.
In this article, we describe the role of the each of these imaging modalities in benign and malignant hepatobiliary disease, summarize their use
in commonly encountered conditions, such as gallstones, cirrhosis and
focal liver lesions, and delineate their advantages and disadvantages.
Often, a combination of different modalities is required to reach the
final diagnosis. We also describe the complementary role of other less
commonly used modalities.
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Figure 2 Acute cholecystitis with gallstone and acoustic shadow. Note the thickened wall (**) of the gallbladder and the acoustic shadowing caused by the
gallstone (arrow). Not all stones cause a shadow on ultrasound as demonstrated in b (arrow).
Figure 3 Normally the intrahepatic ducts (IHD) are not seen on ultrasound.
When visualized it is usually indicative of biliary obstruction (arrow). Note
the adjacent portal vein (pv). The proximity of the dilated IHD to the pv
produces the so-called parallel sign.
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Figure 4 The normal portal vein (pv) and common bile duct (**).
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Figure 5 The liver is normally slightly isoechoic or hyperechoic to the right kidney (a). In disease states, such as a fatty liver (b), the liver appears brighter
than the adjacent kidney. Fatty liver is a non-specific appearance and can result from a range of conditions such as diabetes, hypercholesterolaemia and
excessive alcohol intake.
Doppler and colour US: colour flow and Duplex are used to assess
hepatic vessels and tumour vascularity. The velocity and waveform of the portal veins, hepatic vein and the hepatic artery can be
reliably assessed. The portal veins are of low velocity (10e20 cm/
second) with a respiratory variation (Figure 7). In portal hypertension, there is loss or attenuation of the portal vein flow. On
Duplex US, the hepatic veins have a triphasic flow pattern similar
to the inferior vena cava (IVC) with respiratory and cardiac cycle
variation. The normal flow in the hepatic veins is towards the IVC.
In tricuspid regurgitation, there is reverse flow in the hepatic veins.
In cirrhosis, there is loss of the triphasic pattern since the encased
hepatic vein is less compliant. The hepatic artery has a high
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Figure 7 The flow in the normal portal vein is monophasic. Colour Doppler
with the cursor placed in the middle of the portal vein.
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Arterial phase: the blood supply of the liver is via the hepatic
artery (25%) and the portal vein (75%). Most tumours have
a predominantly arterial supply.
Imaging the liver 20 seconds after the start of the injection of
contrast is ideal for detecting most lesions. It is a very short phase
because iodinated contrast diffuses rapidly from the intravascular compartment into the extravascular space. Highly vascular
lesions are highlighted against a background of unenhanced
normal liver parenchyma. Such lesions will become isodense if
scanned later during the equilibrium phase, and may be missed.
Portal venous phase: this the commonest phase scan performed
for the evaluation of the liver. It is performed with a delay of
50e70 seconds after contrast injection. There is maximum
enhancement of the liver parenchyma. Many liver metastases are
supplied primarily by the hepatic artery and may therefore
appear as hypodense compared with the normal surrounding
liver parenchyma during this phase (Figure 8).
General uses of CT: CT is useful for assessing the overall background of the liver as well as giving an overview of the
remainder of the abdominal contents. Multiphase MDCT is an
effective method for detecting liver tumours and characterizing
focal lesions.
The main indication for CT in biliary disease is for the diagnosis
and staging of GB carcinoma and in the evaluation of complications of cholecystitis, such as perforation and pericholecystic
abscess. It is also used in identifying the cause of biliary
obstruction, such as periampullary pancreatic tumours and nodal
masses at the porta hepatis (Figure 9). Often, it will differentiate
benign from malignant causes of obstruction and provides guidance for biopsy and radiological staging of biliary tumours.
Despite the immense usefulness of CT in modern medical
practice there are some limitations that should be borne in mind.
First, its high radiation dose, especially in MDCT with multiphase
Unenhanced: unenhanced CT is not done routinely unless haemorrhage or calcification is suspected within liver lesions.
Figure 9 Dilated common bile duct (**) on US. The cause on US was unknown. On CT, there is intrahepatic bile duct dilatation (*). The dilated ducts on CT
are of lower density compared to the adjacent intrahepatic branches of the portal vein, which contain contrasts within them. CT was useful in identifying
the cause of the obstruction in this patient as being due to malignancy of the pancreatic head (not shown).
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scanning; second, its low sensitivity for detecting and characterizing lesions smaller than 1 cm; and third, iodinated contrast is
contraindicated in those with history of previous anaphylaxis
and should be used with extreme caution in patients with renal
impairment.
Table 1
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Figure 12 This patient had undergone previous radiofrequency ablation (RFA) for this malignant liver lesion. On the follow-up CT scan (a), it was not easy
to determine whether the low-density lesion (*) was due to residual disease or post-RFA changes. PET-CT was used as a problem-solving tool. The fused
images from PET-CT (b) show that this lesion was highly metabolically active () compared with the surrounding liver and therefore confirmed that it was
due to residual disease activity rather than pure post-RFA changes.
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