a VRT image from portal venous phase CT presents a type II Abernethy malformation. b Late arterial phase contrast-enhanced MDCT images demonstrate this was a partial shunting, as we can see small branches arising from the main PV and left PV for both lobes, Congenital extrahepatic portosystemic shuntAbernethy malformation. 3b), and right anterior segmental branch arising from the left PV [1, 5]. Aggarwal S, Fiel MI, Schiano TD. (Fig.1414). 10.1594/ecr2015/C-0314, http://creativecommons.org/licenses/by/4.0/, Peripheral shunt localized in one hepatic segment, with single or multiple communications between branches of portal and hepatic veins, Portal and hepatic veins connected through an aneurysm, Multiple communications between peripheral portal and hepatic veins in several segments, Complete absence of intrahepatic portal venous flow, Congenital absence of the PV with separate drainage of the SMV and splenic vein into systemic veins, SMV and splenic vein join to form a short extrahepatic PV which drains into a systemic vein, Partial shunt with preserved hepatic portal venous flow. One should note that no significant venous dilatation might be present in PH in case of compensatory portosystemic collateral pathways. Abstract Acute pancreatitis is associated with a number of well-known complications and imaging findings. The net difference results in arterial hyper-enhancement of the involved segment/region, in contrast to the low-attenuating remaining parenchyma. Its etiology and pathogenesis remain unclear, but primary lesions remain in portal tracts, with varying degrees of thrombosis, fibrosis, and sclerosis [17, 18]. 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. 19). In addition, a dilated paraumbilical vein with a maximum diameter of 3.7 cm was seen in the paramedial abdominal wall, leading from the left portal vein into the left inferior epigastric vein. Unable to process the form. The superficial epigastric vein drains to the femoral vein which ultimately drains into the inferior vena cava directly through the external iliac and common iliac vein, thereby bypassing the liver. The most common drainage pattern of paraumbilical veins is through the epigastric veins into the external iliac veins (Fig. 28). Provided by the Springer Nature SharedIt content-sharing initiative. Gastrorenal shunt. Received 2018 Nov 7; Accepted 2019 Feb 4. and drain into a main channel, which extends anteriorly to the UV from the epigastric and cutaneous veins around theumbilicus to the peripheral portal branches1,3 . Background: Persistent right umbilical vein (PRUV) is one of the most common prenatally detected venous anomaly. 12 The majority of paraumbilical veins drain into the SVC through the inferior epigastric veins 9 . THED are frequently observed, because the central regions of the liver are better supplied by the cavernomatous PV than the peripheral ones. As the arterial flow enters the PVS, it follows the lowest gradient pressure, filling retrogradely the PV. 21) is frequently present, considered when splenic bipolar diameter is increased (>130mm in males and >120mm in females) [8]. The most common drainage pattern of paraumbilical veins is through the epigastric veins into the external iliac veins (Fig. 5). 26). Diagrammatic representation of the embryological development of the PV. Congenital extrahepatic arterioportal fistula. Clinically significant PH is defined as a portal venous pressure above 10mmHg, and it is associated with an increased risk of developing varices and variceal bleeding [4, 14, 16]. Surg Radiol Anat. 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. PVS calcification has a strong association with long standing PH, regardless of the underlying etiology (Fig. c Left PV arising from the right anterior segmental branch. OPV diagnosis remains a challenge and patients are often misdiagnosed as cryptogenic cirrhosis. 3a), right posterior segmental branch arising from the main PV (Fig. The https:// ensures that you are connecting to the b Late arterial phase CT images reveal multiple liver nodules (orange arrows), frequently associated with Abernethy malformation [12]. You can help Wikipedia by expanding it. Cavernomatous transformation of PV. Note the THED associated with cavernoma, Portal biliopathy. J Pediatr Surg 32(3):494497, Nacif LS, Paranagu-Vezozzo DC, Galvo FH et al (2015) Significance of CT scan and color Doppler duplex ultrasound in the assessment of Abernethy malformation. Sometimes, it is difficult to differentiate a bland PV thrombus from a malignant thrombus, and this differentiation is critical since malignant thrombi are associated with a poorer prognosis, and have huge impact on patient management. 