(Radiographics. 2001;21:65-81.)
© RSNA, 2001
Improved Diagnosis of Hepatic Perfusion Disorders: Value of Hepatic Arterial Phase Imaging during Helical CT1
Sergi Quiroga, MD,
Carmen Sebastià, MD,
Esther Pallisa, MD,
Eva Castellà, MD,
Mercedes Pérez-Lafuente, MD and
Agustí Alvarez-Castells, MD
1 From the Department of Radiology and Institut de Diagnòstic per la Imatge, Hospital General Universitari Vall d'Hebron, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain. Presented as a scientific exhibit at the 1999 RSNA scientific assembly. Received March 2, 2000; revision requested April 5 and received May 22; accepted May 26. Address correspondence to S.Q. (e-mail: squiroga@hg.vhebron.es).
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Abstract
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The liver has a unique dual blood supply, which makes helical computed tomography (CT) a highly suitable technique for hepatic imaging. Helical CT allows single breath-hold scanning without motion artifacts. Because of rapid image acquisition, two-phase (hepatic arterial phase and portal venous phase) evaluation of the hepatic parenchyma is possible, improving tumor detection and tumor characterization in a single CT study. The arterial and portal venous supplies to the liver are not independent systems. There are several communications between the vessels, including transsinusoidal, transvasal, and transplexal routes. When vascular compromise occurs, there are often changes in the volume of blood flow in individual vessels and even in the direction of blood flow. These perfusion disorders can be detected with helical CT and are generally seen as an area of high attenuation on hepatic arterial phase images that returns to normal on portal venous phase images; this finding reflects increased arterial blood flow and arterioportal shunting in most cases. Familiarity with the helical CT appearances of these perfusion disorders will result in more accurate diagnosis. By recognizing these perfusion disorders, false-positive diagnosis (hypervascular tumors) or overestimation of the size of liver tumors (eg, hepatocellular carcinoma) can be avoided.
Index Terms: Computed tomography (CT), helical, 761.12115 • Computed tomography (CT), perfusion study, 761.12116 • Liver, blood supply, 761.12115, 761.12116 • Liver, diseases, 761.14, 761.20, 761.30, 761.49
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LEARNING OBJECTIVES FOR TEST 2
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After reading this article and taking the test, the reader will be able to:
- Describe the various intrahepatic communications between the arterial and portal venous systems.
- Identify the increasing number of hepatic perfusion disorders detected with dual-phase helical CT.
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Introduction
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A distinctive feature of the liver is its unique dual blood supply, which comes from the hepatic artery (25% of vascularization) and the portal vein (75% of vascularization) (1–4). This characteristic is useful for detecting tumors that are usually hypervascular, such as hepatocellular carcinoma (HCC), hemangioma, focal nodular hyperplasia, and hepatic adenoma, as well as metastases from neuroendocrine tumors (islet cell, carcinoid), renal cell carcinoma, and breast carcinoma. These tumors receive arterial blood primarily and are better detected during the hepatic arterial phase (HAP) of helical computed tomography (CT) because they demonstrate greater enhancement than the normal hepatic parenchyma, which has a predominantly venous supply. In contrast, during the portal venous phase (PVP), these tumors sometimes enhance to a degree similar to that of the hepatic parenchyma and may escape detection (2,3,5). Before faster helical CT scanners were available, the hypervascularity during the HAP could be demonstrated only with single-level evaluation of isolated lesions (6–8); the whole hepatic parenchyma could not be imaged during the HAP (2).
Helical CT has become a useful method for studying the liver. Single breath-hold scanning without motion artifacts is achievable, and rapid data acquisition allows two-phase (HAP and PVP) evaluation of the hepatic parenchyma, thus improving tumor detection rates (1–3,5) and tumor characterization in a single CT study (9). At the beginning of the HAP (20–30 seconds after the start of contrast material administration), hepatic parenchymal enhancement is minimal because no contrast material reaches the portal vein. Although the portal vein itself shows faint enhancement during the middle and late HAP, the contrast material does not reach the peripheral portal vein sinusoids; thus, there is diffusion of nonenhanced portal vein blood into the extravascular spaces. This part of the HAP is the optimal time to image hypervascular tumors.
During the PVP, the normal hepatic parenchyma enhances markedly. However, in most cases, there is still contrast material within the arterial system; thus, both normal hepatic parenchyma and hypervascular tumors can enhance to the same degree, making differentiation difficult. The PVP is the best phase for imaging hypovascular tumors, such as metastases, which receive minimal hepatic arterial flow (3).
