Gastrointestinal Intervention 2018; 7(1): 21-28
Portosystemic collateral pathways and interventions in portal hypertension
Murad Feroz Bandali1, and Anirudh Mirakhur2,*
1Department of Radiology, Stanford University, Stanford, CA, USA, 2Department of Radiology, University of Calgary, Calgary, AB, Canada
Department of Diagnostic Imaging, Division of Interventional Radiology, Peter Lougheed Medical Centre, 3500 26 Avenue NE, Calgary, AB T1Y 6J4, Canada. E-mail (A. Mirakhur). ORCID:
Received: February 14, 2018; Revised: April 10, 2018; Accepted: April 10, 2018; Published online: April 30, 2018.
© Society of Gastrointestinal Intervention. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Pathologic increase in portal pressure can be caused by increased resistance to blood flow at the level of the portal vein (pre-hepatic), hepatic sinusoids (hepatic) or hepatovenous outflow (post-hepatic). This results in recruitment and dilatation of tiny portosystemic collateral pathways, diverting portal venous blood flow to low pressure systemic veins. Based on the location of the causative factor of portal venous resistance, different collateral pathways and shunts may develop, resulting in unique syndromes of portal hypertension and in-turn requiring unique treatment options. Knowledge of the common and less-common portosystemic collateral pathways have important implication for clinicians and interventionalists. The objective of this pictorial review is to illustrate the various collateral pathways using diagrammatic and conventional non-invasive and invasive radiologic examples. Additionally, we will briefly address minimally invasive interventional techniques used to treat the sequelae of portal hypertension.

Keywords: Hypertension, portal, Portal hypertension, Radiology, interventional, Varices

Portal venous system is a distinctive network of vessels that connect two separate vascular beds, the gastrointestinal/splanchnic veins and the hepatic sinusoids. The mesenteric and splenic veins join to form the portal vein, which in turn branches at the liver and terminates in the hepatic sinusoids. While the main feeding branches of the portal vein include the superior mesenteric vein (SMV) and splenic vein, and sometimes the inferior mesenteric vein (IMV), other tributaries also feed into the portal venous vasculature—creating a complex network of vessel that is functionally isolated from systemic circulation (Fig. 1). The portal vein functions to carry blood and nutrients from the splanchnic vasculature to the liver for metabolism, nutrient storage and detoxification.

A pathologic increase in portal pressure (above 5–10 mmHg) can be caused by increased resistance to blood flow at the level of the portal vein (pre-hepatic), hepatic sinusoids (hepatic) or hepatovenous outflow (post-hepatic). Portal pressure is measured by catheter-based hepatic venography, which indirectly measures the portal venous pressure and compares it to the systemic venous pressure in the inferior vena cava (IVC), termed the hepatovenous pressure gradient (HVPG). The HVPG is normally between 1–5 mmHg and portal hypertension is defined by HVPG greater than 10 mmHg.14 Caused by increased resistance to hepatopetal flow, portal hypertension is further aggravated by reactive and progressive splanchnic vasodilatation, as well as, hepatic sinusoidal endothelial dysfunction. Eventually, this leads to recruitment of collateral venous channels that bypass the liver and connect directly to systemic venous circulation, forming a network of shunts and end-organ varices. This is a complex process involving the recanalization, dilatation and hypertrophy of pre-existing portosystemic vascular channels, as well as, a possible component of angiogenesis.1,57

Based on the location of the causative factor of portal venous resistance, different collateral pathways and shunts may develop, resulting in unique syndromes of portal hypertension and in-turn requiring unique treatment options. Understanding of common, clinically relevant, portosystemic collaterals pathways is integral for any physician who aims to treat this complex condition.

In this review, we aim to discuss the spectrum of portosystemic collateral pathways in the abdomen and thorax, using imaging and pictorial examples. Additionally, a brief overview of minimally invasive interventional techniques will also be presented.

