Noninvasive GI Imaging: Ultrasound, Computed Tomography, and Magnetic Resonance Imaging

How has multidetector computed tomography (MDCT) changed the evaluation of the liver, pancreas, and biliary system?

MDCT allows for the rapid acquisition of images using very thin collimation (0.6 mm) and reconstruction intervals (0.5 mm). Using these true isotropic volumetric data sets, exquisite multiplanar reformations (MPR) in the coronal, sagittal, or any other imaging plane can be created ( Figure 69-1 ).

Imaging can be performed in the noncontrast computed tomography (NCCT) phase, early hepatic arterial phase (HAP), late HAP, and the portal venous phase (PVP) depending on the clinical indication. The early HAP is approximately 20 seconds after injection, the late HAP is 35 to 40 seconds after injection and the PVP is 60 to 70 seconds after injection, with the dominant contrast effect in the liver occurring in the PVP. This ability to image rapidly can take advantage of the dual blood supply of the liver—75% from the portal vein (PV) and 25% from the hepatic artery.

MDCT improves the imaging of the hepatic vasculature. It is very helpful in preoperative or preintraarterial chemotherapy planning and for the detection of hepatic infarctions, aneurysms and pseudoaneurysms, PV thrombosis, or strictures. Liver volumes prior to hepatic resection can also be estimated using volume-rendered images.

How is segmental liver anatomy defined?

The liver is divided into four lobes based on the surface configuration and the hepatic veins (HVs). The different hepatic segments are divided by intersegmental fissures, which are traversed or are in the same plane as the HVs.

The main lobar fissure divides the liver into right and left lobes and is represented by a line extending from the gallbladder recess through the inferior vena cava (IVC). It is represented by the middle HV. The right intersegmental fissure divides the right lobe of the liver into anterior and posterior segments and is approximated by the right HV. The left intersegmental fissure divides the left lobe of the liver into medial and lateral segments. It is marked on the external liver margin by the falciform ligament, and it is represented by the left HV. The caudate lobe is the portion of liver located between the IVC and the fissure of the ligamentum venosum ( Figure 69-2 A and B ).

Couinaud’s anatomy further subdivides the liver into eight segments, each with its own blood supply. The eight segments are the caudate lobe (I), the left superior (II) and inferior (III) lateral segments, the left superior (IVa) and inferior (IVb) medial segments, the right anterior (V) and posterior (VI) inferior, and the right posterior (VII) and anterior (VIII) superior segments.

Describe the ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) findings of fatty infiltration of the liver.

• US: Fatty infiltration is seen as areas of focal or diffuse increased echogenicity that do not demonstrate mass effect on adjacent biliary structures or blood vessels. Fatty infiltration may limit or prevent visualization of intrahepatic vessels, the deeper posterior portion of the liver, and the diaphragm posterior to the liver. Hepatitis or cirrhosis can also present with diffusely increased liver echogenicity.

• CT: On NCCT, the liver is normally 8 Hounsfield units (HU) greater in density than the spleen. In fatty infiltration, the spleen is 10 HU more dense than the liver. In diffuse fatty infiltration, the hepatic vessels are more conspicuous and may appear as if they contain contrast even on a NCCT scan. In focal fatty infiltration, the normal hepatic vessels traverse the area of decreased attenuation, a finding not usually present in malignancy. Focal fatty infiltration tends to be in a lobar distribution (wedge shaped) with linear margins ( Figure 69-3 ). Areas where fatty infiltration or sparing typically occur include the gallbladder fossa, subcapsular, left lobe medial segment near the fissure for the ligamentum teres, anterior to the porta hepatis, and around the IVC.

  

• MRI: Signal differences in focal fatty infiltration of the liver may be subtle. As with CT, vessels should course normally through the area of signal abnormality without mass effect on adjacent structures. MRI with fat suppression is more sensitive than T1-weighted (T1-w) and T2-weighted (T2-w) imaging for fatty infiltration, with fatty infiltration having decreased signal intensity compared with normal liver. Areas of fatty infiltration will also reliably demonstrate decreased signal on opposed-phase T1-w imaging.

Describe the US, CT, and MRI findings in cirrhosis.

