Portal Vein: a Review of Pathology and Normal Variants on MDCT E-Poster: EE-005

Home , Cystic vein, Systemic venous system

Portal vein: a review of pathology and normal variants on MDCT e-Poster: EE-005

Congress: ESGAR2016

Type: Educational Exhibit

Topic: Diagnostic / Abdominal vascular imaging

Authors: C. Carneiro, C. Bilreiro, C. Bahia, J. Brito; Portimao/PT

MeSH:

Abdomen [A01.047]

Portal System [A07.231.908.670]

Portal Vein [A07.231.908.670.567]

Hypertension, Portal [C06.552.494]

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To review the embryology and anatomy of the portal venous system.

To describe and illustrate the normal variants and congenital anomalies that may affect the portal vein.

To exhibit acquired abnormalities involving the portal venous system.

2. Background

The portal vein is the main vessel of the portal venous system, which drains blood from the gastrointestinal tract (apart from the lower section of rectum), spleen, pancreas and gallbladder to the liver, contributing to approximately 75% of its blood flow [1,2,3].

Embryology

The embryologic development of the portal venous system is a complex process that occurs from the 4th to the 12th week of gestation [1]. The portal venous system originates from the vitelline venous system, in close relation to the umbilical venous system (Fig.1). Embryology

Fig.1 - Diagrammatic representation of the embryological development of the portal vein. The vitelline venous system arrives at the primitive liver as two paired veins (right and left), branches into the hepatic sinusoids, coalesce, pierce the septum tranversum (primitive diaphragm) and drain into the sinus venosus (primitive heart). This two vitelline veins communicate through three pre-hepatic anastomoses around the developing duodenum (cranial-ventral, dorsal, and caudal-ventral).

Over time the dorsal and cranial-ventral anastomoses persist and give rise to the main portal vein and to the left portal vein, respectively (Fig.2). Embryology

Fig.2 - Diagrammatic representation of the embryological development of the portal vein. 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. Then the dorsal and cranial-ventral anastomoses persist and give rise to the main portal vein and to the left portal vein, respectively. The paired umbilical veins initially lie more lateral than the vitelline veins, 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.

The remnant left umbilical vein cranially bifurcates forming two new communications: one with the inferior vena cava through the ductus venosus, carrying oxygenated blood from the placenta directly to the fetus; and one other with the left portal vein, supplying directly the liver (Fig.3). Embryology

Fig.3 - Diagrammatic representation of the embryological development of the portal vein.

After birth, the ductus venosus and the left umbilical vein involute and become the ligamentum venosum and ligamentum teres, respectively.

Normal anatomy and imaging appearance

Typically, splenic and superior mesenteric veins join anterior to the inferior vena cava and posterior to the pancreatic neck to form the portal vein, which ascends within the hepatoduodenal ligament, posterior to the hepatic artery and common bile duct, toward the hepatic hilum, where it divides into right and left portal veins [1,2,3] (Fig.4). Normal anatomy

Fig.4 – Normal anatomy. A maximum intensity projection (MIP) contrast-enhanced CT image shows the typical branching pattern of the portal venous system.

The left portal vein is horizontal for a short distance before it turns cranially and branches, supplying Couinaud hepatic segments I, II, III, and IV.

The right portal vein subdivides into anterior and posterior branches, the anterior one supplying segments V and VIII, and the posterior branch supplying segments VI and VII.

This typical branching pattern of the main portal vein occurs in 65% of individuals in the general population [1].

The inferior mesenteric vein joins the splenic vein (40%), the superior mesenteric vein (40%), or the splenomesenteric confluence (20%) [1].

Additional tributaries of the portal vein include the left and right gastric veins, cystic vein, and paraumbilical veins.

Normal portal vein has a diameter of 11-13 mm [4]. This venous system is valveless and respiration can affect its caliber, which is greatest at deep inspiration [2].

Role of computed tomography (CT)

Every imaging technique has advantages and disadvantages for the noninvasive evaluation of the portal venous system.

Imaging modality choice will always depend on the case scenario, patient characteristics, local availability and on the radiologist's preference.

Contrast-enhanced CT is used, in most centers, as the imaging modality of choice for the evaluation of the portal venous system [1].