2b). 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. Congenital intrahepatic portosystemic shunts are uncommon and their pathogenesis remains unclear. Dilated cystic veins, epicholedocal plexus (of Saint) and paracholedocal plexus (of Petren), dilated gastric venous branches (left and right gastric veins), and the stenotic/occluded main PV itself may also form the portal cavernoma. There are several variants affecting the PV, and quite a number of congenital and acquired pathologies. The net difference results in arterial hyper-enhancement of the involved segment/region, in contrast to the low-attenuating remaining parenchyma. Acute thrombus usually presents as a high-attenuating luminal defect on plain CT (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]. Inferior mesenteric collateral vessels are less frequent but of great importance because of their association with rectal bleeding, since the PVS (superior hemorrhoidal vein) and the systemic venous circulation (middle and inferior hemorrhoidal veins) connect via the hemorrhoidal plexus (Fig. Variants of the PV branching pattern. Function. 9), in contrast to other arteriovenous malformations, which usually have a complex plexiform vascular nidus. b MPR image from portal venous phase CT show PV invasion by a pancreatic adenocarcinoma, a malignant cause of pre-sinusoidal PH. government site. Hereditary hemorrhagic telangiectasia, also known as Osler-Weber-Rendu disease, is a rare autosomal dominant trait affecting approximately 1 in 5000 people [13]. Additionally, the round ligament located in the free margin of the falciform ligament enters the umbilicus and serves as a significant landmark for the inner anterior abdominal wall. The inferior veins of Sappey accompany the UV in the lower falciform ligament and drain into a main channel, . a Late arterial phase CT axial image shows a heterogeneous low-attenuation PV content, due to pseudothrombosis phenomena. The portal vein (PV) is the main vessel of the PVS, resulting from the confluence of the splenic and superior mesenteric veins, and drains directly into the liver, contributing to approximately 75% of its blood flow [1]. The veins are usually insufficient to maintain the normal portal pressure and thus other signs of PH eventually develop. In this case, it was a suprasplenic type. c Left PV arising from the right anterior segmental branch. In circumportal pancreas, the pancreatic parenchyma from the uncinate process is fused with the body of the pancreas, encasing the PV and/or the SMV. 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]. Additional findings are contiguity of the thrombus with a tumor (most frequently a hepatocellular carcinoma)and vessel dilatation due to the tumoral casts growing inside. At portal venous (b) and late phases (c) the hepatic parenchyma homogenizes, and there is persistent absence of venous enhancement due to bland thrombus. MIP image from portal venous phase CT shows a metallic stent connecting the PV with the hepatic vein. Note aberrant origin of the hepatic artery emerging from superior mesenteric artery. Imaging findings of portal vein thrombosis depend on the type of thrombus, degree of thrombosis, extent of collateralization, and age of the thrombus. Hereditary hemorrhagic telangiectasia. Collateral vessels draining into the left renal vein are fairly common, and they are not associated with gastrointestinal bleeding either. https://doi.org/10.1007/s00276-013-1189-y, Park JH, Cha SH, Han JK, Han MC (1990) Intrahepatic portosystemic venous shunt. Some PH stigmata are present, as such splenomegaly, permeable umbilical vein (red arrow), and other varices. volume10, Articlenumber:38 (2019) Note the THED associated with cavernoma, Portal biliopathy. Liver involvement is characterized by hepatic telangiectasia and usually arteriovenous and less commonly arterioportal, shunts [14]. 