What makes portal vein

Here, learn about its anatomy, functions, and the kinds of health problems that can occur. The fimbriae of the uterine tube, also known as fimbriae tubae, are small, fingerlike projections at the end of the fallopian tubes, through which…. Health Conditions Discover Plan Connect. Common hepatic duct. Intermediate branch of hepatic artery. Hepatic artery proper. Read this next.

Medically reviewed by Alana Biggers, M. Common hepatic duct Medically reviewed by the Healthline Medical Network. Intermediate branch of hepatic artery Medically reviewed by the Healthline Medical Network. Hepatic artery proper Medically reviewed by the Healthline Medical Network. In this pictorial review, we assess the embryological development and normal anatomy of the PVS, displaying selected cases consisting of normal variants, congenital anomalies, and a large and heterogeneous group of acquired conditions that may affect the PV.

Portal venous system drains blood from the gastrointestinal tract apart from the lower section of rectum , spleen, pancreas, and gallbladder to the liver. From an embryological point of view, the portal venous system is formed from the 4th to the 12th gestation week, developing from the vitelline venous system in close relation with the umbilical venous system.

The imaging modality of choice for portal venous system evaluation will depend on the clinical context, patient characteristics, local availability, and expertise.

Imaging findings of portal vein thrombosis depend on the type of thrombus, degree of thrombosis, extent of collateralization, and age of the thrombus. Portal venous system PVS drains blood from the gastrointestinal tract apart from the lower section of rectum , spleen, pancreas, and gallbladder to the liver.

Hepatic artery provides the remaining hepatic blood flow. Once in the liver, PV ramifies and reaches the sinusoids, with downstream blood being directed to the central vein at the hepatic lobule level, then to the hepatic veins and inferior vena cava IVC to reach the systemic venous system.

The embryology of the PVS is a complex process that occurs from the 4th to the 12th gestation week, developing from the vitelline venous system in close relation with the umbilical venous system [ 2 ] Fig. Over time, there is a selective involution of the venous network, with the dorsal and cranial-ventral vitelline anastomoses giving rise to the main PV and left PV, respectively [ 2 ].

Diagrammatic representation of the embryological development of the PV. These two vitelline veins communicate through three pre-hepatic anastomoses around the developing duodenum cranial-ventral, dorsal, and caudal-ventral. The dorsal and cranial-ventral anastomoses persist and give rise to the main PV and to the left PV, respectively. Initially, the paired umbilical veins lie more lateral than the vitelline ones, and also pierce the septum tranversum and drain into the sinus venosus.

With the development of the liver, the umbilical veins fragment and connect to the hepatic sinusoids. Over time, a selective involution of the right umbilical vein and cranial portion of the left umbilical vein also occurs. After birth, the ductus venosus and the left umbilical vein involute and become the ligamentum venosum and ligamentum teres , respectively. On normal anatomy, typically, the splenic vein SV joins the superior mesenteric vein SMV anteriorly to the IVC and posteriorly to the pancreatic neck to form the PV, which ascends within the hepatoduodenal ligament, posteriorly to the hepatic artery and common bile duct, toward the hepatic hilum, where it divides into right and left Fig.

Additional tributaries of the PV include the left and right gastric veins, cystic veins, and Sappey veins. Every imaging technique has advantages and disadvantages for the noninvasive evaluation of the PVS. The imaging modality of choice will depend on the clinical context, patient characteristics, local availability, and expertise.

In most centers, CT is the preferred technique for the evaluation of the PVS, permitting the evaluation of the portal vasculature using high-resolution isotropic acquisition in a short time, and allowing high-quality multiplanar reformations MPR and three-dimensional reconstructions [ 3 ]. In addition, multiphasic CT allows a comprehensive evaluation of the entire porta hepatis with high temporal and spatial resolution. The major advantage is the possibility to anatomically evaluate and obtain information about the contents of vascular structures without administering intravenous contrast product and non-using ionizing radiation.