• US: The hepatic parenchyma in cirrhosis is typically heterogeneous and hyperechoic with “coarsened” echoes and poorly defined intrahepatic vasculature. Unfortunately, these findings are nonspecific, with increased parenchymal echogenicity also present in fatty infiltration, and parenchymal heterogeneity also present in infiltrating neoplasms. Sonographic features with greater specificity for cirrhosis include nodularity of the liver surface and relative enlargement of the caudate lobe. A caudate-to-right lobe volume ratio of more than 0.65 is highly specific but not sensitive in diagnosing cirrhosis.

• MDCT: In cirrhosis, the caudate lobe and left-lateral segment typically enlarge, and the right lobe and left-medial segment typically atrophy, resulting in an enlarged gallbladder fossa. Enlargement of the hilar periportal space, as a result of atrophy of the left lobe medial segment, is more than 90% sensitive and specific for early cirrhosis. In advanced cirrhosis, liver volume usually decreases and periportal fibrosis and regenerative nodules can compress the portal and hepatic venous structures, which may result in altered hepatic perfusion and portal hypertension. The presence of isodense regenerating nodules can often only be inferred from the nodular contour of the liver edge. Complications of portal hypertension, especially varices, are exquisitely demonstrated with MDCT; however, unlike sonography, CT cannot determine the direction of vascular flow ( Figure 69-4 ). Increased attenuation of the mesenteric fat is also noted.

  

• MRI: MRI findings in cirrhosis are similar to those on MDCT, with early changes manifesting as enlargement of the hilar periportal space as a result of atrophy of the left lobe medial segment and later findings presenting as a caudate/right hepatic lobe ratio of more than 0.65 and an expanded gallbladder fossa sign. Regenerative nodules are usually smaller than 1 cm in diameter, have variable T1-w signal, and usually iso to decreased T2-w and gradient-recalled echo (GRE) signal. Regenerative nodules are usually isointense to liver following contrast.

  Dysplastic nodules are considered premalignant and are usually larger than regenerative nodules. They often demonstrate increased T1-w and decreased T2-w signal; however, there is overlap with hepatocellular carcinoma (HCC). Imaging findings of portal hypertension are similar to those on MDCT and initially include dilation of the portal and splenic veins with later occlusion and cavernous transformation of the PV and development of portosystemic collaterals and ascites.

Which is the most sensitive examination for detecting hemochromatosis?

• MRI: Because many patients with hemochromatosis will develop cirrhosis and 25% will develop HCC, it is important to diagnose early.

• US: US examination is normal despite iron deposition, unless underlying cirrhosis is present.

• NCCT: Liver attenuation is typically more than 70 HU in hemochromatosis, compared with a normal level of approximately 45 to 60 HU.

• MRI: More sensitive and specific than CT in detecting hemochromatosis. On MRI, the paramagnetic effects caused by iron deposition result in decreased T2-w and GRE signal intensity ( Figure 69-5 ).

  

How do liver metastases appear on US, CT, and MRI?

• US: Appearance is variable. Gastrointestinal and more vascular tumors (e.g., islet cell, carcinoid, choriocarcinoma, renal cell carcinomas) tend to produce hyperechoic metastases, which may mimic a hemangioma ( Figure 69-6 A ). Hypoechoic lesions are also common, particularly with lymphoma, breast, lung, and cystic or necrotic metastases. Hypoechoic halos surrounding liver masses produce the nonspecific but common “bull’s-eye” appearance often seen with malignant lesions; these require additional work-up.

  

• MDCT: Most liver metastases have decreased attenuation compared with the surrounding parenchyma on NCCT. Most metastases are hypovascular (e.g., colon adenocarcinoma) and are best imaged in the PVP. Hypervascular metastases (i.e., renal cell, carcinoid, thyroid, melanoma, and neuroendocrine tumors) are best imaged during the HAP, which should be added to PVP imaging to increase lesion detection ( Figure 69-6 B ). Calcified metastases are most commonly seen with mucinous colon carcinoma.

• MRI: In general, metastases are hypointense on T1-w and hyperintense on T2-w images. However, hemorrhagic and melanoma metastases are hyperintense on T1-w images. Dynamic gadolinium enhanced MRI increases the sensitivity for the detection of liver metastasis.