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. in 1990 [9] (Table1). Coronary collateral veins at the lesser omentum are the most frequently depicted varices [5] (Fig. paraumbilical veins because, following interruption of umbilical ow after birth, the UV, including the stricture, The most useful imaging finding to distinguish between malignant from bland thrombi relies on the demonstration of heterogeneous contrast enhancement of the tumoral thrombus, especially seen at the arterial phase. Lafortune M, Constantin A, Breton G, Lgar A, Lavoie P. The Recanalized Umbilical Vein in Portal Hypertension: A Myth. Preduodenal PV (Fig. 25). If considering this focal varix as an aneurysm, we can classify this shunt as a type 3 either, Congenital extrahepatic portosystemic shuntAbernethy malformation. The right PV subdivides into anterior and posterior branches; the anterior one supplying segments V and VIII, and the posterior branch supplying segments VI and VII. Individual segmental branches arising away from their usual point of origin are also common variants [5]. 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. 7. Radiographics 31:905926 [. Normal PV usually enhances uniformly in the portal venous phase (6070s after intravenous contrast administration), measures 1113mm in diameter and 78cm in length [3, 4] (Fig. Portal vein thrombosis, chronic evolution. Collateral vessels draining into the left renal vein are fairly common, and they are not associated with gastrointestinal bleeding either. Nacif LS, Paranagu-Vezozzo DC, Galvo FH et al (2015) Significance of CT scan and color Doppler duplex ultrasound in the assessment of Abernethy malformation. (1998) ISBN: 9780865777163 -. 7. Collateral vessels draining into the left renal vein are fairly common, and they are not associated with gastrointestinal bleeding either. MPR image from early arterial phase CT shows heterogeneous enhancing PV thrombus, despite absent enhancement of both splenic and SMV (not shown). 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. Dilation of this particular portacaval anastomosis results in what is referred to as caput medusae . Obliterative portal venopathy (OPV), also known as idiopathic PH and hepatoportal sclerosis, is a major cause of non-cirrhotic PH [17]. These veins drain either directly or indirectly into the portal system. Acute vs. subacute/chronic PV thrombosis. Venous Drainage The gastric veins are similar in position to the arteries along the lesser and greater curvatures. Note also gastric varices due to PH. It can be classified into three subtypessuprasplenic, infrasplenic, or mixed, depending upon the level of the pancreatic annulus [6,7,8]. Knowledge of typical features of congenital and acquired PV pathologies allows the radiologist to make a confident diagnosis potentially impacting patient management. 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. Insights Imaging 10, 38 (2019). Congenital arterioportal fistulas are rare and generally solitary connections between hepatic arteries and portal veins (Fig. MIP image showing extensive calcification of PV and its tributaries, in a patient with a long-standing PH. At the time the article was created Mohammed Al Khader.O.Thabet had no recorded disclosures. Caput medusae is one of the cardinal features of portal hypertension 2. Transjugular intrahepatic portosystemic shunt. 19). The creation of a TIPS in the context of PH is one of the most common percutaneous interventional procedures involving PVS, where a parenchymal channel between a large hepatic vein and a major PV branch is created by inserting an expandable stent, in most cases connecting the right PV with the right or middle hepatic vein (Fig. These include the paraumbilical veins as well as veins of the lesser omentum, falciform ligament, and those draining the gallbladder wall. Acute thrombus usually presents as a high-attenuating luminal defect on plain CT (Fig. 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. Acquired extrahepatic portosystemic shunts are the most common shunts among PVS. 21). 22b)]; sinusoidal (e.g., cirrhosis, sinusoidal obstruction syndromepreviously known as hepatic veno-oclusive disease); and post-sinusoidal (e.g., Budd-Chiari syndrome). 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. Imaging of the porta hepatis: spectrum of disease. 10.1007/s00276-015-1436-5 [, Tappouni R, Perumpillichira J, Sekala M, Hosseinzadeh K, Clark C, Leyendecker J (2015) Circumportal pancreas: imaging findings in 40 patients. Hepatopetal venous flow is rerouted away from the liver (hepatofugal) through collateral pathways to reach the low-pressure systemic vessels. Four types are classically described, as proposed by Park et al. 10.1594/ecr2011/C-0972, Covey AM, Brody LA, Getrajdman GI, Sofocleous CT, Brown KT (2004) Incidence, patterns, and clinical relevance of variant portal vein anatomy. National Library of Medicine Variants of the PV branching pattern. 4) is a very rare condition. 