However, compared to CT, it is still a more time-consuming, expensive, and less accessible imaging technique, generally with less spatial and temporal resolution necessary to evaluate vascular structures, and also more susceptible to artifacts.

Doppler ultrasound is a useful imaging technique in the evaluation of the PVS, is highly available, and the major advantage is allowing a detailed evaluation of the venous flow besides the anatomical information.

Sometimes it is conditioned by the biotype and lack of collaboration of the patient, and still have to recur to other techniques if necessary an overall PVS assessment or dynamic contrast information. Normal PV usually enhances uniformly in the portal venous phase 60—70 s after intravenous contrast administration , measures 11—13 mm in diameter and 7—8 cm in length [ 3 , 4 ] Fig. Since this venous system is valveless, pressure modifications caused by respiration can affect its diameter; therefore, measurements on every imaging technique should be made at deep inspiration, when the caliber is at its greatest [ 1 ].

Common variant patterns include trifurcation of the main PV Fig. Individual segmental branches arising away from their usual point of origin are also common variants [ 5 ].

Other variant branching patterns are less frequently observed, as the left PV arising from the right anterior segmental branch Fig. Variants of the PV branching pattern. MIP oblique reconstruction images from portal venous phase CT. Awareness of PV branching pattern is important to accurately interpret imaging findings, in planning liver surgery to ensure that portal perfusion to the future liver remnant is not compromised , liver transplantation to enable appropriate graft selection so as to avoid complex anastomosis that might compromise the graft or the residual liver in a living donor , and percutaneous interventional procedures.

Normal PV lies posterior to the first part of the duodenum, as it derives embryologically from the dorsal anastomosis of vitelline veins. Preduodenal PV Fig. Its main clinical significance is the frequent association with intestinal obstruction or other congenital malformations, with two-thirds of cases presenting in the first week of life [ 1 , 2 ]. Preduodenal PV. MPR image from portal venous phase CT shows the main PV coursing in front of the duodenum and pancreas, an incidental finding in this case.

Circumportal pancreas is a normal anatomic finding in pigs but a relatively uncommon anatomic variant in humans 1—3. It can be classified into three subtypes—suprasplenic, infrasplenic, or mixed, depending upon the level of the pancreatic annulus [ 6 — 8 ]. It can exhibit either an anteportal or an unusual retroportal main pancreatic duct. Combination of an anteportal duct and suprasplenic fusion is the most common subtype [ 7 ] Fig.

Circumportal pancreas. Portal venous phase CT axial image shows pancreatic parenchyma surrounding PV like an annulus. In this case, it was a suprasplenic type. Portal venous shunts are abnormal communications between portal and systemic venous systems portosystemic shunts , or between the PVS and the hepatic artery arterioportal shunts. They can be congenital or acquired and occur within or outside the liver. In this section, we will discuss the congenital ones.

Portosystemic shunts are diversions of portal venous blood into the systemic venous system bypassing the liver. Patients may be asymptomatic, but high-flow shunts are prone to develop hepatic encephalopathy, hepatopulmonary syndrome, and portopulmonary syndrome.

Depending on the case, these shunts are managed conservatively, with trans-catheter embolization, or surgery. Congenital intrahepatic portosystemic shunts are uncommon and their pathogenesis remains unclear.

Interestingly, they are more frequent in the right hepatic lobe [ 1 ] Fig. Four types are classically described, as proposed by Park et al. Intrahepatic portosystemic shunts may also be acquired, resulting from trauma may be iatrogenic and portal hypertension PH , as described later. Classification of congenital intrahepatic portosystemic shunts based on Park et al.

Congenital intrahepatic portosystemic shunt. MPR image from late arterial phase CT displaying the most common type of congenital intrahepatic portosystemic shunt type 1 , with a single vessel connecting the right PV with the IVC.

Note the large caliber of both afferent PV branch and efferent hepatic vein, and the presence of a variceal dilatation between both, appearing as a rounded enhancing mass. If considering this focal varix as an aneurysm, we can classify this shunt as a type 3 either.