Multidetector CT (MDCT) allows evaluation of the portal vasculature using a high-resolution isotropic acquisition in a short acquisition time, permitting three dimensional reconstructions, possibility to identify associated complications and can be used to guide interventional procedures. Disadvantages are the classic ones (ionizing radiation and nephrotoxicity of iodinated contrast material) and the lack of qualitative flow information. we present an overview of normal variants and congenital and acquired anomalies of the portal venous system.

3. Imaging Findings/Procedure Details

Anatomic variants and congenital malformations

Variants in the normal branching pattern of the portal vein occur in approximately 20% of the population [2,5].

The most common variant patterns include trifurcation of the main portal vein (Fig.5A), right posterior segmental branch arising from the main portal vein (Fig.5B), and right anterior segmental branch arising from the left portal vein (Fig.5C) [1,2,5].

Anatomic variants

Fig.5 - Anatomic variants. Contrast-enhanced MDCT oblique axial MIP reformatted images showing the most common anatomic variants of portal vein branching pattern. (A) Portal vein trifurcation - portal vein divides into three branches: left portal vein, right anterior portal vein, and right posterior portal vein. (B) right posterior portal vein branch as first branch arising directly from the main portal vein. (C) right anterior segmental branch arising from the left portal vein, instead of right portal vein bifurcation.

Other variant branching patterns are less frequently observed, as the left portal vein arising from the right anterior segmental branch (Fig.6A), and the right anterior segmental branch arising from a common trunk with the left portal vein (Fig.6B).

Anatomic variants

Fig.6- Anatomic variants. Contrast-enhanced MDCT oblique axial MIP reformatted images showing not so common other anatomic variants of portal vein branching pattern. (A) Left portal vein arising from the right anterior segmental branch. (B) Right anterior segmental branch and left portal vein arising from a common left trunk.

Individual segmental branches arising away from their usual point of origin are common variants [2].

Major anatomic anomalies such as portal vein duplication, congenital absence of the portal vein, absent branching of the portal vein, and preduodenal portal vein are very rare [1].

The normal portal vein lies posterior to the first part of the duodenum, as it derives embryologically from the dorsal anastomosis of vitelline veins. Preduodenal portal vein is a very rare condition (Fig. 7). Its main clinical significance is the frequent association with intestinal obstruction and with other congenital malformations, two-thirds of cases presenting in the first week of life [2].

Preduodenal portal vein

Fig.7 - Preduodenal portal vein. Portal venous phase contrast-enhanced MDCT oblique MPR shows the main portal vein coursing in front of the duodenum and pancreas, in this case an incidental finding. Circumportal pancreas is a normal anatomic finding in pigs but a relatively uncommon anatomic variant in humans (1-3,4%) [6]. It is usually an incidental finding at imaging, where the pancreatic parenchyma from the uncinate process is shown to be fused with the body of the pancreas, encasing the portal vein and/or the superior mesenteric vein. Circumportal pancreas can be classified into three subtypes - suprasplenic, infrasplenic or mixed, depending upon the level of the pancreatic annulus [6,7,8]. 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 (Fig.8) [7].

Circumportal pancreas

Fig.8 - Circumportal pancreas. Portal venous phase contrast-enhanced MDCT images of two different cases, both incidental findings. (A-C) axial, sagittal and oblique coronal MPR's, and (D) a second case depicted on an axial image. Both cases are suprasplenic type. Note the pancreatic parenchyma surrounding the portal vein like an annulus.

Knowledge of these anatomic variants in the portal venous system is particularly important during planning of pancreatic surgery, liver resection, liver transplantation and percutaneous interventional procedures.

Portal venous shunts are abnormal communications between the portal venous system and the systemic venous system (portosystemic shunts) or between the portal venous system and the hepatic artery (arterioportal shunts). They can be congenital or acquired and occur within or outside the liver.

— Portosystemic shunts are diversions of portal venous blood into the systemic venous system without the passage of blood through the hepatic sinusoids. Patients may be asymptomatic, but high-flow shunts are prone to develop hepatic encephalopathy. They can be managed conservatively, with transcatheter embolization, surgical ligation or partial hepatectomy.

Congenital extrahepatic portosystemic shunts are rare and frequently associated with additional congenital malformations. Patients may be asymptomatic but are prone to develop intrahepatic tumors and hepatic encephalopathy [1]. Extrahepatic portosystemic shunts as an acquired pathology are the most common portal venous shunts and occur more frequently in the context of portal venous hypertension discussed here later.