Basic Anatomy of Portosystemic Collaterals

Shunts are defined as collateral veins that simply bridge the portal venous and systemic venous systems. Varices, in contrast, are dilated end-organ capillary beds that have a propensity to bleed. The most common pathway of hepatofugal flow is via the coronary vein, forming esophageal, paraesophageal and cardiophrenic varices.3,8,9 Other pathways include gastric, paraumbilical and mesenteric venous channels. Pleuro-pericardial, peritoneal, pancreaticoduodenal, splenoazygos and mesocaval collaterals are far less common but may also be recruited to decompress the portal vein (Fig. 2). On cross-sectional imaging such as computed tomography (CT) or magnetic resonance imaging (MRI), shunts appear as well defined smooth, round, serpiginous and tubular structures which are separate from the viscera and enhance to a same degree as the adjacent normal portal or mesenteric veins. Varices have a similar appearance but are in a mural or submucosal location and are commonly seen in the walls of the hollow viscera such as the esophagus, stomach, and rectum.8,10,11

Coronary Vein Pathways

The coronary vein, or the left gastric vein, is situated within the lesser omentum and is the most common collateral pathway recruited in portal hypertension secondary to liver cirrhosis, occurring in an estimated 80% of cross sectional imaging studies.1113 Typically, they appear as dilated collateral veins along the lesser curvature of the stomach and gastroesophageal junction. A coronary vein larger than 5 to 6 mm is a strong indicator of portal hypertension. These are also commonly accompanied by esophageal or paraesophageal varices. The anterior branch of the coronary vein typically supplies esophageal varices, while the posterior branch supplies paraesophageal varices (Fig. 3).3,14,15

After forming a subepithelial and submucosal venous network within the esophageal wall, esophageal varices usually drain into the azygous or hemiazygous system. Their typical CT/MRI appearance is nodular and intraluminal protrusions with scalloped borders (Fig. 4).11 Formation of these varices is clinically significant in portal hypertension as they have a high propensity to hemorrhage into the esophageal and gastric lumen, at a rate of 10% to 30% per year, with an overall mortality of 20% to 35%.16 While cross-sectional imaging, is highly sensitive at the detection of large, clinically relevant, esophageal varices; endoscopy remains the mainstay of identification and diagnosis.16

Paraesophageal varices, in contrast, surround and are directly adjacent to the esophagus and descending thoracic aorta and form a network of dilated veins which are continuous with the coronary veins and can be followed superiorly to the azygous/hemiazygous veins and paravertebral venous plexus.9,17 Unlike esophageal varices, they cannot be seen on endoscopy and require cross-sectional imaging for diagnosis (Fig. 3A). While they do not result in variceal hemorrhage, the presence of paraesophageal varices on chest CT portends a poor prognosis for patients who have existing esophageal varices irrespective of whether they have undergone sclerotherapy.18

Cardiophrenic varices also result from recruitment of the coronary vein collateral pathway and consist of dilated pericardial and cardiophrenic veins. On imaging, they manifest of as undulating lesions with venous enhancement along the inferior cardiac borders and cardiophrenic angles and may simulate a cardiophrenic mass at radiography. They care commonly seen in patients with post-hepatic causes portal hypertension, appearing in 18% of cases of cirrhosis secondary to membranous obstruction of the IVC.3

Several strategies exist for treating esophageal varices. For patients with medium to large sized esophageal varices, non-selective beta-blockers, endoscopic ligation and/or balloon tamponade should be considered as initial therapies.19 However, patient who do not respond to these therapies, image-guided interventions may be considered. Transjugular intrahepatic portosystemic shunt (TIPS) is an image-guided procedure where a transhepatic shunt is created using a large needle-trocar set, angioplasty balloon and polytetrafluoroethylene (PTFE)-covered stents; creating a parenchymal tract between the portal and hepatic veins and reducing HVPG below 12 mmHg (Fig. 5).20 TIPS has shown up to a threefold decrease in recurrent variceal bleeding when compared to endoscopic therapy.21 Strong evidence also exists for TIPS placement improving transplant-free survival in cirrhotic patients who suffer from refractory ascites, when compared to intermittent large-volume paracentesis.22 Limited evidence exists for additional indications which include: acute gastropathy, hepatopulmonary syndrome, and Budd-Chiari syndrome (Fig. 6).20