3a), right posterior segmental branch arising from the main PV (Fig. Portal venous gas. PubMedGoogle Scholar. This typical branching pattern of the main PV occurs in 65% of individuals in the general population [2] (Fig. a MPR and b MIP images from portal venous phase CT show the evolution of a previous left PV complete thrombosis. Considering the differential diagnosis, it should also be noted that the combination of hypertrophy of the caudate lobe, atrophy of segment IV, and a nodular liver surface are signs more often associated whit true cirrhosis but not with OPV. b Right posterior PV branch arising directly from the main PV. The paraumbilical veins are thick-walled and of similar structure to the umbilical vein. Accessory hepatic portal veins are those veins that drain directly into the liver without joining the hepatic portal vein. Note enlargement of the hepatic vein due to increased flow directly drained from the PVS to its lumen, skipping the hepatic parenchyma. The most common drainage pattern of paraumbilical veins is through the epigastric veins into the external iliac veins (Fig. Over time, a selective involution of the right umbilical vein and cranial portion of the left umbilical vein also occurs. Can be found on ultrasound, on CT are best depict at portal venous phase as tubular enhancing structures and on MRI as flow voids. b Late arterial phase CT images reveal multiple liver nodules (orange arrows), frequently associated with Abernethy malformation [12]. Federal government websites often end in .gov or .mil. Portal venous system (PVS) drains blood from the gastrointestinal tract (apart from the lower section of rectum), spleen, pancreas, and gallbladder to the liver. The major vessel in this system is the inferior vena cava. Hepatic parenchyma displays heterogeneous peripheral enhancement in arterial phase (b) due to compensatory increased arterial flow. Some PH stigmata are present, as such splenomegaly, permeable umbilical vein (red arrow), and other varices. Most common locations are the splenomesenteric venous confluence, main PV, and intrahepatic branches at bifurcation sites (Fig. We can also see portal and hepatic venous dilatation, hepatomegaly, and lobulated hepatic contour. Liver surgery. VRT image from portal venous phase CT shows an increase in size of SV (green arrow) and SMV (red arrow), an extensive collateral network of varices fed by SMV (blue arrows), communicating with a huge-caliber right ovarian vein (yellow arrow), and giving rise to varices along the ovarian venous plexus. Patients may be asymptomatic, but high-flow shunts are prone to develop hepatic encephalopathy, hepatopulmonary syndrome, and portopulmonary syndrome. The left umbilical vein, which drains into the left branch of the portal vein, remains patent until birth. b Here, we can precisely individualize the arteriovenous malformation, as an aberrant tortuous hepatic artery branch connecting with the left PV, with an attenuation similar to the hepatic artery, filling retrogradely the PV. In this case, we can individualize ingurgitated tortuous vessels (red arrows), but sometimes thickening and hyperenhancement are all we can see. Four types are classically described, as proposed by Park et al. Transjugular intrahepatic portosystemic shunt. 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. Along with these findings, splenomegaly (Fig. 13a), in contrast to the low-attenuating defect usually observed on subacute/chronic stages. 18c). In 1793, 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]. Aneurysms of the PV are rare and represent only 3% of all aneurysms of the venous system [15]. Gastric varices are commonly located in the posterosuperior aspect of the gastric fundus (Fig. OPV imaging findings comprise the similar signs described for other general causes of PH but the most useful features are the disparity in caliber from the central PVbranches (increased) and its first and second order segmental branches (clearly reduced or even not detectable) (Fig. The first scenario is in cases of portal venous hypertension in which dilated superficial thoracoepigastric and paraumbilical veins build the so-called "caput medusa." . Portal venous gas. A more comprehensive classification may also benefit comparative analyses from different institutions (Table2). Portal vein thrombosis, chronic evolution. In this section, we will discuss the congenital ones. We can also see portal and hepatic venous dilatation, hepatomegaly, and lobulated hepatic contour. With the development of the liver, the umbilical veins fragment and connect to the hepatic sinusoids. b Maximum intensity projection (MIP) image from portal venous phase contrast-enhanced CT showing the typical branching pattern of the main PV. The site is secure. The dorsal and cranial-ventral anastomoses persist and give rise to the main PV and to the left PV, respectively. With time, the unsupplied hepatic segments totally disappeared with atrophic involution of the left lobe. Portal venous phase CT images showing a variceal network along, around and within the anorectal wall. Superior mesenteric vein (drains small intestine, ascending colon, transverse colon) 2. 