When vascular compromise occurs, the dual blood supply system can cause changes in the volume of blood flow in individual vessels and even in the direction of blood flow (10). Extensive use of helical CT during the HAP in the study of hepatic tumors and liver cirrhosis increases the detection rates of these hemodynamic changes, which usually go undetected on PVP images (1,2,11–13). To understand the physiology and pathophysiology of the hemodynamic changes that occur, it is important to remember that the arterial and venous supplies to the liver are not independent systems (Fig 1). There can be several communications between the vessels, including transsinusoidal, transvasal, transtumoral, and transplexal (peribiliary) routes (13).
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Figure 1. Hepatic blood supply. Diagram shows that the arterial and venous supplies to the liver are not independent systems. There are numerous communications between them, including the transsinusoidal route (between the interlobular arterioles and portal venules or sinusoids) and the transplexal route (peribiliary plexus), which play an important role when portal venous inflow is compromised. Ao = aorta, GDA = gastroduodenal artery, HV = hepatic vein, IMV = inferior mesenteric vein, IVC = inferior vena cava, SMV = superior mesenteric vein.
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Transient hepatic parenchymal enhancement (THPE) reflects a change in the normal dual blood supply of the liver in which the affected site appears as an area of high attenuation on HAP images and returns to normal on PVP images (1,12). THPE during the HAP reflects an enhanced, redistributing arterial flow to a hepatic segment or lobe, usually due to decreased portal or hepatic venous flow and resulting in an arterioportal shunt (APS) (3). The area of THPE may be lobar, segmental, or subsegmental; it is usually peripheral and triangular or wedge shaped, has a straight margin, and contains normal vessels (12). The causes of such perfusion disorders are portal vein obstruction, liver cirrhosis, hepatic neoplasms, hepatic trauma, hereditary hemorrhagic telangiectasia (HHT), hepatic vein obstruction, steal phenomenon by hypervascular tumors, inflammatory changes, aberrant blood supply, hepatic parenchymal compression, and other causes (1,12).
This article presents the spectrum of hepatic perfusion disorders that can be diagnosed with helical CT but might be overlooked with conventional CT. The radiologist should be mindful of areas of high attenuation on HAP images because they can represent perfusion disorders. With biphasic helical CT, such areas of high attenuation can be correctly interpreted according to their typical location, shape, and association with hepatic lesions (12). Although most cases of hepatic perfusion disorders are asymptomatic, it is important to recognize them to avoid false-positive diagnoses (hypervascular tumors) or overestimation of the size of liver tumors, such as HCC.
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Arterioportal Shunt
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An APS is an organic or functional communication between a hepatic arterial branch and the portal venous system, resulting in redistribution of arterial flow into a focal region of portal venous flow. The shunt can occur by several routes: (a) through a macroscopic fistula, usually of iatrogenic origin; (b) transsinusoidal route (between microscopic interlobular arterioles and portal venules) (Fig 1); (c) transvasal route (due to a tumor thrombus); (d) transtumoral route (via a draining vein from a hypervascular tumor); or (e) transplexal (peribiliary) route (Fig 1). These shunts play an important role when the portal vein is obstructed or compressed (9). APSs are a relatively common cause of pseudolesions at hepatic imaging, and differentiation of pseudolesions from hypervascular tumors is not always easy (14). The causes of APS include hepatic neoplasms such as HCC (7,8), hemangioma (3), and cholangiocarcinoma (11); hepatic trauma or interventional procedures such as hepatic biopsy, percutaneous abscess drainage, ethanol injection, and biliary drainage; liver cirrhosis (3); and other less frequent causes of functional APSs. Metastatic tumors, rupture of a hepatic artery aneurysm, and congenital malformations can also be associated with APS (15).
The helical CT findings of APS are as follows: (a) early enhancement of the peripheral portal vein branches during the HAP and before the main portal vein is enhanced; (b) enhancement of the peripheral portal vein branches and main portal vein without enhancement of the superior mesenteric and splenic veins (3), an appearance that has been considered diagnostic on hepatic angiograms (11,16); and (c) transient, peripheral, wedge-shaped hepatic parenchymal enhancement—usually with a straight margin—during the HAP (THPE) (3,13,17). The last finding usually results from a peripheral APS (15), which manifests as a transient area of high attenuation due to passage of contrast material from high-pressure arterial blood into a low-pressure portal vein branch, thus enhancing a focal area of the liver before the adjacent parenchyma is enhanced through the portal venous system (14,17).
