Portal and Hepatic Veins

Anatomy

Hepatic Segmentation

The distributions of the right and left hepatic arteries and portal vein branches are not reflected by surface landmarks such as the ligamentum teres and falciform ligament. The most widely accepted schema is by Couinaud with a modification by Bismuth ( Fig. 14-1 ). The liver is divided into right and left halves by a plane that passes through the inferior vena cava (IVC) and the gallbladder fossa along the path of the middle hepatic vein. Each liver half is then further divided into four portions for a total of eight hepatic segments. The left-sided segments are numbered from 1 to 4 beginning with the caudate lobe. The right-sided segments are 5-8. Bismuth’s modification divides segment 4 into 4a (superiorly) and 4b (inferiorly).

Venous Anatomy

The portal and hepatic veins are distinct but interrelated systems responsible for the venous drainage of all of the abdominal viscera except the kidneys and adrenal glands. The linkage of the two systems occurs in the liver. Blood collected by the tributaries of the portal vein passes through the hepatic sinusoids. After traversing the sinusoids, blood is collected in the hepatic veins and flows to the right atrium. The portal vein supplies two thirds of the blood flow into the liver but carries only one third of the liver’s oxygen supply. The hepatic artery provides the bulk of the liver’s oxygen.

The portal vein is formed beneath the neck of the pancreas by the confluence of the splenic and the superior mesenteric veins and travels in the free edge of the gastrohepatic ligament ( Fig. 14-2 ). The normal portal vein is about 8 cm in length and 10-12 mm in diameter. At the liver hilum (porta hepatis) the portal vein bifurcates into right and left branches that further ramify as they penetrate through the liver ( Fig. 14-3 ). The portal vein bifurcation is extrahepatic in 40%-48% of individuals but is generally surrounded by dense fibrous connective tissue in the porta hepatis. A trifurcation of the main portal vein, resulting in absence of a right portal trunk, is encountered in about 11% of cases. Occasionally the left portal vein provides a branch to a portion of the right lobe of the liver (4%), usually the anterior segments (5 and 8). The left portal vein is critical to the fetal circulation, receiving blood from the placenta via the left umbilical vein and delivering it across the liver to the IVC via the ductus venosus. The ductus venosus eventually atrophies and becomes the ligamentum venosum while the umbilical vein becomes part of the ligamentum teres. Persistence of the ductus venosus is very rare ( Fig. 14-4 ). Valves are present in the portal vein in utero but rarely persist into adult life.

Blood in the portal system is collected from the gastrointestinal tract, pancreas, and the spleen by a network of major tributaries (see Fig. 14-2 ). The superior mesenteric vein (SMV) collects blood from the small bowel and the right colon (cecum to the mid transverse colon). Pancreaticoduodenal veins drain both into the SMV and directly into the main portal vein. The inferior mesenteric vein (IMV) collects blood from the left colon (mid transverse colon to rectum). The IMV drains into the splenic vein in roughly two thirds of individuals and in the remaining one third enters the SMV at or just below the confluence. The splenic vein drains the spleen as well as portions of the stomach (short gastric veins) and pancreas. By convention, the terms proximal and distal in the venous system are based on the normal direction of flow, with blood traveling from a proximal (peripheral) to a distal (central) location. The proximal splenic vein is therefore that portion closest to the spleen, whereas the distal portion is closest to the portal confluence.

The left gastric vein, or coronary vein, is a major draining vein of the stomach and lower esophagus. The coronary vein drains into the main portal vein in about two thirds of individuals, and into the splenic vein in the remaining one third.