Congenital extrahepatic portosystemic shunts are rare and represent a group of malformations with high morphological variability, with resultant differences in clinical presentation and optimal operative approach [ 10 ]. In , John Abernethy first described a case of a congenital absence of the PV with a portocaval shunt responsible for the portal venous blood diversion [ 10 , 11 ].

Portal vein. Reference article, Radiopaedia. Vascular , Hepatobiliary. URL of Article. On this page:. Portal vein normal anatomy and variants: implication for liver surgery and portal vein embolization. Semin Intervent Radiol. Related articles: Anatomy: Abdominopelvic.

Promoted articles advertising. Figure 1: portal vein Figure 1: portal vein. Figure 2: portal vein cross-section image Figure 2: portal vein cross-section image. Loading more images Close Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Portosystemic shunts are diversions of portal venous blood into the systemic venous system bypassing the liver.

Patients may be asymptomatic, but high-flow shunts are prone to develop hepatic encephalopathy, hepatopulmonary syndrome, and portopulmonary syndrome. Depending on the case, these shunts are managed conservatively, with trans-catheter embolization, or surgery. Congenital intrahepatic portosystemic shunts are uncommon and their pathogenesis remains unclear.

Interestingly, they are more frequent in the right hepatic lobe [ 1 ] Fig. Four types are classically described, as proposed by Park et al. Intrahepatic portosystemic shunts may also be acquired, resulting from trauma may be iatrogenic and portal hypertension PH , as described later. Congenital extrahepatic portosystemic shunts are rare and represent a group of malformations with high morphological variability, with resultant differences in clinical presentation and optimal operative approach [ 10 ].

In , John Abernethy first described a case of a congenital absence of the PV with a portocaval shunt responsible for the portal venous blood diversion [ 10 , 11 ]. Since , Abernethy malformations became an accepted eponymous to congenital extrahepatic portosystemic shunts, and can be subdivided into two major categories: total shunting with complete absence of intrahepatic portal venous flow—type I; and partial shunting with some preserved hepatic portal venous flow—type II [ 10 , 11 ].

Nowadays, it is increasingly recognized that there is more a continuum than an absolute distinction between type I and type II. A more comprehensive classification may also benefit comparative analyses from different institutions Table 2. In both types, most patients suffer premature mortality, associated with the shunting complications and other congenital abnormalities inherent to the syndrome Figs. Congenital intrahepatic portosystemic shunt.

MPR image from late arterial phase CT displaying the most common type of congenital intrahepatic portosystemic shunt type 1 , with a single vessel connecting the right PV with the IVC. Note the large caliber of both afferent PV branch and efferent hepatic vein, and the presence of a variceal dilatation between both, appearing as a rounded enhancing mass.

If considering this focal varix as an aneurysm, we can classify this shunt as a type 3 either. Congenital extrahepatic portosystemic shunt—Abernethy malformation. After that, the main PV lacks the classic branching pattern into right and left PV.

Taking into account the origin, the route, and the final confluence with IVC, this aberrant left PV-IVC shunt was interpreted as a patent ductus venosus. Note aberrant origin of the hepatic artery emerging from superior mesenteric artery. There is also increase caliber of the common hepatic artery and its branches, consequence of the augmented arterial compensatory flow.

Extrahepatic portosystemic shunts as an acquired pathology are the most common portal venous shunts, discussed here later. Arterioportal shunts may be either congenital presenting as a fistula or as vascular malformations in hereditary hemorrhagic telangiectasia or more frequently acquired, as discussed here later. Congenital arterioportal fistulas are rare and generally solitary connections between hepatic arteries and portal veins Fig. As the arterial flow enters the PVS, it follows the lowest gradient pressure, filling retrogradely the PV.

High-flow shunts may generate a continuous hepatofugal flow, progressing in time to PH. Congenital extrahepatic arterioportal fistula. Hereditary hemorrhagic telangiectasia , also known as Osler-Weber-Rendu disease, is a rare autosomal dominant trait affecting approximately 1 in people [ 13 ]. It is a multi-organ vascular dysplasia characterized by multiple arteriovenous malformations that lack an intervening capillary network.