When THPE is the only finding, it can be difficult to recognize the wedge-shaped margins of small APSs, which can resemble nodular lesions. THPE with the typical peripheral location and wedge-shaped appearance, homogeneous attenuation, portal vein branches visualized early during the HAP, and isoattenuating or slightly hyperattenuating areas during the PVP are suggestive of APSs at two-phase helical CT (13). In cases of macroscopic arterioportal fistulas, transvasal shunts, and transtumoral shunts, the portal veins are demonstrated in the early phase of contrast material–enhanced CT, whereas THPE occurs in cases of transsinusoidal shunts (10). At nonenhanced CT, an APS occasionally appears as a wedge-shaped area of low attenuation (10).
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Portal Vein Obstruction
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Hepatic perfusion disorders are often caused by venous inflow obstruction due to portal vein thrombosis (Figs 2, 3), tumor invasion, compression (Fig 4), or surgical ligation (1–3,10,12). Perfusion alterations are produced by increases in arterial flow through transsinusoidal, transvasal, transtumoral, and especially transplexal (peribiliary) routes to compensate for the diminished portal venous flow (functional APS) and by decreased dilution of the contrast material by the nonenhanced portal venous flow (12). The causes of portal vein thrombosis include infectious processes (eg, sepsis), neoplasms that invade or compress the portal venous system (eg, hepatoma or pancreatic cancer), hypercoagulative states, myeloproliferative disorders, and noninfectious inflammatory processes (eg, pancreatitis) (18,19).
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Figure 2a. Portal vein thrombosis secondary to appendicitis in a 45-year-old woman. (a) CT scan shows transient high attenuation of the right hepatic lobe (arrow) due to obstruction of portal venous inflow and compensatory increase of the arterial inflow. (b) CT scan shows a bland thrombus within the right portal vein (arrow), which produces venous inflow obstruction.
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Figure 2b. Portal vein thrombosis secondary to appendicitis in a 45-year-old woman. (a) CT scan shows transient high attenuation of the right hepatic lobe (arrow) due to obstruction of portal venous inflow and compensatory increase of the arterial inflow. (b) CT scan shows a bland thrombus within the right portal vein (arrow), which produces venous inflow obstruction.
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Figure 3a. Right portal vein thrombosis secondary to abdominal trauma and a foreign body thrust into the hepatic parenchyma. CT was performed after the foreign body had been removed. (a) Helical CT scan shows the course of the foreign body (white arrow) through the right hepatic lobe, which is markedly enhanced during the arterial phase (arrowheads). Black arrow = left hepatic portal vein. (b) Helical CT scan shows thrombosis of the right portal vein (arrow) and THPE of the right hepatic lobe (arrowheads) secondary to compensatory increase of the arterial flow. (c) Shaded-surface display image shows the portal venous system with absence of the right portal vein. A = anterior, H = head, R = right, thick arrow = main portal vein, thin arrow = left portal vein. (d) Shaded-surface display image shows the hepatic parenchyma with arterial supply (red area) through two right hepatic arteries (arrows), one arising from the hepatic artery and the other from the superior mesenteric artery. A = anterior, H = head, R = right.
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Figure 3b. Right portal vein thrombosis secondary to abdominal trauma and a foreign body thrust into the hepatic parenchyma. CT was performed after the foreign body had been removed. (a) Helical CT scan shows the course of the foreign body (white arrow) through the right hepatic lobe, which is markedly enhanced during the arterial phase (arrowheads). Black arrow = left hepatic portal vein. (b) Helical CT scan shows thrombosis of the right portal vein (arrow) and THPE of the right hepatic lobe (arrowheads) secondary to compensatory increase of the arterial flow. (c) Shaded-surface display image shows the portal venous system with absence of the right portal vein. A = anterior, H = head, R = right, thick arrow = main portal vein, thin arrow = left portal vein. (d) Shaded-surface display image shows the hepatic parenchyma with arterial supply (red area) through two right hepatic arteries (arrows), one arising from the hepatic artery and the other from the superior mesenteric artery. A = anterior, H = head, R = right.
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Figure 3c. Right portal vein thrombosis secondary to abdominal trauma and a foreign body thrust into the hepatic parenchyma. CT was performed after the foreign body had been removed. (a) Helical CT scan shows the course of the foreign body (white arrow) through the right hepatic lobe, which is markedly enhanced during the arterial phase (arrowheads). Black arrow = left hepatic portal vein. (b) Helical CT scan shows thrombosis of the right portal vein (arrow) and THPE of the right hepatic lobe (arrowheads) secondary to compensatory increase of the arterial flow. (c) Shaded-surface display image shows the portal venous system with absence of the right portal vein. A = anterior, H = head, R = right, thick arrow = main portal vein, thin arrow = left portal vein. (d) Shaded-surface display image shows the hepatic parenchyma with arterial supply (red area) through two right hepatic arteries (arrows), one arising from the hepatic artery and the other from the superior mesenteric artery. A = anterior, H = head, R = right.