The common bile duct and common hepatic artery lie with the portal vein in the gastrohepatic ligament. The portal vein, hepatic artery, and bile ducts continue together into the liver parenchyma in a grouping referred to as “portal triads.” There is actually a fourth element, the lymphatic ducts. The terminal branches of the portal vein join with the terminal branches of the hepatic artery to perfuse the hepatic sinusoids. Blood percolates through the sinusoids, where it is separated from the hepatocytes by a thin endothelial layer, and drains to the centrilobular hepatic veins. This forms the basic functional unit of the liver. The centrilobular veins join together, forming sublobular veins that unite eventually to form the hepatic veins. The largest of the hepatic veins exit the posterosuperior surface of the liver and join the hepatic segment of the IVC just before it leaves the abdomen, usually about 2 cm below the right atrium. These are the right, middle, and left hepatic veins and are referred to by anatomists as the upper group . The left and middle hepatic veins are oriented anterior and anterolateral (respectively) while the right hepatic vein typically has a lateral or posterolateral orientation ( Fig. 14-5 ). The middle and left hepatic veins form a common trunk before joining the IVC in 65%-85% of individuals. A second, lower group of hepatic veins arising from the caudate and right lobes are also present and vary in number. Large-caliber veins from the lower right lobe (inferior right hepatic veins) are seen in approximately 15% of individuals. These large veins are usually solitary but can be duplicated.

The quantity of blood flow in the portal vein is totally dependent on the perfusion of the spleen, pancreas, and gastrointestinal tract. After a meal, portal vein flow increases dramatically (postprandial portal hyperemia) as a consequence of increased perfusion of these organs. The direction of normal portal blood flow is toward the liver (hepatopetal).

Key Collateral Pathways

Two series of important collateral networks are recognized in the portal circulation. Portal-to-portal collaterals become apparent when focal occlusions develop within the portal circulation. Blood bypasses the occlusion but remains within the portal circulation. Three commonly encountered venous occlusions are in the splenic, portal, and superior mesenteric veins. When the splenic vein occludes, retrograde flow through the short gastric veins to the left gastric vein can occur ( Fig. 14-6 ). Occlusion of the central SMV can result in collateral drainage through mesenteric, paraduodenal, and marginal veins. The collateral pathways for splenic vein and SMV occlusion are frequently submucosal and are therefore prone to bleeding into the gastrointestinal tract. Occlusion of the portal vein results in enlargement of the pericholedochal and epicholedochal veins in the gastrohepatic ligament, termed cavernous transformation ( Fig. 14-7 ). A small, residual, or recanalized main portal vein may exist within this network but can be difficult to identify.

Portal-to-systemic collaterals develop in the setting of portal hypertension and represent pathways for blood to escape the portal circulation and return to the systemic circulation ( Fig. 14-8 ). Termed varices , the majority of these pathways represent enlargement of preexisting small communications between the portal and systemic veins. Unusual portal-to-systemic collaterals can form following abdominal surgery. Both portal-to-portal and portal-to-systemic collaterals may be present in the same patient.

Obstruction of the main hepatic veins frequently results in intrahepatic collateralization to other hepatic veins. If at least one hepatic vein remains patent, obstruction of main hepatic veins is usually well tolerated. Collateral drainage through capsular and diaphragmatic veins may also occur.

Imaging

Transabdominal ultrasound (US) with Doppler interrogation is an excellent noninvasive means for evaluating the patency of the portal vein, hepatic veins, and hepatic artery. Color-flow Doppler and power Doppler provide quick means for locating the vessels and confirming patency, with color-flow Doppler also providing directional information. Spectral Doppler should also be performed and the waveforms evaluated. Each vessel has a typical waveform ( Fig. 14-9 ). The portal vein is a high-flow, low-pressure, low-resistance conduit characterized by a gentle phasic waveform with respiratory variation. The splenic and superior mesenteric veins have similar waveforms. Flow in the portal system increases dramatically after meals. The hepatic veins are characterized by a variable waveform influenced by right atrial contractions. The hepatic artery has a low-resistance arterial waveform. A structural evaluation of the liver should also be performed, noting the overall size and echotexture of the liver, parenchymal masses (cystic or solid), and biliary dilatation. Ascites should be noted and the volume qualitatively estimated (minimal, moderate, large). Ultrasound can be technically demanding depending on the patient’s body habitus, ability to cooperate, and severity of underlying liver disease.