Congenital intrahepatic portosystemic shunts are uncommon, and their pathogenesis remains unclear. Four types are described: the most common type, a single vessel connecting the right portal vein to the inferior vena cava (Fig.9); a localized shunt in a single segment with one or more communications between peripheral branches of portal and hepatic veins; a localized shunt with a focal varix between peripheral branches of portal vein and hepatic veins; and multiple communications between peripheral portal and hepatic veins in several segments [1,2]. These shunts are more common at the right hepatic lobe [2]. Intrahepatic portosystemic shunts may also be acquired resulting from trauma or portal hypertension.

Congenital intrahepatic portosystemic shunt

Fig.9 - Congenital intrahepatic portosystemic shunt. Contrast-enhanced MDCT axial image on portal venous phase (PVP) shows one example of most common type of congenital intrahepatic portosystemic shunt, when a single vessel connects the right portal vein to the inferior vena cava. Note the large caliber of afferent portal vein branch and the efferent hepatic vein branch and the focal varix, appearing as a rounded, enhancing mass.

— Arterioportal shunts may be either congenital (presenting as a fistula or vascular malformations in hereditary hemorrhagic telangiectasia) or more frequently acquired (resulting from cirrhosis, tumor - as discussed later Fig.20 -, iatrogenic interventions or trauma).

Rare congenital arterioportal fistulas (Fig.10) are generally solitary connections between hepatic arteries and portal veins, in contrast to other arterial vascular malformations, which usually have a complex plexiform vascular nidus with multiple feeding arteries and draining veins. As the arterial flow enters the portal venous system following the low gradient pressure, retrograde fulfilling the portal vein, subsequently may generate a continuous hepatofugal flow, after time developing portal hypertension. Congenital extrahepatic arterioportal fistula

Fig.10 – Congenital extrahepatic arterioportal fistula. Contrast-enhanced MDCT volume-rendering technique reconstruction (VRT) (A) and oblique axial MIP reformatted images (B)(C) on hepatic arterial phase (HAP) shows an aberrant branch of hepatic artery connecting portal venous system. Consequently, an early enhancement of main portal vein is seen, similar to the arterial phase enhancement of the hepatic artery, depicting the arterial flow entering the venous portal system by the presented shunt.

Acquired portal vein pathologies

Portal vein thrombosis

Portal vein thrombosis (or pylethrombosis) is uncommon, despite the association with a number of conditions [1] (Fig.11). Common causes include cirrhosis, upper abdominal tumors (especially hepatocellular carcinoma), intraabdominal inflammation, hypercoagulable states, abdominal trauma, and iatrogenic complications [1,4]. Portal vein thrombosis

Fig.11 – Portal vein thrombosis. Contrast-enhanced MDCT axial image depict classic venous thrombus imaging appearance in PVP, a low-attenuation filling defect within the lumen of the vessel, in this particular case of left portal vein.

We must be alert to portal vein pseudothrombosis phenomena, which consists on a low-attenuation filling defect appearance in the main portal vein lumen due to mixed flow from the enhanced splenic vein return and the nonenhanced superior mesenteric vein return during the hepatic arterial phase. This false filling defect disappear on portal venous phase (Fig.12), in contrast to a real thrombus. Pseudothrombosis of portal vein

Fig.12 - Pseudothrombosis of portal vein. (A) Contrast-enhanced MDCT late arterial phase axial image shows contrasted splenic vein converging with portal vein which present a heterogeneous low-attenuation content, which could correspond to a portal vein thrombus. (B) Contrast-enhanced MDCT PVP axial image shows a homogenous fulfilling of the portal vein, proving that it was pseudothrombosis phenomena.

In portal vein thrombosis the MDCT appearance depends on the degree of thrombosis, extent of collateralization, and duration of the thrombus.