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. In addition, multiphasic CT allows a comprehensive evaluation of the entire porta hepatis with high temporal and spatial resolution. a Plain CT axial image shows high-attenuation content within a left PV branch (blue arrow)acute thrombus. in 1990 [9] (Table1). a Axial fat suppressed T2-weighted MR image shows increased caliber of the hepatic artery and its branches (orange arrows). Retroperitoneal varices. Gross. Portalvenous phase CT axial imageshows pancreatic parenchyma surrounding PV like an annulus. Most patients are asymptomatic and both congenital and acquired causes are proposed. 2001;21 Spec No(suppl_1):S81-96. 19). Obliterative portal venopathy. SV converges with the SMV giving rise to the main PV. Sometimes, cavernomatous transformation of PV can encircle the common bile duct at porta hepatis, causing biliary obstruction with subsequent dilatation of the biliary treean entity described as portal biliopathy (Fig. Common variant patterns include trifurcation of the main PV (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. The imaging modality of choice will depend on the clinical context, patient characteristics, local availability, and expertise. Thus, the arterial flow takes the role and is responsible for keeping the blood supply to that segment/region, in contrast to the remaining liver, that continues to receive the vast majority of its blood supply from PVS. The paraumbilical veins are small accessory portal veins confined between the layers of the falciform ligament. The portal vein in children: radiological review of congenital anomalies and acquired abnormalities. 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. 6). AJR Am J Roentgenol 183:10551064, Connelly TM, Sakala M, Tappouni R (2015) Circumportal pancreas: a review of the literature and image findings. Nowadays, other recognized causes of portal venous gas include inflammatory bowel disease, diverticulitis, bowel distention, intra-abdominal sepsis, trauma, iatrogenic, and idiopathic causes. 2b). The veins on left side of esophagus drain into hemiazygos veins. Normal PV lies posterior to the first part of the duodenum, as it derives embryologically from the dorsal anastomosis of vitelline veins. Mesocaval shunts are portosystemic collateral vessels between the SMV and IVC that are established through retroperitoneal veins, and are not associated with an increased risk of rectal bleeding (Fig. They join the caval and portal systems by communicating with systemic veins at one end and the portal circulation at the other. References 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. Tumoral PV thrombosis. Paraumbilical veins can become enlarged in portal hypertension 3. 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. 5). 22b)]; sinusoidal (e.g., cirrhosis, sinusoidal obstruction syndromepreviously known as hepatic veno-oclusive disease); and post-sinusoidal (e.g., Budd-Chiari syndrome). THED are frequently observed, because the central regions of the liver are better supplied by the cavernomatous PV than the peripheral ones. The imaging modality of choice will depend on the clinical context, patient characteristics, local availability, and expertise. 11) [15]. The portal vein transports blood from abdominal viscera and ramifies - much like an artery - at the liver, ending into the hepatic sinusoids. The communication of the SVS and IVS with the superior epigastric or internal thoracic veins may be indirect, in a descending way from the xyphoid venous arch or plexus through a vein known. 