Computed tomography angiography (CTA) is an excellent modality for imaging the hepatic and portal veins. Furthermore, detection of mass lesions is highly sensitive. The three-dimensional (3-D) relationships of the vascular structures (notably the portal vein and hepatic veins) can be easily appreciated from the axial CT images and postprocessed data ( Fig. 14-10 ). Dedicated vascular CTA of the liver requires a minimum of two acquisition phases: hepatic arterial and portal venous. The first scan through the liver is obtained during the arterial phase of enhancement. Approximately 30-60 seconds after the initiation of the bolus, the scan should be repeated to obtain the portal venous phase. Addition of preliminary noncontrast and delayed postcontrast images optimizes evaluation of the hepatic parenchyma for any mass lesion (triple or quadruple phase examination). The arterial phase should be performed with thin effective collimation and overlapping slices to ensure longitudinal resolution appropriate for the size of the hepatic artery. Wider collimation can be used for the portal venous phase and to cover the remainder of the abdominal contents if necessary.

Magnetic resonance imaging (MRI) and MR venography (MRV) are also excellent tools for evaluating the portal venous system and hepatic veins, as well as the liver parenchyma. Dedicated anatomic sequences should be obtained in multiple planes for overall anatomic evaluation. The relatively slow and nonpulsatile flow in the portal venous system is well suited for MRV with time-of-flight (TOF) and phase-contrast (PC) techniques. However, the complex geometry of the vessels limits the utility of these sequences. Gadolinium-enhanced 3-D gradient echo volume acquisitions, in both arterial and portal venous phases, provide dramatic angiographic images of these structures unaffected by signal loss due to complex or in-plane flow (see Fig. 14-3 ). Image postprocessing is an essential tool when interpreting hepatic and portal venous MRV.

Hepatic venography can be performed from either the femoral vein or internal jugular vein approaches. Femoral venous access is convenient if no other procedure is to be performed. A Cobra-type curved catheter can be used; however, a recurved catheter such as a Simmons-1 is very effective for engaging the hepatic veins from the femoral approach. Access from the jugular vein is mechanically more advantageous, providing a direct line for the catheter into the hepatic vein. A multipurpose angled-tip catheter is generally effective in selecting the hepatic veins. The junction of the diaphragm with the right cardiac border represents a convenient fluoroscopic landmark for the hepatic vein orifices. The main trunk of the right hepatic vein is characteristically oriented in a lateral or slightly posterolateral direction while the middle and left hepatic veins are more anterior in orientation (see Fig. 14-5 ). A test injection of contrast should be performed by hand to ensure that the catheter tip is not wedged in a small hepatic vein branch. Some angiographers advocate the addition of a side hole near the tip of the catheter to prevent an inadvertent wedged injection. A formal venogram can then be obtained by injecting contrast at a rate of 5-6 mL/sec for a total of 15-18 mL during suspended respiration ( Fig. 14-11 ).

Balloon occlusion hepatic venography can be used to image the small hepatic veins as well as the portal vein ( Table 14-1 ). An 8- to 11-mm diameter occlusion balloon is gently inflated with 2-3 mL of dilute contrast (or room air for rapid deflation) until the hepatic vein wall is circumferentially engaged (see Fig. 2-26 ). Standard iodinated contrast material or carbon dioxide (CO ₂ ) gas can then be injected through the catheter by hand. In a normal liver, the portal vein is usually not visualized because contrast drains into other hepatic vein branches. With cirrhosis, opacification of the portal vein and even retrograde flow may be seen. Because of its extremely low viscosity, CO ₂ gas easily traverses the hepatic sinusoids, providing superior opacification of the portal vein. When sinusoidal hypertension (discussed later) is present, the contrast enters the portal vein and a portal venogram can be obtained. Aggressive injection of either iodinated contrast or CO ₂ gas can result in hepatic fracture, a potentially lethal complication ( Fig. 14-12 ).