Acute portal vein thrombosis can be asymptomatic, manifest with a nonspecific abdominal pain, can exacerbate preexisting portal hypertension, or can result in variceal bleeding and shock [1,4]. Acute portal vein thrombosis is usually present as high-attenuating lumen defect on plain CT, in contrast to a low-attenuating defect on subacute/cronic stages (Fig.13). Acute vs subacute/cronic portal vein thrombosis

Fig.13 - Acute vs subacute/cronic portal vein thrombosis. (A) MDCT plain axial image shows a discrete high-attenuating lumen defect of a left portal vein branch (blue arrow) and a low-attenuating defect at distal right portal vein and right posterior portal vein branch (red arrow). (B) Contrast-enhanced MDCT PVP axial image shows more clearly both defects presented differently on plain MDCT image, in this phase after contrast administration, as a low-attenuation filling defect.

Contrast-enhanced MDCT onthrombosis acute stages shows a partial or complete filling defect in the portal vein at the portal venous phase. Despite absolute lack of enhancement of the portal vein lumen, a peripheral rim enhancement can be present, due to preserved blood flow through the vasa vasorum of the portal vein wall [5] (Fig.14). Acute portal vein thrombosis

Fig.14 - Acute portal vein thrombosis. Contrast-enhanced MDCT PVP oblique MPR image shows a low-attenuation filling defect of portal vein – thrombus, and enhancement of the portal vein wall presumed due to still normal flow in the vasa vasorum of the vessel.

Imaging findings of subacute and chronic thrombosis, beasides the defect filling, usually consist of: transient hepatic attenuation differences (THAD); portal hypertension stigmata (ascites, splenomegaly - Fig.15, extensive extrahepatic portosystemic collateralization discussed here later, and portal vein calcification); and can evolve to total disappearance of the trombosed segment with involution of the reliant structures - Fig.16, or even with cavernous transformation of the portal vein.

THAD in portal vein thrombosis results from a decrease in the portal venous flow to a region usually irrigated by the occluded venous segment. Then, that area will be supplied by arterial flow, resulting in a high-attenuation of this area at the hepatic arterial phase, disappearing at portal venous and late phases (Fig.17). THAD at portal vein thrombosis

Fig.17 - THAD at portal vein thrombosis. Contrast-enhanced MDCT (A) plain image shows a subtle low-attenuation at right anterior portal vein branch, aspect that may raise the suspicion of a subacute/chronic portal venous thrombosis. (B) HAP image confirms the suspect showing the low-attenuation defect filling – thrombus, and also a high-attenuation area corresponding to the parenchyma supplied by the occluded branches - portal hypoperfusion, now supplied by arterial flow. At PVP (C–D) the hepatic parenchyma homogenizes. Splenomegaly

Fig.15 - Splenomegaly. Contrast-enhanced MDCT PVP axial image shows an engorged splenic vein and an enlarged spleen in the context of portal hypertension caused by portal vein thrombosis. The blood flow rerouted to low pressure pathways, including splenic vein, congesting splenic venous drainage. Portal vein thrombosis chronic evolution

Fig.16 - Portal vein thrombosis chronic evolution. (A) Contrast-enhanced MDCT PVP axial image and (B) oblique axial MIP reformatted image shows an evolution of a previous left portal vein thrombosis. With time the trombosed segment solved and total disappear with associated involution of the left hepatic lobe.

Cavernous transformation of portal vein consists of venous channels formation within and around a previously stenosed or occluded portal vein, acting as portoportal collateral vessels. Dilated biliary branches (cystic and pericholecystic veins), dilated gastric branches (left and right gastric veins), and the stenosed/occluded main portal vein segment compose the portal cavernoma.

This transformation can occur as soon as 6-20 days after a thrombotic event, even if partial recanalization of the thrombus develops. The veins are usually insufficient to bypass the entire inflow and signs of portal hypertension eventually develop.

THAD in cavernous portal vein transformation are frequently seen at hepatic arterial phase because the central regions of the liver are better supplied by the cavernous portal vein than are the peripheral regions. As portal flow decreases peripherally, arterial inflow increase, so an inhomogeneous, peripheral, patchy areas of transient high attenuation can be seen at hepatic arterial phase, that are not seen at plain CT neither on portal venous phase, as at this late stage blood already recirculated and contrast arrives the central regions (Fig.18). Cavernous transformation of portal vein

Fig.18 - Cavernous transformation of portal vein. (A) Plain MDCT image shows dysmorphic/enlarged porta hepatis with low-attenuation at usual topography of portal vein, raising the suspicion for thrombosis. (B) Contrast-enhanced MDCT late arterial phase axial image shows the low-attenuation portal vein defect filling and multiple enhancing vessels within and around the occluded segment – portoportal collaterals vessels/portal cavernoma. Note the cavernoma associated THAD. (C) At contrast-enhanced MDCT PVP axial image the hepatic parenchyma homogenizes. Ascites and fine calcifications in the pancreatic head are other gross findings in this case.