What are the three growth patterns of HCC?

• A.

  Large solitary mass (50%)

• B.

  Multifocal HCC (40%)

• C.

  Diffuse infiltration (10%)

How does HCC appear on US, CT, and MRI?

• General: In the United States, more than 80% of patients with HCC have underlying liver disease (e.g., cirrhosis). Men are three times more commonly affected.

• US: Appearance is variable, sometimes simulating metastatic disease. HCCs smaller than 5 cm are often hypoechoic, whereas larger lesions have mixed echogenicity. Fat within the tumor may cause internal hyperechoic foci. Vascular invasion is common; PV invasion is more common than HV invasion. Doppler US can depict tumor thrombus, which typically has an arterial waveform.

• MDCT: On NCCT, HCCs are typically hypodense but may appear hyperdense in fatty livers, with 5% to 10% containing calcification. In the HAP, small HCCs (< 3 cm) typically demonstrate homogeneous and large HCCs heterogeneous enhancement, often with central necrotic areas of low attenuation. Imaging in the HAP allows detection of up to 30% more tumor nodules compared with NCCT and PVP imaging alone ( Figure 69-7 ). In the PVP, HCC is usually iso- to hypodense in appearance. Even so, sometimes contour deformity, mass effect, or vascular, especially venous, invasion might be the only clues to detection. Hemoperitoneum, caused by rare spontaneous rupture, and intratumoral hemorrhage may also occur.

  

• MRI: MRI can usually distinguish between regenerative nodules, dysplastic nodules, and HCC. HCC is usually hypointense on T1-w images, but HCC may be iso- or hyperintense depending on the degree of fatty change and internal fibrosis. Findings that suggest HCC include increased T2-w signal (in more than 70% of HCCs) and a diameter of more than 2 to 3 cm. A “nodule within a nodule” appearance (increased T2-w nodule within a decreased T2-w mass) is highly suggestive of HCC within a dysplastic nodule. Gadolinium-enhanced images increase the detection of HCC as HCC has marked enhancement in the HAP phase, late washout, and a peripherally enhancing pseudocapsule on PVP images. As the degree of malignancy increases, there is increased hepatic arterial and decreased portal flow to the nodules ( Figure 69-8 ). HCC may also enhance after gadoxetic acid administration.

  

Both fibrolamellar HCC and focal nodular hyperplasia (FNH) have a central scar with multiple fibrous septa; however, fibrolamellar HCC has a high prevalence of calcification. The central scar in fibrolamellar HCC is typically T2-w hypointense and calcified, whereas in FNH the central scar is T2-w hyperintense and not calcified. Fibrolamellar HCC occurs at a younger age, has equal male to female incidence, and a better prognosis.

What MRI contrast agents are commercially available in the United States for use in hepatobiliary imaging?

Gadobenate diglumine (Multihance, Bracco Diagnostics) and gadoxetic acid (Eovist, Bayer Healthcare Pharmaceuticals) are both conventional, nonspecific extracellular as well as hepatocyte-specific contrast agents (outside the United States, Eovist is marketed as Primovist). The hepatocyte-specific contrast agent mangafodipir trisodium and the superparamagnetic iron oxide ferumoxides and carboxydextran-coated particles are not currently available in the United States.

Gadobenate diglumine is taken up by functioning hepatocytes and excreted in the bile in addition to being in the extracellular space. The maximal benefit in the detection of lesions with this agent occurs with imaging 1 to 2 hours after injection, which is the time of peak liver-to-lesion contrast. Imaging in the hepatobiliary phase can differentiate between FNH (with biliary ducts) and hepatocellular adenoma (HCA).

Gadoxetic acid is similar to gadobenate diglumine except that the time of peak liver-to-lesion contrast occurs 20 to 45 minutes after injection. Recently, studies have shown that Gadobenate diglumine is more accurate than CT arterial portography (CTAP) in detecting even small HCC lesions. In addition, imaging with Gadobenate is noninvasive and does not require radiation, unlike CTAP.

What is the most common benign neoplasm of the liver?

Cavernous hemangioma is the most common benign liver neoplasm.

Describe the US, CT, and MRI characteristics of hepatic hemangiomas.