Unfortunately, TIPS is not without disadvantages. Deterioration of hepatic function can result from diversion of portal venous blood flow. Hepatic encephalopathy may develop due to the flow of non-detoxified blood to systemic circulation; now being allowed to bypass the liver parenchyma unimpeded.23,24 Additionally, frequent surveillance and potential maintenance procedure may also be needed to ensure long-term stent patency.20

In some instances, optimal tract creation via the right or middle hepatic vein is not possible. In such cases, direct intrahepatic portocaval shunt (DIPS) may be created. Using intravascular ultrasound, a trans-caudate tract may be created directly from the IVC to the portal vein. DIPS has demonstrated shorter procedure times, as well as, may be ideal in cases of hepatic vein thrombosis, challenging anatomy or in where ideal parenchymal tract is not possible.25

Gastric Venous Collateral Pathways

Gastric varices are less prevalent than esophageal varices but can be seen in up to 33% of patients with portal hypertension. Esophageal and gastric varices frequently co-exist with esophageal varices, as described in the commonly used Sarin classification for gastric varices (Table 1).10 Gastric varices are more likely to be supplied by the short gastric and posterior gastric veins, while esophageal varices are more likely to be supplied by the coronary veins. Rarely they are they supplied by the gastroepiploic vein, typically in the context of endovascular or surgical exclusion of other feeding veins.10,26 Short gastric varices usually course along the lesser curvature of the stomach and drain into the splenic vein. Isolated short gastric varices are seen in the context of splenic vein stenosis or thrombosis. On cross sectional imaging, they typically appear as a tangle of vessels in the region of the splenic hilum and gastric fundus. It can often be difficult to distinguish between the gastric walls and individual vessels.

Gastric veins may drain into esophageal/paraesophageal varices in approximately 84% of cases.27 Occasionally gastric varices may drain via a gastrorenal shunt, which appears as a large left-sided inferior phrenic vein which connects the gastric varices to a dilated renal vein. This shunt may be recruited by existing tiny portosystemic collaterals from the adrenal venous system.27 Large gastric varices are commonly seen in the absence of esophageal varices when a gastrorenal shunt is seen. Alternative pathways include direct drainage into the IVC by way of the left inferior phrenic vein or pericardiophrenic veins. Other smaller drainage pathways include paravertebral venous plexus, intercostal veins ascending lumbar veins and azygous veins.10,27,28

Gastric varices tend to bleed at a lower rate than esophageal varices but they are associated with a higher overall mortality secondary to their larger size and higher flow rate.29 Additionally, life-threatening gastric variceal hemorrhage can occur at HVPG below 12 mmHg, making TIPS placement a less favorable option.30,31 Balloon-occluded retrograde transvenous obliteration of gastric varices (BRTO) is a technique which involves advancing paired catheters from femoral vein access through the outlet of a gastrorenal shunt (Fig. 7). Following balloon-occlusion of the shunt, the distal catheter is placed in the gastric variceal bed and is used to inject a sclerosing agent to obliterate the varices. The sclerosing agent and balloon-catheter are left in-place for 4 to 48 hours, prior to removal.3032

BRTO has shown excellent efficacy at controlling variceal bleeding with low re-bleed rates and some have advocated for its employment as a prophylactic measure.32,33 BRTO is advantageous in that it diverts the blood flow away from collateral pathways; improving hepatopetal flow and overall hepatic reserve. As such, BRTO is also an excellent treatment option for refractory encephalopathy. It is also advantageous in that it does not require general anesthesia (unlike TIPS).32 However, occlusion of certain portosystemic shunts may aggravate other symptoms of portal hypertension: either worsening abdominopelvic ascites or aggravating esophageal varices. Additionally, severe adverse reactions may result from extended exposure to a sclerosing agent such as: anaphylaxis, portal vein thrombosis, diffuse intravascular coagulopathy, renal dysfunction and pulmonary edema.31,34