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Figure 3d. Right portal vein thrombosis secondary to abdominal trauma and a foreign body thrust into the hepatic parenchyma. CT was performed after the foreign body had been removed. (a) Helical CT scan shows the course of the foreign body (white arrow) through the right hepatic lobe, which is markedly enhanced during the arterial phase (arrowheads). Black arrow = left hepatic portal vein. (b) Helical CT scan shows thrombosis of the right portal vein (arrow) and THPE of the right hepatic lobe (arrowheads) secondary to compensatory increase of the arterial flow. (c) Shaded-surface display image shows the portal venous system with absence of the right portal vein. A = anterior, H = head, R = right, thick arrow = main portal vein, thin arrow = left portal vein. (d) Shaded-surface display image shows the hepatic parenchyma with arterial supply (red area) through two right hepatic arteries (arrows), one arising from the hepatic artery and the other from the superior mesenteric artery. A = anterior, H = head, R = right.
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Figure 4a. Transient high attenuation secondary to portal vein compression in a 52-year-old woman with an intrahepatic cholangiocarcinoma in the left lobe. (a) Preoperative maximum-intensity projection image shows the portal venous anatomy with absence of the left portal vein due to tumor invasion. Note the normal appearance of the anterior branch of the right portal vein (arrow). (b) Postoperative CT scan obtained during the HAP shows marked high attenuation of the anterior segments of the right hepatic lobe and a straight border (arrows). (c) CT scan obtained caudad to b shows a stricture of the anterior branch of the right portal vein (arrow) (cf a) and compensatory increase of hepatic arterial inflow.
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Figure 4b. Transient high attenuation secondary to portal vein compression in a 52-year-old woman with an intrahepatic cholangiocarcinoma in the left lobe. (a) Preoperative maximum-intensity projection image shows the portal venous anatomy with absence of the left portal vein due to tumor invasion. Note the normal appearance of the anterior branch of the right portal vein (arrow). (b) Postoperative CT scan obtained during the HAP shows marked high attenuation of the anterior segments of the right hepatic lobe and a straight border (arrows). (c) CT scan obtained caudad to b shows a stricture of the anterior branch of the right portal vein (arrow) (cf a) and compensatory increase of hepatic arterial inflow.
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Figure 4c. Transient high attenuation secondary to portal vein compression in a 52-year-old woman with an intrahepatic cholangiocarcinoma in the left lobe. (a) Preoperative maximum-intensity projection image shows the portal venous anatomy with absence of the left portal vein due to tumor invasion. Note the normal appearance of the anterior branch of the right portal vein (arrow). (b) Postoperative CT scan obtained during the HAP shows marked high attenuation of the anterior segments of the right hepatic lobe and a straight border (arrows). (c) CT scan obtained caudad to b shows a stricture of the anterior branch of the right portal vein (arrow) (cf a) and compensatory increase of hepatic arterial inflow.
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Biphasic helical CT can demonstrate (a) decreased attenuation of the affected hepatic parenchyma on nonenhanced scans due to edema, depletion of hepatocytes, or fibrosis (9,10); (b) transient high attenuation during the HAP due to increased arterial flow; and (c) portal vein thrombosis (bland or tumor thrombus) or compression.
When cavernous transformation of the portal vein occurs, the central part of the liver (caudate lobe and lateral segment) is well supplied by collateral venous vessels, whereas the peripheral zone (mainly the right lobe) receives less portal venous flow. To compensate, arterial flow increases and thus gives rise to scattered areas of high attenuation in the periphery during the HAP (1,9,19). Sometimes, laminar flow in the portal vein produces pseudolesions, which are seen as multiple or solitary wedge-shaped areas (Fig 5) (9). It is important to emphasize that venous compromise (portal or hepatic veins) results in increased arterial flow that can be demonstrated at helical CT, whereas decreased hepatic arterial flow does not cause an increase in portal venous flow or changes in hepatic parenchymal attenuation at nonenhanced CT (9,10). The coexistence of hepatic arterial occlusion and decreased portal venous flow results in hepatic infarction, producing a hypoattenuating area on nonenhanced HAP and PVP images (10).