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. Right PV is hypoattenuating before and after contrast material administration (yellow arrows), a feature suggesting non-acute thrombus. By using this website, you agree to our Correspondence to Variants of portal architecture can be found in 2035% of individuals [1, 5]. This THED fades in portal venous phase (c). Springer Nature. Radiology 263(3):741750. At portal venous (b) and late phases (c) the hepatic parenchyma homogenizes, and there is persistent absence of venous enhancement due to bland thrombus. Since 1997, 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 flowtype I; and partial shunting with some preserved hepatic portal venous flowtype II [10, 11]. CAS 3c), and major anatomic anomalies such as PV duplication and absent branching of thePV are very rare [2]. Normal anatomy of the PVS and the typical branching pattern of the main PV. Despite the thrombus age, in portal venous phase, it always appears as a luminal filling defect (Fig. Dilated cystic veins, epicholedocal plexus (of Saint) and paracholedocal plexus (of Petren), dilated gastric venous branches (left and right gastric veins), and the stenotic/occluded main PV itself may also form the portal cavernoma. Initially, the paired umbilical veins lie more lateral than the vitelline ones, and also pierce the septum tranversum and drain into the sinus venosus. 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. Esophageal and paraesophageal varices. Hereditary hemorrhagic telangiectasia. Check for errors and try again. Typically, the hepatic synthetic function is preserved, and the laboratory evaluation reveals only mild nonspecific hematological abnormalities, mostly related to hypersplenism. Obliterative portal venopathy. 3c), and major anatomic anomalies such as PV duplication and absent branching of thePV are very rare [2]. There is also increase caliber of the common hepatic artery and its branches, consequence of the augmented arterial compensatory flow. The imaging modality of choice for portal venous system evaluation will depend on the clinical context, patient characteristics, local availability, and expertise. official website and that any information you provide is encrypted b Portal venous phase CT axial image clearly reveals an additional low-attenuation filling defect in the right PV, extending into its right posterior branch (red arrow)subacute/chronic thrombus, Acute portal vein thrombosis. Depending on the case, these shunts are managed conservatively, with trans-catheter embolization, or surgery. They can be congenital or acquired and occur within or outside the liver. MIP image from portal venous phase CT shows a metallic stent connecting the PV with the hepatic vein. FOIA Mihai F, Bar C, Savin ML, Cucuteanu B, Negru D (2011) CT appearance of collateral pathways in portal hypertension. There are several variants affecting the PV, and quite a number of congenital and acquired pathologies. Pseudothrombosis phenomena. Congenital extrahepatic arterioportal fistula. Together they constitute an accessory portal system which is confined between the layers of the falciform ligament and is in communication with the veins of the ventral abdominal wall. The most common drainage pattern of paraumbilical veins is through the epigastric veins into the external iliac veins (Fig. Nodular regenerative hyperplasia (focal nodular hiperplasia-like nodules) and perfusion disorders are also more frequent in cases of OPV than in cirrhosis. Causes of PH can be easily identified, and categorized according to its relation to the hepatic sinusoids: pre-sinusoidal [e.g., PV thrombosis, extrinsic compression of PV (Fig. The best marked of these small veins is one which commences at the navel (umbilicus) and runs backward and upward in, or on the surface of, the round ligament (ligamentum teres) between the layers of the falciform ligament to end in the left portal vein. a VRT image from arterial phase CT of the same patient in Fig. Coronary collateral veins at the lesser omentum are the most frequently depicted varices [5] (Fig. 10.1007/s00261-014-0242-6 [, Arora A, Velayutham P, Rajesh S, Patidar Y, Mukund A, Bharathy KG (2014) Circumportal pancreas: a clinicoradiological and embryological review. 12). Obliterative portal venopathy: a clinical and histopathological review. Along with these findings, splenomegaly (Fig. 11) [15]. 19). Typically, the hepatic synthetic function is preserved, and the laboratory evaluation reveals only mild nonspecific hematological abnormalities, mostly related to hypersplenism. Portal venous system drains blood from the gastrointestinal tract (apart from the lower section of rectum), spleen, pancreas, and gallbladder to the liver. Congenital arterioportal fistulas are rare and generally solitary connections between hepatic arteries and portal veins (Fig. b Accordingly, on portal venous phase, the PV shows homogeneous fulfilling, discarding a hypothesis of a true thrombosis. All authors read and approved the final manuscript. In more advanced cases, ascites may occur as a result of decompensated PH. The SMV drains the major portion of the small bowel and the colon up to the splenic flexure. 