A potential solution to this is employment of other occlusion methods at the level of the gastrorenal shunt. Coil-assisted retrograde transvenous obliteration of gastric varices is a modified version of BRTO, where dual microcatheters are employed but rather than balloon occlusion, the gastrorenal shunt is coil-embolized.34 A microcatheter is placed beyond the coil-pack and gel-foam slurry is injected into the variceal bed. Both catheters are then immediately withdrawn with coil-pack left in place; alleviating the need for a sclerosing agent.34 A similar modification using a vascular plug instead of embolization coils (termed PARTO: vascular plug-assisted transvenous obliteration of gastric varices) has demonstrated similar technical success and clinical efficacy for the treatment of gastric varices and hepatic encephalopathy.35

Splenic Vein Collateral Pathways

Splenic/perisplenic varices are seen in the anteroinferior region of the splenic hilum where they traverse the splenocolic ligament. This collateral pathway may also communicate and serve as a drainage pathway for gastric varices. Dilated and tortuous splenic vein within the hilum of an enlarged spleen should not be confused with perisplenic varices (Fig. 8).11

Splenic venous flow also commonly circumvents the liver by way of large splenorenal or splenocaval shunts. Splenorenal shunts appear as large tortuous veins connecting the splenic and left renal hilum; although the exact origin of the connection along the splenic vein is usually difficult to discern.11 As with gastrorenal shunts, the left renal vein is usually dilated. Rarely a splenocaval shunt can develop, which extends inferiorly into the pelvis and drains into the IVC via the internal iliac or gonadal veins. Splenoazygous shunts are even less common, where a dilated venous connection can be seen from the splenic vein to the hemiazygous or posterior abdominal wall/chest wall veins.10

Paraumbilical and Abdominal Wall Collateral Pathways

The paraumbilical vein is a fetal remnant which, when re-canalized in the context of portal hypertension, arises from the left portal vein and courses along the anterior edge of the falciform ligament to the abdominal wall (Fig. 9A). This is a common portosystemic pathway in cirrhosis, seen in up to 30% to 35% of cases.36 Typically this can be seen as 2 to 3 mm tubular and serpiginous vessels within the abdominal wall (Fig. 9B) which drain via the superior epigastric vein and/or internal thoracic veins, superior vena cava or to the IVC by way of the inferior epigastric and external iliac veins.36 For patients with medically refractory encephalopathy, the paraumbilical vein is a common shunt that can serve as a target for transvenous obliteration to achieve symptomatic improvement (Fig. 9C).37,38

Surgically created ileostomies and colostomies within the abdominal wall create portosystemic collaterals which develop in portal hypertension, by way of unique mucocutaneous connections.10,28,39 As a result, stomal varices are very common and reported in up to 50% patient with surgical digestive stomas and concomitant portal hypertension. Hemorrhage from these varices is a common occurrence, present in up to 27% of patients with stomal varices, and can be challenging to manage.39 Stomas that are diffusely engorged with diffuse venous oozing tend to respond favorably to TIPS therapy. Conversely, patients with focal stomal variceal bleeding respond better to manual compression and transvenous obliteration (which include BRTO, percutaneous transhepatic obliteration, or trans-TIPS balloon-occluded antegrade transvenous obliteration) (Fig. 10).40