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Figure 5a. Portal venous laminar flow. (a) Helical CT scan shows THPE in both hepatic lobes (arrows). (b) Helical CT scan clearly shows laminar flow within the main portal vein (arrow), which is probably causing the THPE.
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Figure 5b. Portal venous laminar flow. (a) Helical CT scan shows THPE in both hepatic lobes (arrows). (b) Helical CT scan clearly shows laminar flow within the main portal vein (arrow), which is probably causing the THPE.
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Liver Cirrhosis
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Liver cirrhosis is caused mainly by parenchymal necrosis, which is followed by deposition of connective tissue, nodular hepatocyte regeneration, and distortion of the lobular and vascular hepatic architecture, producing portal hypertension (16). Liver cirrhosis is known to alter normal hepatic blood flow dynamics, resulting in increased arterial flow and decreased portal venous flow to the liver.
Although the presence of an APS in a cirrhotic patient makes the diagnosis of HCC very likely, cirrhosis alone is a known but uncommon cause of APS (Figs 6, 7) (3,12–14,16). APS is believed to be secondary to occlusion of the small hepatic venules and retrograde filling of the small portal vein branches by way of arterioportal anastomoses (transsinusoidal route) (13,14). The portal vein becomes a draining vein rather than a supplying vein, and there is a compensatory increase in hepatic arterial flow (9). In advanced cirrhosis, the hepatic artery is frequently enlarged and tortuous, and Doppler ultrasonography (US) can easily demonstrate increased flow (16).
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Figure 6a. APS secondary to liver cirrhosis. (a) Helical CT scan obtained during the HAP shows early enhancement of the right portal vein branch (thick arrow), whereas the main portal vein remains nonenhanced (thin arrow). (b) Helical CT scan shows transient high attenuation (large arrow) in segment VI of the right hepatic lobe. Note the nonenhanced main portal vein (small arrow). (c) Maximum-intensity projection image shows early filling of the right portal vein branches (arrow).
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Figure 6b. APS secondary to liver cirrhosis. (a) Helical CT scan obtained during the HAP shows early enhancement of the right portal vein branch (thick arrow), whereas the main portal vein remains nonenhanced (thin arrow). (b) Helical CT scan shows transient high attenuation (large arrow) in segment VI of the right hepatic lobe. Note the nonenhanced main portal vein (small arrow). (c) Maximum-intensity projection image shows early filling of the right portal vein branches (arrow).
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Figure 6c. APS secondary to liver cirrhosis. (a) Helical CT scan obtained during the HAP shows early enhancement of the right portal vein branch (thick arrow), whereas the main portal vein remains nonenhanced (thin arrow). (b) Helical CT scan shows transient high attenuation (large arrow) in segment VI of the right hepatic lobe. Note the nonenhanced main portal vein (small arrow). (c) Maximum-intensity projection image shows early filling of the right portal vein branches (arrow).
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Figure 7a. THPE in the left hepatic lobe secondary to liver cirrhosis. (a) Helical CT scan shows THPE in the left hepatic lobe with a straight border (small arrow) and early filling of the left portal vein (large arrow) similar to that of the adjacent left hepatic artery. (b) CT scan obtained caudad to a also shows THPE with a straight border (small arrow). Note that the right portal vein (large arrow) and main portal vein remain nonenhanced.
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Figure 7b. THPE in the left hepatic lobe secondary to liver cirrhosis. (a) Helical CT scan shows THPE in the left hepatic lobe with a straight border (small arrow) and early filling of the left portal vein (large arrow) similar to that of the adjacent left hepatic artery. (b) CT scan obtained caudad to a also shows THPE with a straight border (small arrow). Note that the right portal vein (large arrow) and main portal vein remain nonenhanced.
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APSs in the cirrhotic liver are rarely of sufficient magnitude to result in total hepatofugal portal venous flow (14). Hypertrophy of the peribiliary plexus and direct anastomosis in the peripheral area of the liver are the major routes of APS in experimental studies (20). Abnormal permeability of the sinusoid also has a role in the development of arterioportal communications in the cirrhotic liver (13). Moreover, cirrhotic patients often undergo percutaneous hepatic biopsy for histologic evaluation, increasing the risk of APS. In cases of severe cirrhosis, thromboses of portions of the portal venous system are sometimes seen.
Occasionally, a tiny tumor with a wedge-shaped transtumoral APS shows findings similar to those of a nontumorous APS on HAP images; thus, a second study during the PVP is always mandatory to detect focal lesions. However, radiologists should remember that a hyperattenuating focal lesion in a cirrhotic liver at HAP helical CT usually represents an HCC. If the findings are not characteristic of an arterioportal fistula, the lesion is so small that its morphology cannot be established (wedge-shaped margins), or there may be an associated focal lesion, helical CT follow-up or other studies such as arteriography, iodized oil CT, or magnetic resonance imaging must be performed to exclude the possibility of coexisting tumors (13).