Cavernous transformation of portal vein can encage the common bile duct at porta hepatis, causing biliary obstruction with consequent dilatation of the biliary tree – portal biliopathy (Fig.19). Portal biliopathy

Fig.19 – Portal biliopathy. Contrast-enhanced MDCT PVP MIP reformatted (A) sagittal and (B)(C) axial images shows common bile duct encased and obstructed by portal cavernoma, conditioning dilation of peripheral branches. Also note the innumerous gastric varices, classic stigmata of portal hypertension.

Sometimes it is difficult to differentiate a bland portal thrombus from a malignant portal venous thrombus, but this differentiation is critical since malignant thrombi are associated with a poorer prognosis, and their curative resection is unlikely. The most useful imaging finding to distinguish malignant from bland thrombi is diffuse or heterogeneous contrast enhancement of the thrombus mass at hepatic arterial phase. Additional findings are contiguity of the thrombus with the tumor and vessel expansion due to tumor thrombus growth (Fig.20).

Malignant portal venous thrombus frequently manifests as an acquired tumoral form of arteroportal fistula. The arterial flow enters the portal venous system following the low gradient pressure, retrogradelly fulfilling the portal vein or collateral vessels. Tumoral portal venous thrombus

Fig.20 - Contrast-enhanced MDCT HAP MIP reformatted (A) sagittal and (B)(C) axial images shows a network of multiple aberrant arterial branches feeding a neoplastic thrombus, which uptakes contrast material. This case also presents an arteriovenous fistula between the arterial hypervascularized tumoral mass and the recanalized paraumbilical vein, which presents an early enhancement.

Portal venous gas

Portal venous gas (aeroportia) was traditionally considered a life threatening sign and was thought to be associated with advanced mesenteric ischemia. Nowadays, although mesenteric ischemia is still identified as the most common cause of portal venous gas, the increased use of MDCT allows its earlier diagnosis, decreasing reported mortality. Other causes of portal venous gas include inflammatory bowel disease, diverticulitis, bowel distention, intraabdominal sepsis, trauma, iatrogenic and idiopathic causes.

Imaging findings on MDCT are linear, branching pattern, or ovoid areas with attenuation similar to that of air in the main portal vein or its peripheral venous branches. Intrahepatic portal venous gas locules may be seen near the liver capsule, predominantly in the left lobe, because of its nondependent location when the patient is positioned supine (Fig.21). Aeroportia

Fig.21 - Portal vein gas. Two cases of aeroportia at contrast-enhanced abdominal MDCT MIP images. (A,B) First case shows air branching pattern fulfilling some segments of peripheral right portal vein branches. Note the pneumatosis intestinalis on the colonic wall covered, this was a case of volvulus. (C,D) Second case shows a more extensive aeroportia.

Portal hypertension and extra-hepatic portosystemic shunts

Acquired extra-hepatic portosystemic shunts are the most common shunts among portal venous system. A large group of pathologies can trigger the development of this shunts, but the most common cause of portosystemic collateral vessels is portal hypertension [1,5]. Other causes include splenic, splenomesenteric, or superior mesenteric venous stenosis or obstruction.

Portal hypertension causes can be split in their relation to the hepatic sinusoids: pre-sinusoidal (e.g. portal vein thrombosis, extrinsic compression of portal vein - Fig.22, tumor invasion - Fig.23); sinusoidal (e.g. cirrhosis) and post-sinusoidal (e.g. hepatic veno-occlusive disease). Portal hypertension pre-sinusoidal cause

Fig.22 - Pre-sinusoidal cause of portal hypertension. Contrast-enhanced MDCT MIP PVP image shows a large hepatic cyst exerting extrinsic compression on portal vein, representing one benign cause of pre-sinusoidal portal hypertension. Portal hypertension pre-sinusoidal cause

Fig.23 - Pre-sinusoidal cause of portal hypertension. Contrast-enhanced MDCT MIP PVP (A) coronal (B) axial images shows portal vein malignant invasion by a pancreatic adenocarcinoma, representing a malignant cause of pre-sinusoidal portal hypertension.