Mesenteric and Omental Collateral Pathways

Omental varices can be seen in up to 30% of patients with cirrhosis but are not considered common collateral pathways by interventionalist, as they are not commonly seen at the time of angiography.11 They tend to be much smaller than their counterparts elsewhere in the abdomen but are typically quite numerous and should not be mistaken for peritoneal metastasis at cross sectional imaging. On imaging, they appear as sparse tubular vessels coursing through the greater omentum (Fig. 11). They arise from the SMV or IMV and drain into retroperitoneal or pelvic veins.10 There have been few but fatal reports of bleeding and rupture from omental varices.41,42

Mesenteric varices appear as dilated and tortuous branches of the SMV and IMV within the mesenteric fat.11 They also drain into systemic circulation by way of the retroperitoneal or pelvic veins but rarely mesororenal shunts may develop between the mesenteric varices and the right renal vein or mesocaval shunts directly to the IVC.43 Of note, inferior mesenteric varices may drain into systemic circulation via the superior or middle rectal veins to the internal iliac veins. Rectal varices more commonly result in encephalopathy rather than life-threatening hemorrhage.44

Other Collateral Pathways

Intrahepatic portal veins may also create direct venous connections with hepatic venous branches or direct communication with the coronary vein, typically via the left hepatic lobe.43 Pleuropericardial-peritoneal collaterals may develop as a loose venous plexus which pierces the diaphragm to join the pericardial, pleural and pulmonary veins.45 Pericholecystic varices in or outside the gallbladder wall are present in up to 12% of patients with portal hypertension but are most common in patients with extrahepatic portal vein obstruction.28


A strong background knowledge of the basic anatomy of portosystemic collateral pathways is a necessity for any physician treating patients with portal hypertension. Not only is it essential for accurate diagnosis, appropriate characterization of portosystemic collateral pathways can lead to identification of causative factors, therapy selection and mitigate potential procedure-related complications. As non-invasive imaging techniques continue to advance, so too does the ability to visualize this complex disease process.


We would like to acknowledge Salima Hirji for her contribution in creating the anatomic illustrations.

M.F.B. and A.M. contributed to this review article with conception, literature review and analysis, image preparation and editing, manuscript drafting and critical revision and editing, and approval of the final version.