18c), and drain into the esophageal or paraesophageal veins, or occasionally into the left renal vein. 24). Liver surgery. Their presence has a high sensitivity rate to PH diagnosis. 10). AJR Am J Roentgenol 183:10551064 [, Connelly TM, Sakala M, Tappouni R (2015) Circumportal pancreas: a review of the literature and image findings. Tirumani SH, Shanbhogue AKP, Vikram R, Prasad SR, Menias CO. MIP oblique reconstruction images from portal venous phase CT. a PV trifurcationPV divides into three branches: left PV, right anterior PV, and right posterior PV. Portal venous phase CT images showing a variceal network along, around and within the anorectal wall. Portal venous shunts are abnormal communications between portal and systemic venous systems (portosystemic shunts), or between the PVS and the hepatic artery (arterioportal shunts). MPR images from portal venous phase CT shows air branching pattern fulfilling some segments of peripheral right PV branches. b Over time, a selective involution occurs, involving the caudal part of the right vitelline vein, the cranial part of the left vitelline vein, and the caudal-ventral anastomosis. Additionally, the round ligament located in the free margin of the falciform ligament enters the umbilicus and serves as a significant landmark for the inner anterior abdominal wall. Partial drainage of the esophagus also occurs into bronchial and pulmonary veins. . Intrahepatic portosystemic venous shunt. Other causes include splenic, splenomesenteric, and SMV stenosis or obstruction. The creation of a TIPS in the context of PH is one of the most common percutaneous interventional procedures involving PVS, where a parenchymal channel between a large hepatic vein and a major PV branch is created by inserting an expandable stent, in most cases connecting the right PV with the right or middle hepatic vein (Fig. 8600 Rockville Pike MIP image from portal venous phase CT shows right hepatectomy findings: section and ligation of the right PV at its origin; shift of left liver toward the right with horizontalization of PV; prominent caliber of left PV and hypertrophy and rounded contours of the remaining liver. As a library, NLM provides access to scientific literature. Late arterial phase CT shows absence of a well-defined PV and multiple enhancing veins instead, representing portoportal collateral vesselsportal cavernoma. Note also the enlarged liver with heterogeneous texture. Radiographics 31:905926, Tirumani SH, Shanbhogue AKP, Vikram R, Prasad SR, Menias CO (2014) Imaging of the porta hepatis: spectrum of disease. 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. Despite the PH etiology, acquired extrahepatic portosystemic shunts may develop over time in an attempt to reduce the hepatofugal venous flow (discussed below). If considering this focal varix as an aneurysm, we can classify this shunt as a type 3 either. Inferior mesenteric collateral vessels are less frequent but of great importance because of their association with rectal bleeding, since the PVS (superior hemorrhoidal vein) and the systemic venous circulation (middle and inferior hemorrhoidal veins) connect via the hemorrhoidal plexus (Fig. Other iatrogenic findings may result from post-surgical changes. 7 and 8) [12]. 22a), tumor invasion (Fig. not via the portal system)into the liver from the anterior abdominal wall is considered the cause of focal fatty infiltrationand focal fatty sparingof the liver, and when there is systemic venous obstruction, may cause hepatic pseudolesions1,2. Gastric varices are commonly located in the posterosuperior aspect of the gastric fundus (Fig. Inferior Vena Cava The inferior vena cava is the common convergence of venous drainage from all structures below the diaphragm. b Accordingly, on portal venous phase, the PV shows homogeneous fulfilling, discarding a hypothesis of a true thrombosis. 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. b Portal venous phase CT axial image clearly reveals an additional low-attenuation filling defect in the right PV, extending into its right posterior branch (red arrow)subacute/chronic thrombus, Acute portal vein thrombosis. Segmentectomy always involves portal venous branches ligation and rearrange of the remaining system, conducing to an increased vessel caliber and/or adaptive shifting (Fig. 10). Paraumbilical veins may also be connected with numerous subcutaneous . 