Hepatopetal blood flow is rerouted away from the liver through collateral pathways to low-pressure systemic vessels. More than 20 pathways have been described, the most common being gastroesophageal, paraesophageal, paraumbilical, splenorenal, and inferior mesenteric venous collateral vessels, in order of decreasing frequency [1;5].

On MDCT collaterals appear as enlarged, tubular, tortuous, enhancing structures in characteristic locations:

Gastroesophageal vessels - Fig.24

Coronary collateral veins at the lesser omentum are the most frequently depicted varices at MDCT [5]. Gastric varices are located at the posterosuperior aspect of the gastric fundus, and most drain into the esophageal or paraesophageal veins, but occasionally they drain into the left renal vein. Gastric varices

Fig.24 – Gastric varices. Contrast-enhanced MDCT PVP axial images shows multiple engorged gastric varices in a pre-sinusoidal cause of portal hypertension – portal cavernoma.

Esophageal and paraesophageal vessels - Fig.25

Varices here are of major clinical importance because they are a frequent source of gastrointestinal bleeding. Endoscopy is more sensitive than CT to the presence esophageal varices, instead for evaluation of paraesophageal collateral vessels CT is more sensitive. Esophageal and paraesophageal varices

Fig.25 – Esophageal and paraesophageal varices. Contrast-enhanced MDCT PVP axial image shows multiple varices esophageal (blue arrow) and paraesophageal (red arrow). (Esophagus – green arrow)

Paraumbilical vessels - Fig.26

Paraumbilical vessels are an accepted pathway to decompression of the portal venous system because they are not associated with gastrointestinal bleeding. The most common pattern of drainage of paraumbilical veins is through the epigastric veins into the external iliac veins. Recanalized paraumbilical vein

Fig.26 - Recanalized paraumbilical vein. Contrast-enhanced MDCT PVP axial images shows recanalized paraumbilical vein, fulfilled with contrast material, emerging from left portal vein.

Splenorenal Collateral Vessels

Collateral vessels from the splenic hilum to the left renal vein are fairly common, and they are not associated with gastrointestinal bleeding either. However, enlarged shunts are significantly associated with hepatic encephalopathy. A common feature depicted at cross-sectional imaging is an enlarged left renal vein and dilatation of the inferior vena cava at the level of the left renal vein in the presence of a splenorenal shunt.

Mesenteric Collateral Vessels

Inferior mesenteric collateral vessels are less frequent but of great importance because of their association with rectal bleeding. The portal venous system (superior hemorrhoidal vein) and the systemic venous circulation (middle and inferior hemorrhoidal veins) connect via the hemorrhoidal plexus.

Mesocaval shunts are portosystemic collateral vessels between the inferior mesenteric vein and inferior vena cava that are established through lumbar and retroperitoneal veins, are not associated with an increased risk of rectal bleeding (Fig.27). Retroperitoneal varices

Fig.27 - Retroperitoneal varices. Contrast-enhanced MDCT (A) VRT and (B) PVP axial image shows multiple large retroperitoneal varices (green arrows).

If obstruction occurs near the splenic hilum, collateral vessels develop at the gastric fundus and the greater and lesser omentum.

When splenic vein occlusion is near the splenomesenteric confluence, mesocaval, hemorrhoidal, splenorenal, or splenoretroperitoneal collateral vessels are the usual portosystemic pathways of decompression.

In occlusion of the superior mesenteric vein, mesenteric varices and mesentericorenal collateral vessels develop.

Portal vein calcification has a strong association with long standing portal venous hypertension regardless of the underlying aetiology (Fig. 28). Sometimes splenic vein and superior mesenteric vein calcification is also present. Portal vein calcification

Fig.28 - Portal vein calcification. Contrast-enhanced MDCT MIP reformatted oblique axial image shows a case of portal hypertension with extensive calcification of portal vein, splenic-mesenteric confluence and distal segment of superior mesenteric and splenic veins. Note the incidental finding of the gallbladder stones.