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Hepatic Neoplasms
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Hepatic tumors (usually HCC) are sometimes associated with portal vein compromise and, less frequently, hepatic vein compromise. In cases of HCC, APS is induced via the transvasal route (due to portal vein tumor thrombosis), the transtumoral route (through the tumor itself), or the transsinusoidal route (between microscopic hepatic arterioles and portal venules distal to portal vein compression or thrombosis) (12). In addition, a transplexal (peribiliary) route may play a role when the portal vein is compromised. A hepatic tumor can produce fan-shaped transient high attenuation on HAP images due to portal vein compression, with the tumor located at the apex of the perfusion disorder (Fig 8). A hepatic tumor can also produce wedge-shaped transient high attenuation on HAP images due to proximal tumor thrombosis or APS, with the tumor located within the perfusion alteration (Fig 9) (1,9,10,15). In both cases, the hepatic tumor can be isoattenuating to the hyperattenuating adjacent parenchyma and difficult to detect on HAP images (1,15). In these cases, images obtained in the PVP and delayed phase are essential for detection (11).
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Figure 8a. APS secondary to HCC. (a) Helical CT scan shows a 2-cm-diameter HCC in segment VII (curved arrow), which is difficult to distinguish because of distal transient, peripheral, wedge-shaped enhancement due to APS (straight arrows). Note also the small peripheral HCC in the left hepatic lobe (arrowhead). (b) Helical CT scan obtained during the HAP shows early enhancement of right portal vein branches (arrow) while the main portal vein remains nonenhanced. (c) Shaded-surface display image (anterosuperior view) shows early filling of the right portal vein branches (arrow) and transient enhanced hepatic parenchyma (blue area) due to APS. (Reprinted, with permission, from reference 17.)
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Figure 8b. APS secondary to HCC. (a) Helical CT scan shows a 2-cm-diameter HCC in segment VII (curved arrow), which is difficult to distinguish because of distal transient, peripheral, wedge-shaped enhancement due to APS (straight arrows). Note also the small peripheral HCC in the left hepatic lobe (arrowhead). (b) Helical CT scan obtained during the HAP shows early enhancement of right portal vein branches (arrow) while the main portal vein remains nonenhanced. (c) Shaded-surface display image (anterosuperior view) shows early filling of the right portal vein branches (arrow) and transient enhanced hepatic parenchyma (blue area) due to APS. (Reprinted, with permission, from reference 17.)
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Figure 8c. APS secondary to HCC. (a) Helical CT scan shows a 2-cm-diameter HCC in segment VII (curved arrow), which is difficult to distinguish because of distal transient, peripheral, wedge-shaped enhancement due to APS (straight arrows). Note also the small peripheral HCC in the left hepatic lobe (arrowhead). (b) Helical CT scan obtained during the HAP shows early enhancement of right portal vein branches (arrow) while the main portal vein remains nonenhanced. (c) Shaded-surface display image (anterosuperior view) shows early filling of the right portal vein branches (arrow) and transient enhanced hepatic parenchyma (blue area) due to APS. (Reprinted, with permission, from reference 17.)
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Figure 9a. APS secondary to diffuse HCC in the right hepatic lobe. (a) Helical CT scan obtained during the HAP shows marked early enhancement of portal vein branches in both hepatic lobes and extensive THPE in the right lobe (arrows) secondary to APS, making detection of a tumor difficult. (b) Helical CT scan obtained during the PVP shows diffuse HCC in the right lobe and tumor thrombosis of a branch of the right portal vein (arrow).
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Figure 9b. APS secondary to diffuse HCC in the right hepatic lobe. (a) Helical CT scan obtained during the HAP shows marked early enhancement of portal vein branches in both hepatic lobes and extensive THPE in the right lobe (arrows) secondary to APS, making detection of a tumor difficult. (b) Helical CT scan obtained during the PVP shows diffuse HCC in the right lobe and tumor thrombosis of a branch of the right portal vein (arrow).
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In cases of HCC, it is important to detect macroscopic invasion of the portal vein branches because such invasion substantially worsens the prognosis and may result in the patient being excluded from surgery (3). Helical CT can demonstrate arterial enhancement within a tumor thrombus, thus allowing differentiation from a bland, nonenhancing thrombus (3,16,18). When proximal APS occurs in the hepatofugal direction, tumor cells can disseminate into the splanchnic area (15).