2b). Note also gastric varices due to PH. Congenital intrahepatic portosystemic shunts are uncommon and their pathogenesis remains unclear. With the development of the liver, the umbilical veins fragment and connect to the hepatic sinusoids. which drain into the omphalomesenteric veins. At present, the diagnosis of OPV is based on pathologic findings, excluding cirrhosis and other causes of PH. TA98: A12.3.12.010: TA2: 5103: FMA: 70317: Anatomical terminology [edit on Wikidata] The umbilical vein is a vein present during fetal development that carries oxygenated blood from the placenta into the growing fetus. 21) is frequently present, considered when splenic bipolar diameter is increased (>130mm in males and >120mm in females) [8]. Coronal maximum intensity projection of contrast enhanced CT shows enlarged recanalized paraumbilical vein (arrow) communicating with bilateral inferior epigastric veins (dashed arrows) to drain into the external iliac veins (asterisk). Privacy Portal venous gas (aeroportia) was traditionally considered a life-threatening sign thought to be a finding almost exclusive of advanced mesenteric ischemia. Patients may be asymptomatic, but high-flow shunts are prone to develop hepatic encephalopathy, hepatopulmonary syndrome, and portopulmonary syndrome. Nowadays, it is increasingly recognized that there is more a continuum than an absolute distinction between type I and type II. Malignant portal venous thrombus may also present as an arterioportal fistula, as arterial flow enters the PVS following its low gradient pressure, retrogradelly filling the PV or collateral vessels (Fig. c The remnant left umbilical vein cranially bifurcates, forming two new communications: one with the IVC through the ductus venosus, carrying oxygenated blood from the placenta directly to the fetus; and another with the left PV, supplying directly the liver. Paraumbilical vessels may anastomose with the superior epigastric or internal thoracic veins and drain into the superior vena cava (SMV), or anastomose with the inferior epigastric vein and then drain into the IVC through the external iliac vein (Fig. Imaging findings of portal vein thrombosis depend on the type of thrombus, degree of thrombosis, extent of collateralization, and age of the thrombus. a The vitelline venous system arrives at the primitive liver as two paired veins (right and left), branches into the hepatic sinusoids, and then coalesce, pierce the septum tranversum (primitive diaphragm) and drain into the sinus venosus (primitive heart). Systemic Venous System The systemic venous system transports deoxygenated blood to the right atrium of the heart. Hepatology 65(1):310335. Thus, the function of the umbilical vein is to carry oxygenated blood from the placenta to the ductus venosus, bypassing the liver and draining directly into the inferior vena cava. In the initial stages of PH increased diameter and tortuosity of hepatic artery and its branches may also be seen, as a result of hepatic venous inflow disturbance. Hereditary hemorrhagic telangiectasia, also known as Osler-Weber-Rendu disease, is a rare autosomal dominant trait affecting approximately 1 in 5000 people [13]. A large group of pathologies can trigger its development, but the most common cause is PH [2, 15]. The left gastric vein runs to the left along the lesser curvature, receiving the esophageal veins below the esophageal hiatus in the diaphragm. 26). 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 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. All about portal vein: a pictorial display to anatomy, variants and physiopathology, https://doi.org/10.1186/s13244-019-0716-8, https://doi.org/10.1007/s00276-015-1436-5, https://doi.org/10.1007/s00261-014-0242-6, https://doi.org/10.1007/s00276-013-1189-y, https://doi.org/10.1186/s12880-015-0079-7, https://doi.org/10.1007/s10456-017-9585-2, https://doi.org/10.1007/s10620-013-2736-4, http://creativecommons.org/licenses/by/4.0/. The small bowel and the colon up to the arteries along the lesser omentum are the most common pattern... Common drainage pattern of paraumbilical veins are similar in position to the low-attenuating defect observed., Breton G, Lgar a, Breton G, Lgar a, Breton G, Lgar a Breton. 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