Iatrogenic findings

Transjugular intrahepatic portosystemic shunt (TIPS) is used to control symptomatic complications of portal hypertension. Its creation is one of the most common percutaneous interventional procedures involving portal venous system, where a parenchymal channel between a large hepatic vein and a major portal vein branch is created by inserting an expandable stent, in most cases created between right portal vein and the right or middle hepatic vein (Fig.29). TIPS

Fig.29 - MIP contrast-enhanced MDCT image shows a metallic stent connecting right portal vein with middle hepatic vein. Notice that the receiver hepatic vein tends to enlarged due to increased flow directly drained from the central venous system to its lumen, skipping the hepatic parenchyma.

Liver surgery mainly consists in anatomical segment-oriented resections, based on the intrahepatic distribution of portal branches and hepatic veins [9]. Segmentectomy always involves portal venous branches ligation and rearrange of the remaining system, like increasing caliber and adaptive shifting (Fig. 30). Liver surgery

Fig.30 - MIP contrast-enhanced MDCT image shows imaging liver findings after a right hepatectomy: section and ligation of the right portal vein at its origin; shift of left liver towards the right with horizontalisation of portal vein; prominent caliber of left portal vein and hypertrophy and rounded contours of the remaining liver.

4. Conclusion

Understanding the embryology, normal anatomy, and anatomical variants of the portal venous system is important to accurately interpret abdominal CT findings.

Knowledge of typical features of congenital and acquired portal vein pathologies allows the radiologist to make a confident diagnosis.

Due to its superior spatial and temporal resolution, CT is an outstanding method to evaluate the portal venous system.

5. References

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et al. AJR 1997;168:233.-2370361-803X/97/1681-233. 4. Imaging of the Porta Hepatis: Spectrum of Disease. S.H. Tirumani, A.K.P. Shanbhogue, R. Vikram et al. RadioGraphics 2014; 34:73–92. 5. Congenital and Acquired Anomalies of the Portal Venous System. C. Gallego, M. Velasco, P. Marcuello et al. RadioGraphics 2002; 22:141–159. 6. Circumportal pancreas: a review of the literature and image findings. T.M. Connelly; M. Sakala; R. Tappouni; Surg Radiol Anat (2015) 37:431–437. DOI 10.1007/s00276-015-1436-5. 7. Circumportal pancreas: imaging findings in 40 patients. R. Tappouni, J. Perumpillichira, M. Sekala, et al. Abdom Imaging (2015) 40:521–530. DOI: 10.1007/s00261-014-0242-6. 8. Circumportal pancreas: a clinicoradiological and embryological review. A. Arora, P. Velayutham, S. Rajesh, et al. Surg Radiol Anat (2014) 36:311–319. DOI 10.1007/s00276-013-1189-y. 9. Imaging of the Post-operative Liver: Review of Normal Appearances and Common Complications. S. Mule, A. Colosio, J. Cazejust, et al. ECR 2015 C-0314. DOI: 10.1594/ecr2015/C-0314.

6. Author Information

Carolina Carneiro,

Centro Hospitalar do Algarve - EPE,

Sitío do Poço Seco 8500-338 Portimão email: [email protected] 7. Mediafiles

Acute portal vein thrombosis

Anatomic variants

Embryology

Fig.3 - Diagrammatic representation of the embryological development of the portal vein. Embryology

Fig.25 – Esophageal and paraesophageal varices. Contrast-enhanced MDCT PVP axial image shows multiple varices esophageal (blue arrow) and paraesophageal (red arrow). (Esophagus – green arrow) Gastric varices

Fig.24 – Gastric varices. Contrast-enhanced MDCT PVP axial images shows multiple engorged gastric varices in a pre-sinusoidal cause of portal hypertension – portal cavernoma. Liver surgery

Fig.4 – Normal anatomy. A maximum intensity projection (MIP) contrast-enhanced CT image shows the typical branching pattern of the portal venous system. Portal biliopathy

Portal hypertension pre-sinusoidal cause

Preduodenal portal vein

Fig.26 - Recanalized paraumbilical vein. Contrast-enhanced MDCT PVP axial images shows recanalized paraumbilical vein, fulfilled with contrast material, emerging from left portal vein. Retroperitoneal varices

Fig.27 - Retroperitoneal varices. Contrast-enhanced MDCT (A) VRT and (B) PVP axial image shows multiple large retroperitoneal varices (green arrows). Splenomegaly