Hepatic hemangiomas can also show a distal THPE effect due to associated APSs (Fig 10) (1,3). However, it is easier to differentiate hemangiomas from other hypervascular tumors because (a) they demonstrate nodular, peripheral higher enhancement (similar to that of the aorta) on HAP images, with progressive enhancement from the periphery to the center of the lesion; (b) they retain contrast material; and (c) they remain hyperattenuating on PVP images. The presence of an APS can help differentiate hemangioma from HCC. An APS usually occurs in small (<1 cm in diameter), early, homogeneous, high-attenuation hemangiomas, whereas an APS in HCC is probably secondary to vascular system invasion and occurs in large lesions (21,22).
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Figure 10. APS secondary to hepatic hemangioma. Helical CT scan obtained during the HAP shows a small, homogeneous lesion (arrow) of high attenuation (similar to that of the aorta) with distal wedge-shaped parenchymal enhancement (arrowhead), an appearance corresponding to a small APS.
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Hepatic Trauma
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Abdominal trauma and interventional procedures sometimes cause an organic communication between the arterial and portal venous systems or produce functional APSs due to portal vein injury, such as portal vein thrombosis (Fig 3). Interventional procedures (eg, hepatic biopsy, biliary or abscess drainage) can produce iatrogenic arterioportal fistulas (Figs 11–13) (11,12).
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Figure 12. APS in a 25-year-old man with toxic hepatitis secondary to antituberculous therapy, acute liver failure, and a heterotopic liver transplant. Percutaneous biopsy of the native liver after graft removal resulted in a peripheral APS. Helical CT scan obtained during the HAP shows early enhancement of a small branch of the right portal vein (large arrow), indicative of an APS, and THPE (small arrows) in segment VI. Follow-up CT performed 9 months later showed spontaneous resolution of the arterioportal fistula.
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Figure 13. Transient hepatic attenuation difference due to APS in a 64-year-old man with obstructive jaundice after percutaneous transhepatic biliary drainage. Helical CT scan shows a hyperattenuating area (arrows) corresponding to an APS affecting hepatic segments V and VIII. The APS was confirmed with celiac angiography and treated with embolization.
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These procedures can also be the cause of hepatic artery pseudoaneurysms, which appear on CT scans obtained during the HAP as focal, round, enhancing lesions, simulating vascular tumors. Differentiation between tumors and fistulas is particularly important in cirrhotic patients, the population most at risk for HCC, a highly vascularized neoplasm (3).
Because percutaneous hepatic biopsy has been widely used in histologic diagnosis of hepatic tumors, it may be difficult to know if an APS is secondary to a biopsy or to an intratumoral shunt unless helical CT was performed before the interventional procedure. The frequency of APS secondary to hepatic biopsy is as high as 50% during the first week but drops to 10% afterward, since these shunts tend to close spontaneously (11).
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Hereditary Hemorrhagic Telangiectasia
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HHT (Osler-Weber-Rendu disease) is a vascular disease with autosomal dominant transmission characterized by multiple telangiectases, which are thin-walled, dilated vascular channels with arteriovenous communications. HHT affects mucocutaneous tissue most frequently, but any part of the body can be affected, including the liver (23,24). Telangiectases are nearly universal in HHT, and arteriovenous malformations—direct connections between arteries and veins—are also prominent. In the liver, arteriovenous shunts are often numerous and can occur between hepatic artery branches and branches of the hepatic or portal veins (Figs 14, 15).
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Figure 14. HHT in a 60-year-old man with a family history of HHT, repeated episodes of epistaxis, and telangiectases on the skin and mucosa. Results of liver function tests were normal. Helical CT was performed to investigate vague epigastric pain. CT scan obtained during the HAP shows dilated and tortuous intrahepatic arterial branches (arrows) and mosaic perfusion of the hepatic parenchyma with multiple transient enhancing areas, an appearance that probably corresponds to multiple APSs. On images obtained during the PVP, the liver was homogeneous and the hepatic veins were not dilated.
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Figure 15a. HHT in a 66-year-old man with a family history of HHT and nasopharyngeal bleeding. Abdominal US was performed to investigate recurrent vague epigastric pain. The results of three hepatic biopsies in this area were normal. The results of liver function tests were also normal. (a) Transverse US scan shows a heterogeneous hepatic parenchyma with a subdiaphragmatic hypoechoic pseudonodular area (arrow). (b) Helical CT scan obtained during the HAP shows marked heterogeneous (reticular-mosaic) enhancement with multiple peripheral, wedge-shaped areas of transient enhancement, especially in segments VII and VIII, an appearance that probably corresponds to APSs. On images obtained during the PVP, no abnormalities were seen and the hepatic veins were not dilated. The hypoechoic areas on the US scan (a) probably correspond to focal sparing of fatty infiltration in the areas where APSs are present.