Direct opacification of the portal system can be accomplished with a transhepatic approach analogous to that employed during a transhepatic cholangiogram ( Fig. 14-13 ). Local anesthetic is infiltrated into the skin and a narrow-gauge needle (typically 21-gauge) is advanced into the liver under fluoroscopic control. Transpleural puncture should be avoided, and the needle should pass over, not under, the rib. As the needle is slowly withdrawn, contrast is carefully injected with continuous fluoroscopic monitoring. The portal branches must be differentiated from hepatic arterial branches, because both flow in the same direction; arterial flow is faster with less arborization. Once a suitable portal vein radicle is opacified, a 0.018-inch guidewire can be introduced and the needle exchanged for a coaxial introducer set with a 4- or 5-French outer catheter. A 0.035-inch guidewire can then be inserted into the portal system and the introducer set exchanged for a pigtail catheter positioned deep in the splenic vein or SMV. The same transhepatic tract can be used to insert larger instruments if interventions are to be performed. Depending on the size of the catheters used and the patient’s coagulation status, it may be appropriate to embolize the tract with Gelfoam pledgets or coils at the end of the procedure to reduce the risk of intraperitoneal bleeding.

Transvenous portal access is obtained by using a special directional cannula introduced into a hepatic vein from the jugular vein (see Transjugular Intrahepatic Portosystemic Shunt). When performed correctly this method avoids puncture of the liver capsule and thus reduces the risk of bleeding complications. The portal system can also be opacified by inserting a needle percutaneously into the splenic pulp and injecting either iodinated contrast or CO ₂ . This method, known as splenoportography, is rarely used for diagnostic imaging but can be a useful alternative approach for splenic vein interventions. Lastly, percutaneous retrograde catheterization of a recanalized umbilical vein allows access to the left portal vein ( Fig. 14-14 ).

Indirect opacification of the portal venous system can be achieved by arterioportography. Injection of the SMA and/or IMA results in opacification of the mesenteric tributary veins and portal vein as the contrast drains from the splanchnic capillary bed. The rate and density of opacification of these veins can be significantly improved by injecting a vasodilator such as nitroglycerin (NTG; 200-300 μg) through the arterial catheter immediately before the contrast injection. Dilution of the NTG to 50-100 μg/mL provides a sufficient volume. The NTG is injected through the selective SMA or IMA catheter, followed by 5-10 mL of saline flush. The angiogram should be performed immediately (5-8 mL/sec in the SMA and 2-4 mL/sec in the IMA for 6-10 seconds), with rapid filming (at least 4 frames/sec) for a few seconds followed by 1 frame/sec during the venous phase. Breathholding is essential to minimize motion artifacts, and glucagon (1 mg intravenously) may be used to decrease peristalsis.

Injection of the celiac artery also opacifies the portal vein with blood draining from the spleen, stomach, and pancreas. Selective catheterization of the splenic artery results in greater portal venous opacification ( Fig. 14-15 ). For selective splenic artery injections, volumes between 20 and 60 mL may be needed depending on the size of the spleen. Vasodilators are not of assistance in this vascular bed. This technique is less effective in the presence of congestive splenomegaly, which requires very large volumes of contrast and has significantly increased transit time through the spleen.

Portal Hypertension

Portal hypertension can be defined as an absolute portal venous pressure of greater than 10 mm Hg. More commonly, the pressure gradient between the portal and systemic veins is used to guide therapy; normal gradient is less than 5 mm Hg. Elevated pressures can exist in the entire portal venous system, or focally in isolated segments. Portal hypertension is just one manifestation of chronic liver disease ( Box 14-1 ).

In industrialized countries, portal hypertension is most commonly encountered in patients with cirrhosis (schistosomiasis is the most common etiology globally). The usual diseases in industrialized nations leading to cirrhosis and portal hypertension are alcoholic liver disease, chronic viral hepatitis (hepatitis B and C viruses), and steatohepatitis ( Box 14-2 ). The incidence of cirrhosis in the United States is 3.6/1000 adults. End-stage liver disease was the 12th leading cause of death in the United States in 2009. In at least 50% of these patients alcohol is the most significant cause of liver failure. Patients in whom a cause cannot be identified are said to have “cryptogenic cirrhosis.”

The many causes of portal hypertension are organized into three categories based on the level of obstruction: posthepatic, intrahepatic, and prehepatic ( Box 14-3 ). Pathologists further divide the intrahepatic causes as presinusoidal, sinusoidal, and postsinusoidal on the basis of histologic findings. The level of obstruction in alcoholic cirrhosis is primarily sinusoidal. In schistosomiasis, a common cause of portal hypertension in parts of Africa and South America, the obstruction is presinusoidal.