Liver involvement is characterized by hepatic telangiectasia and usually arteriovenous and less commonly arterioportal, shunts [ 14 ]. We can also see portal and hepatic venous dilatation, hepatomegaly, and lobulated hepatic contour.

Doppler ultrasound may raise the suspicion of an arterioportal shunt when increased systolic velocity and decreased resistance index of hepatic artery are present, increased velocity of the PV flow, and PV wave inversion demonstrating hepatofugal blood flow. Hereditary hemorrhagic telangiectasia. Note also the enlarged liver with heterogeneous texture. An early contrast filling of portal venous branches is also seen, both peripheral b red arrow and central branches c blue arrow , in addition to an increased PV caliber.

Most patients are asymptomatic and both congenital and acquired causes are proposed. Most common locations are the splenomesenteric venous confluence, main PV, and intrahepatic branches at bifurcation sites Fig. Aneurysm of the PVS. Note the left PV branches arising directly from the aneurysm yellow arrow. Portal vein thrombosis, also known as pylethrombosis, is uncommon, although it can be associated with a number of common clinical conditions including cirrhosis, intraabdominal inflammation, hypercoagulability states, abdominal trauma, and iatrogenic complications [ 2 , 3 ].

In PV thrombosis, imaging appearance depends on the degree and chronicity of the thrombosis, as well as the extent of collateralization, but typically imaging findings show a complete or partial filling defect within the portal venous lumen on contrast-enhanced imaging. The reader must be aware that a PV pseudothrombosis may be occasionally depicted, consisting in a low-attenuation filling defect-like appearance in the main PV lumen resulting from the mixing of the enhanced splenic vein flow with the non-enhanced SMV flow during the late arterial phase or early portal venous phase.

However, contrarily to a real thrombus, this pseudo-filling defect disappears on portal venous phase Fig. Pseudothrombosis phenomena. Acute PV thrombosis may have different clinical presentations, ranging from the asymptomatic patient, nonspecific abdominal pain, to deteriorating PH with increased risk of variceal bleeding and shock [ 2 , 3 ]. Acute thrombus usually presents as a high-attenuating luminal defect on plain CT Fig. Despite the thrombus age, in portal venous phase, it always appears as a luminal filling defect Fig.

Sometimes, at its early stages, despite the lack of enhancement of the PV lumen, enhancement of the vein wall may occur, thought to represent either dilated vasa vasorum or a patent thin peripheral lumen [ 15 ] Fig. Acute vs. Acute portal vein thrombosis. MPR image from portal venous phase CT shows a luminal thrombus within the main PV, and enhancement of the vessel wall red asterisk , presumably due to still normal flow through its vasa vasorum.

Additional CT imaging findings of subacute and chronic PV thrombosis include transient hepatic enhancement differences THED , cavernomatous transformation of the PV, and total disappearance of the thrombosed segment with involution of the reliant structures Fig.

Portal vein thrombosis, chronic evolution. With time, the unsupplied hepatic segments totally disappeared with atrophic involution of the left lobe. THED is the end result of the decreased portal venous flow to a liver segment or region and subsequent buffer response of the arterial counterpart via the opening of the physiological distal arterioportal shunts. Portal vein thrombosis with THED.

At portal venous b and late phases c the hepatic parenchyma homogenizes, and there is persistent absence of venous enhancement due to bland thrombus. Cavernomatous transformation of PV consists on the development of multiple venous channels within and around a previously stenotic or occluded PV, acting as portoportal collateral vessels.

This transformation can occur as soon as 6—20 days after a thrombotic event, even if partial recanalization of the thrombus develops [ 15 ]. The veins are usually insufficient to maintain the normal portal pressure and thus other signs of PH eventually develop. THED are frequently observed, because the central regions of the liver are better supplied by the cavernomatous PV than the peripheral ones.

The portal venous flow decrease at the periphery of the liver causes again an arterial compensatory buffer response and inhomogeneous, peripheral, patchy areas of transient high attenuation are recognized in the arterial phase Fig.