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Figure 15b. HHT in a 66-year-old man with a family history of HHT and nasopharyngeal bleeding. Abdominal US was performed to investigate recurrent vague epigastric pain. The results of three hepatic biopsies in this area were normal. The results of liver function tests were also normal. (a) Transverse US scan shows a heterogeneous hepatic parenchyma with a subdiaphragmatic hypoechoic pseudonodular area (arrow). (b) Helical CT scan obtained during the HAP shows marked heterogeneous (reticular-mosaic) enhancement with multiple peripheral, wedge-shaped areas of transient enhancement, especially in segments VII and VIII, an appearance that probably corresponds to APSs. On images obtained during the PVP, no abnormalities were seen and the hepatic veins were not dilated. The hypoechoic areas on the US scan (a) probably correspond to focal sparing of fatty infiltration in the areas where APSs are present.
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Hepatic involvement is more frequent than was originally suspected, although the real frequency is not known because hepatic involvement is often asymptomatic (24). The hepatic changes, including widened and tortuous hepatic arteries, telangiectases, and arteriovenous and portovenous fistulas, affect the extrahepatic and intrahepatic vessels (23–25). Hepatic involvement is especially important because it can cause connective tissue formation with fibrosis and atypical cirrhosis, high cardiac output, and secondary congestive heart failure due to a left-to-right intrahepatic shunt. Moreover, the presence of portosystemic shunts can lead to portal hypertension, gastrointestinal hemorrhage, ascites, or encephalopathy (26).
Helical CT demonstrates hepatic involvement as arterial dilatation (26) and tortuosity, hepatomegaly, hepatic vein dilatation (23), and, when arteriovenous shunts are present, simultaneous enhancement of hepatic arteries and veins. In cases of APSs, helical CT shows heterogeneous perfusion of the hepatic parenchyma with multiple, peripheral, wedge-shaped areas of THPE during the HAP, which probably have a role in the irregular pools of contrast material (diffuse mottled capillary blush) that result in heterogeneous parenchymal opacification at angiography (24). It is important to recognize APSs in HHT because they can lead to portal hypertension, portosystemic encephalopathy, and possibly atypical cirrhosis.
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Hepatic Vein Obstruction
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Occlusion of the hepatic veins results in increased sinusoidal pressure and reverses the pressure gradient between the sinusoidal and portal veins (1,13). The portal vein then becomes a draining vein and there is an increase in hepatic arterial flow, resulting in a functional APS, as in liver cirrhosis (9,10,13).
Hepatic vein occlusion can be secondary to right-sided heart failure, pericardial disease, Budd-Chiari syndrome, or mediastinal fibrosis (1). In such cases, HAP images demonstrate transient hepatic enhancement in the area of obstructed hepatic venous drainage, similar to the CT findings in cases of portal venous flow stoppage. The difference is that the vertex of the wedge-shaped hyperattenuating area points to the hepatic hilum in portal vein obstruction and to the inferior vena cava in hepatic vein obstruction (10). Usually, a heterogeneous, reticular, or mosaic pattern persists on PVP images (12), whereas homogeneous enhancement is seen on delayed images (1). In cases of Budd-Chiari syndrome, the caudate lobe remains unaffected because it has its own draining veins (1).
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Steal Phenomenon by Hypervascular Tumors
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Hypervascular tumors, usually large HCCs or hypervascular metastases, may result in "hypertrophy" of the hepatic arterial blood supply to the lobe or segment of the liver containing the tumor (1,3,12). The effect of this hypertrophy can be transient higher or lower attenuation during the HAP in the segment containing the tumor. The hypervascular tumor can "steal" arterial blood from the surrounding parenchyma, which then appears hypoattenuating on HAP images relative to the contralateral lobe of the liver due to incomplete compensation by the arterial flow increase (1,10). Conversely, the hepatic parenchyma adjacent to the tumor can receive a greater than usual arterial blood supply and show transient high attenuation on HAP images (3,12), while the perfusion of the remainder of the lobe behind this enhancing area is reduced; the remainder of the lobe then appears hypoattenuating relative to the contralateral lobe.
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Inflammatory Changes
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Abstract
LEARNING OBJECTIVES FOR TEST...