• US: Cavernous hemangiomas appear as well-defined hyperechoic masses in a normal liver. Doppler and color flow imaging usually demonstrate no detectable flow within the mass as blood flow is usually very slow; however, a feeding vessel may sometimes be detected. Occasionally hemangiomas have a mixed or hypoechoic appearance, especially in the setting of a fatty liver.

• MDCT: On NCCT, hemangiomas are usually isodense to blood vessels, with 20% containing calcifications. A characteristic peripheral nodular enhancement pattern, isodense to the aorta, is present on HAP imaging; followed by slow central filling of the lesion, which becomes isodense to the blood pool in the PVP. The enhancement typically persists; however, large lesions may not completely enhance. Less frequently, hemangiomas may initially have central or uniform enhancement, similar to the pattern present in malignant lesions.

• MRI: Hemangiomas are usually well defined and have decreased T1-w and increased T2-w signal compared with the normal liver. The signal increases on more heavily T2-w images equal to or greater than the signal of bile. Using dynamic contrast-enhanced MRI, the enhancement pattern is similar to the pattern on CT ( Figure 69-9 ).

  

Describe the appearance of FNH on US, CT, and MRI.

• General: FNH is the second most common benign hepatic tumor and it is more common in women. FNH contains all of the normal liver elements, but in an abnormal arrangement. It is typically smaller than 5 cm in diameter and solitary. The characteristic feature of FNH is the central scar, containing radiating fibrous tissue with vascular and biliary elements. The central scar may be seen with other lesions such as fibrolamellar HCC. Therefore, although a characteristic feature of FNH, it is not specific for FNH.

• US: Often subtle; therefore, minimal contour abnormalities or vascular displacement should raise the possibility of FNH. A well-demarcated hypo- to isoechoic mass, possibly demonstrating a central scar, may be identified. Doppler images, especially if a stellate arterial pattern is present, are suggestive of FNH.

• MDCT: FNH is hypo- to isodense on NCCT and without calcifications. FNH is hyperdense on HAP images because it is supplied by the hepatic artery. On PVP images, it is isodense to normal liver with a hyperdense pseudocapsule. The central scar is present in 35% of lesions smaller than 3 cm and 65% of lesions larger than 3 cm. The scar has lower attenuation than the normal liver on HAP and PVP images, but becomes hyperdense on 5- to10-minute delayed images. Enlarged feeding arteries and draining veins may be seen, especially with the use of MPRs.

• MRI: FNH is T1-w hypo- to isointense and T2-w iso- to hyperintense to liver. The central scar is T1-w hypointense and T2-w hyperintense, unlike HCC in which the central scar is T2-w hypointense. The lesion demonstrates diffuse enhancement in the HAP except for the central scar, which demonstrates delayed enhancement similar to CT. Unlike HCC and HCAs, capsular enhancement is not identified in FNH. FNH has delayed enhancement with gadoxetic acid.

How does HCA appear on US, CT, and MRI?

• General: HCAs are more common in women and are associated with oral contraceptive use. HCAs can cause morbidity and mortality because of their propensity for hemorrhage and rare malignant degeneration to HCC. HCAs are often 8 to 15 cm in diameter when diagnosed. HCAs contain few if any bile ducts or Kupffer cells, but they are more likely to demonstrate calcification or fat than FNH.

• US: Typically shows a heterogeneous, hyperechoic mass caused by internal hemorrhage and high lipid content.

• MDCT: A hypodense mass is typically seen on NCCT resulting from intratumoral fat. Internal areas of higher attenuation may be present as a result of recent hemorrhage, a key distinguishing feature from FNH. Contrast-enhanced CT (CECT) may show centripetal enhancement similar to a hemangioma. In contrast to hemangiomas, the enhancement is transient.

• MRI: HCA is commonly heterogeneous as a result of necrosis and internal hemorrhage. HCA is usually T2-w iso- to slightly hyperintense. The T1-w signal is variable, but often hyperintense because of fat or hemorrhage, although similar findings may be seen in HCC. HCA can demonstrate decreased signal on opposed-phase T1-w imaging because of the high lipid content. Enhancement is most pronounced in the HAP with rapid washout in the PVP. The presence of hemorrhage helps differentiate HCA from HCC.

