The liver uniquely receives a dual blood supply; approximately 1000-1200 ml/min of blood arrives via the portal vein and approximately 400 ml/min arrives via the hepatic artery. In a non-cirrhotic liver, blood perfusion occurs at pressures of approximately 7 mmHg and 100 mmHg, via the portal vein and hepatic artery, respectively. Arterio-portal parenchymal perfusion demonstrates the degree of reciprocity of the arterial and portal venous contributions by virtue of vascular flux through dynamic microcirculatory arterioportal shunts (APS), largely at the level of the portal triad by transplexal, transvasal, or even transtumoral routes [20,24]. These shunts can transiently open under the influence of angiogenic modulators but are frequently related to a pathology that either compromises portal flow or increases arterial perfusion. APS can open to a further extent in response to significant portal blood flow reduction or stoppage, which in turn results in a compensatory increase of the arterial flow through the corresponding liver segments.
Connections between the intrahepatic vascular systems are not restricted to arterioportal communication but may also occur between the portal vein and the hepatic or systemic veins, as seen in conditions such as portal hypertension.
Transsinusoidal shunts are governed by an ar-teriolar inlet sphincter under the influence of an-giogenic factors such as vascular endothelial growth factor (VEGF) and angioproteins. These shunts occur in Budd-Chiari syndrome, or may arise for no apparent reason or in response to focal infection or nodules of disease that compromise the portal perfusion of the subtended liver.
The peribiliary plexus or transplexal route is the most prominent venous system, and is composed of vessels that run around the lobular ducts. This system plays an important role when the portal vein is compromised.
Transvasal plexus often occurs in conjunction with peribiliary shunting and via the vasa vaso-rum of the portal vein. It most commonly occurs in the setting of portal vein occlusion or in cases of invasive hepatocellular carcinoma (HCC) .
Small areas of liver tissue may be supplied by another venous system, the "third inflow" which comprises aberrant veins that enter the liver directly, independently of the portal venous system. Such veins communicate with intrahepatic portal branches to various degrees and lead to focally decreased portal perfusion. However, little overall change in the hepatic arterial perfusion is seen. Because this hemodynamic state is persistent, focal metabolic changes are occasionally observed, typically as sparing in the fatty liver or as accumulations of fat .
Anatomic Variants of the Hepatic Circulation
Anatomic vascular variants of the hepatic circulation may involve the hepatic artery, the portal vein, and the hepatic veins, and may occur in the following manner:
A) The hepatic artery may have many collateral vessels including the pancreatic-duodenal arteries, the gastro-duodenal artery, and the phrenic inferior right artery. Collateral routes by aberrant hepatic arteries may originate from the superior mesenteric artery, the left gastric artery or by extrahepatic collateral arteries, such as the left gastroepiploic artery, the gas-troduodenal artery, and the right gastric artery. Outside the celiac trunk, collateral flow may occur via the inferior phrenic artery .
B) The portal vein has variants and collateral vessels. Frequently, portal vein variants result in a "third inflow" in which aberrant veins that are not connected with the portal vein system enter the liver directly. These aberrant veins, which are not derived from the gut venous drainage, are poor in nutritional factors. The third inflow may involve the cystic vein, which drains the gallbladder bed, and the parabiliary venous system, which is within the hepatoduodenal ligament just anterior to the main trunk of the portal vein. The parabiliary venous system collects venous blood from the head of the pancreas, the distal part of the stomach, and the biliary system near the gallbladder [13,32]. These veins usually join the main trunk of the portal venous system's major branches, but occasionally enter the liver directly around the porta hepatis, which sometimes results in isolated perfusion.
The epigastric-paraumbilical venous system is another variant of the portal vein and consists of small veins around the falciform ligament that drain the venous blood from the anterior part of the abdominal wall directly into the liver. These veins are roughly divided into three subgroups: the superior and inferior veins of Sappey that drain the upper and lower portions of the falciform ligament, respectively, and the vein of Burow . When obstruction of the vena cava occurs, each of these veins may serve as collateral channels for blood flow into the liver.
C) There are numerous hepatic vein variants and accessories. Most hepatic vein variants drain directly into the inferior vena cava. These usually enter the vena cava on the right side both caudally and dorsally with respect to the level of the portal vein. The detection of these vessels is important in Budd-Chiari syndrome and also for surgical planning, since they represent the main drainage route from the right liver lobe .
Due to the interrelationship between different vessels, when individual vessels become compromised, this immediately changes the blood flow in surrounding vessels (Fig. 1).
A decrease in portal blood flow may occur in response to thrombosis, stenosis, or to compression of the main portal trunk or peripheral intrahepat-ic branches. On dynamic computer tomography (CT) or magnetic resonance (Mr) studies of the liver, the decreased portal blood flow leads to areas of parenchymal enhancement during the arterial phase, referred to as transient hepatic attenuation difference (THAD). This area of enhancement, representing increased compensatory arterial flow, is no longer visible during the subsequent portal venous phase due to rapid equilibration of contrast density. Potential clinical problems associated with THAD are that focal liver lesions may be obscured if they are located within the areas of hy-perattenuation, and that the THAD areas themselves may be mistaken for hypervascular lesions if they have a round or oval shape.
THAD are frequently seen around liver ab-
scesses or acute cholecystitis and these may develop as a result of increased arterial perfusion deriving from local hyperemia related to the inflammatory process itself and/or because of locally reduced portal flow due to parenchymal compression by the lesion. In cirrhotic and non-cirrhotic patients, THAD are typically fan- or wedge-shaped and may be lobar, segmental, subsegmental, or subcapsular in location.
Another cause of reduced portal blood flow to the liver, especially at the periphery, is portal cav-ernoma .
Hepatic Artery Compromise
The hepatic arteries communicate with each other in the central portion of the liver and thus the blockage of these large arteries induces new routes of flow. However, acute obstruction of peripheral arterial flow does not induce recognizable changes in portal blood flow .
Hepatic Vein Compromise
When the hepatic vein is acutely obstructed, the portal vein becomes a draining rather than a supplying vein. The result is a compensatory increase in hepatic arterial flow as a result of functional portal flow elimination. Liver tumors may obstruct the hepatic vein, in which case prominent hepatic enhancement is induced at a site that corresponds to the area of obstructed hepatic venous drainage.
A reduction in the afferent blood flow via the hepatic vein is seen in Budd-Chiari syndrome. In the acute phase, the post-sinusoidal obstruction causes a severe reduction in the portal vein flow and a compensatory increase in the arterial flow delivered through the hepatic artery. Since blood flow is not able to perfuse the more peripheral liver areas properly, and because there is a pressure gradient between the arterial vessels and liver veins, functional intrahepatic APS develop, that may ultimately lead to complete flow reversal within the portal vein. In the latter phases of liver enhancement, the appearance of the parenchyma is characterized by stasis. This imaging finding is also seen in right side cardiac failure, and is ascrib-able to the same hemodynamic effects.
In the chronic phase of Budd-Chiari syndrome, an intrahepatic network of venous collateral vessels is prominent, which develops to bypass the obstruction. These abnormal vessels are more evident at the periphery, and are most prominent around the caudate lobe, due to its separate autonomous venous drainage .
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