Describe the appearance of a hepatic abscess on US, CT, and MRI.

• General: Hepatic abscesses can develop from (1) biliary, (2) portal venous, (3) arterial, (4) local extension, and (5) traumatic etiologic factors.

• US: A hepatic abscess appears as a complex fluid collection, typically with septations, an irregular wall, and internal debris or air. Air is seen as a focal area of echogenicity with posterior shadowing. An abscess can also appear as a simple fluid collection, similar to a cyst.

• MDCT: CT is the most sensitive imaging modality; however, the CT findings vary with the size and age of the abscess. Generally, an abscess is a well-defined, low-attenuating uni- or multilocular mass with a well-defined enhancing wall that may contain internal septations. Air bubbles within the abscess cavity, although present in a minority of cases, are the most specific sign for an abscess ( Figure 69-10 ).

  

• MRI: An abscess appears as a well-defined homogeneous or heterogeneous lesion with decreased T1-w and increased T2-w signal. The cavity may contain septations and is surrounded by a low-signal enhancing capsule. Other complex cystic lesions, such as necrotic or hemorrhagic neoplasms, may have a similar appearance.

What is a “normal” Doppler waveform?

The “normal” Doppler waveform depends on the vessel being imaged. In general, veins have continuous low-velocity flow that varies with respiration. The PV normally has hepatopetal flow (flow toward the liver) that ranges from 15 to 18 cm/sec ( Figure 69-11 A ). The HVs have triphasic and pulsatile flow directed away from the liver into the IVC (see Figure 69-11 B ). Arterial flow varies dramatically with the cardiac cycle, with high-velocity flow during systole and relatively high flow (i.e., low resistance) during diastole.

The change in frequency of reflected sound waves from flowing blood (the Doppler frequency shift) and the angle at which the US beam interfaces with the flowing blood (the Doppler angle) are used to calculate the velocity and direction of blood flow. The Doppler angle should be less than 60 degrees to avoid erroneous velocity calculations. The operator determines whether flow directed toward the transducer is displayed above or below the baseline on grayscale imaging and whether blood flowing toward the transducer is blue or red on color imaging, with flow in arteries and veins normally assigned a different color.

Describe the sonographic findings of portal hypertension.

Portal hypertension can be suggested when (1) PV diameter is larger than 13 mm, (2) there is less than 20% increase in the PV diameter with deep inspiration, (3) a monophasic waveform is present, and (4) flow velocity is decreased. Specific measurements may be unreliable given PV diameter variability and the formation of portosystemic collaterals, which often develop in response to portal hypertension, reducing the PV diameter. Common collaterals include (1) a recanalized paraumbilical vein, which runs in the falciform ligament to the abdominal wall and drains the left PV; (2) splenorenal shunts; (3) retroperitoneal veins; (4) hemorrhoidal veins; and (5) the coronary vein, which connects with the portosplenic confluence and ascends to the gastroesophageal junction, producing esophageal varices. A coronary vein diameter larger than 7 mm is highly associated with severe portal hypertension. Retrograde (hepatofugal) PV flow indicates advanced disease and is a useful but late finding ( Figure 69-12 ).

How are Doppler waveforms altered in PV thrombosis?

In acute PV thrombosis, flow in the PV is markedly diminished or absent, with no Doppler waveform or color flow. Cavernous transformation of the PV, manifested by multiple tubular channels in the porta hepatis demonstrating Doppler and color flow with nonvisualization of the native PV, may develop within 12 months. Echogenic material representing thrombus is usually seen in the PV. An arterial waveform within the thrombus is highly specific for malignancy.

How does Budd-Chiari syndrome affect Doppler waveforms?

Budd-Chiari syndrome refers to obstruction of hepatic venous outflow. It can occur anywhere from the small hepatic venules to the IVC. It is diagnosed when echogenic thrombus or absent flow is present in one or more of the HVs or the suprahepatic IVC. Intrahepatic collaterals extending from the HVs to the liver surface are common, and the liver parenchyma is usually diffusely heterogeneous. Associated PV thrombosis is present in 20% and ascites is often present. The caudate lobe is frequently spared as it has separate drainage to the IVC.

Describe the CT findings in acute cholecystitis.

Findings are similar to those of US; wall thickening, pericholecystic fluid, and gallstones are seen. CT is better than US at detecting stranding in the adjacent tissues. CECT can also demonstrate enhancement in the adjacent liver. CT can depict intramural gas in emphysematous cholecystitis.

What other conditions can result in gallbladder wall thickening?

Numerous conditions exist. These are (1) congestive heart failure; (2) constrictive pericarditis; (3) hypoalbuminemia; (4) renal failure; (5) portal venous congestion or portal hypertension; (6) hepatic venoocclusive disease; (7) chronic cholecystitis; (8) acquired immune deficiency syndrome–related cholangitis; (9) adenomyomatosis; (10) primary sclerosing cholangitis; (11) leukemic infiltration; and (12) inflammation from hepatitis, pancreatitis, and colitis.

Gallbladder carcinoma also causes wall thickening but is usually differentiated from other causes by a masslike appearance, adenopathy, and liver metastases.

Describe the differential imaging features seen in the common causes of biliary obstruction.

• A.

  Intrahepatic ductal dilatation (> 2 mm) with a normal common bile duct (CBD) suggests an intrahepatic mass or abnormality. Dilatation of the pancreatic duct typically localizes the obstruction to the pancreatic or ampullary level.

• B.

  An abrupt transition from a dilated to a narrowed or obliterated CBD is more characteristic of a neoplasm or stone. Gradual tapering of the CBD at the pancreatic head is more typical of fibrosis associated with chronic pancreatitis, but chronic pancreatitis also can present as a focal mass, and biopsy may be required for differentiation.

• C.

  Cholangiocarcinoma often arises around the liver hilum (Klatskin tumor). It should be suspected when abrupt biliary obstruction is present but no mass or stone is identified.

  • US: The primary mass is difficult to identify.

  • MDCT: Low-attenuating mass with mild delayed (10-20 minutes postinjection) peripheral enhancement is typical. Unlike HCC, cholangiocarcinoma usually encases but does not invade adjacent vessels.

  • MRI: Usually has low T1-w and high T2-w signal and progressive delayed enhancement caused by fibrous tissue. This can help determine the area to biopsy.

What is magnetic resonance cholangiopancreatography (MRCP) and how does it compare to endoscopic retrograde cholangiopancreatography (ERCP)?

MRCP is a noninvasive way to evaluate the hepatobiliary tract using heavily T2-w images. MRCP can reliably demonstrate the CBD, the pancreatic duct, the cystic duct, and aberrant hepatic ducts, and can differentiate dilated from normal ducts. MRCP exceeds the accuracy of CT and US in detecting choledocholithiasis, because CBD stones do not always exhibit acoustic shadowing. This is one reason why US is only 60% to 70% accurate in detecting CBD stones ( Figure 69-13 ).

MRCP is comparable to ERCP in detecting choledocholithiasis and extrahepatic strictures, and in diagnosing extrahepatic biliary and pancreatic duct abnormalities ( Figure 69-14 A and B).

Describe the radiologic work-up of suspected biliary tree obstruction.

• US: US is the screening examination of choice for suspected biliary ductal disease. Doppler can readily differentiate biliary ducts from vasculature in the portal triad. A CBD diameter larger than 6 mm is more sensitive than dilated intrahepatic ducts in assessing early or partial biliary obstruction; however, the extrahepatic ductal diameter may increase with age, following cholecystectomy or previous resolved obstruction. Normal intrahepatic ducts are smaller than 2 mm in diameter and less than 40% of the diameter of the adjacent PV. With intrahepatic ductal dilatation (> 2 mm), tubular, low-echogenicity structures are seen to parallel the PVs, producing the “too many tubes” sign ( Figure 69-15 A ).

  

• MDCT and MRI/MRCP: Once biliary disease is detected, MDCT or MRI are more efficacious in depicting the degree, site, and cause of obstruction because bowel gas commonly obscures US visualization of the distal CBD (see Figure 69-15 B ). MDCT and MRI/MRCP also provide more complete delineation of the entire CBD, especially with the use of coronal imaging.

• ERCP or percutaneous transhepatic cholangiography: These imaging methods provide a more detailed evaluation than US, MDCT, or MRI/MRCP, but both modalities are invasive.