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Fig. 1. Normal portal venous anatomy. Main portal vein (MPV) most commonly forms from the joining of the splenic vein (SV) and superior mesenteric vein (SMV). The inferior mesenteric vein (IMV) has a variable draining position but most common location is into the SV. Coronary vein (or left gastric vein [LGV]) courses along the lesser curvature of the stomach and drains directly into the MPV. As the MPV reaches the liver, it branches into the right portal vein and left portal vein, respectively.
Fig. 2. Hepatofugal portosystemic pathways in portal hypertension. Progressive resistance to portal venous blood flow results in decompression through pre-existing collateral pathways. Paraumbilical (PuVa) and abdominal wall (AwVa) varices develop after recanalization of the paraumbilical vein. Esophageal (EsoVa), Paraesophageal (PEsoVa), and Cardiophrenic (CPVa) develop when blood flow decompresses via the left gastric vein (LGV). Mesenteric (MVa) and rectal (RVa) varices may also develop to allow passage of portal venous blood into systemic circulation. MPV, main portal vein; GrSh, gastrorenal shunt; SrSh, splenorenal shunt; SV, splenic vein; SMV, superior mesenteric vein; IMV, inferior mesenteric vein.
Fig. 3. Axial contrast-enhanced computed tomography image (A) and thick-slab three-dimensional reformat image (B) of the abdomen and pelvis in a 54-year-old female with hepatitis C induced cirrhosis. Massive paraesophageal varices are seen surrounding the distal esophagus (asterisk) with a markedly dilated feeding coronary vein which arises from the proximal main portal vein (arrow).
Fig. 4. Axial computed tomography image through the esophagus demonstrating nodular and tubular lesions within the submucosal region of the distal esophagus consistent with esophageal varices (arrow). Note abdominal ascites surrounding the dome of the liver.
Fig. 5. Illustration demonstrating the conventional position of a transjugular intrahepatic portosystemic shunt from the right portal vein to the right hepatic vein. After a parenchymal tact is created with an angioplasty balloon, the tract is lined with a partially polytetrafluoroethylene-covered stent with covered portion lining the parenchymal tract and hepatovenous outflow and the uncovered portion within the portal vein.
Fig. 6. A 27-year-old male with a history of schistosomiasis associated portal hypertension presents with recurrent upper gastrointestinal bleeding secondary to esophageal varices. (A) Digital subtraction angiography (DSA) performed through a pigtail catheter within the main portal vein after a Rosch-Uchida transjugular intrahepatic portosystemic shunt trochar-needle set (Cook Medical) are advanced from the right hepatic vein through the hepatic parenchyma into the right portal vein. Note the dilated coronary vein arising from the main portal vein and Linton balloon in the stomach. (B) Delayed DSA images demonstrate prominent and extensive esophageal varices and gastric varices along the lesser curvature of the stomach (asterisk). (C) Subsequently, polytetrafluoroethylene-covered stent was placed across the parenchymal tract (arrow). (D) Transvenous injection of liquid embolic agent in the coronary vein and esophageal varices.
Fig. 7. Schematic drawing demonstrating the BRTO procedure. Via femoral vein access, a pair of catheters are advanced into the outlet of the gastrorenal shunt. A balloon catheter is inflated and sclerosant is injected in the gastric varices. The sclerosant and balloon are left inflated for 4 to 48 hours while the patient is under close clinical surveillance. The balloon catheter is then deflated and removed.
Fig. 8. Axial computed tomography image depicting cirrhosis, splenomegaly and associated perisplenic varices within the left upper quadrant. Note a large dominant splenic varix posterior to stomach (arrow).
Fig. 9. A 62-year-old female with a history of hepatitis C induced cirrhosis presents with refractory encephalopathy despite maximal medical management. Axial (A) and coronal (B) contrast-enhanced computed tomography images demonstrate large recanalized paraumbilical vein which follows a markedly tortuous course to the umbilicus. (C) Angiographic images demonstrate coil-assisted retrograde transvenous obliteration-variant procedure where venous access was obtained trans-abdominally directly into the peripheral aspect of the periumbilical collateral. After a coil-embolization was performed at the central and peripheral aspect of the periumbilical collateral; the entire length was embolized using gelfoam to ensure complete obliteration of the shunt.
Fig. 10. A 67-year-old female with a history of metastatic colorectal cancer who has a past surgical history of low anterior resection and diverting sigmoid colostomy. She subsequently developed portal hypertension and stomal varices (arrow) after undergoing multiple microwave ablation procedures for recurrent liver metastases. (A) Axial fat-suppressed T1-weighted contrast enhanced images demonstrate multiple serpiginous tubular varices within the region of the stoma (arrow). (B) Ultrasound-guided access of a prominent stomal varix was obtained and catheter-directed coil embolization was performed of prominent feeding mesenteric collaterals. (C) Post-procedural coronal computed tomography image demonstrates resolution of stomal varices (arrow) but aggravation of ascites.
Fig. 11. Axial computed tomography image depicting tiny omental collaterals along the left ventral abdomen (arrow).

Table 1

Sarin Endoscopic Classification for Grading Gastric Varices

Gastroesophageal varix type 1 (GOV-1)2–5 cm below the gastroesophageal junction and continuous with esophageal varices which extend along the lesser curvature of the stomach.
Gastroesophageal varix type 2 (GOV-2)Continuation from esophageal varices which extend along the lesser curvature of the stomach but are more tortuous than GOV-1.
Isolated gastric varix type 1 (IGV-1)Absence of esophageal varices and are located at the gastric fundus. Varices are tortuous and complex.
Isolated gastric varix type 2 (IGV-2)Absence of esophageal varices and are located at the gastric body, antrum or pylorus.
  1. Berzigotti, A, Seijo, S, Reverter, E, and Bosch, J (2013). Assessing portal hypertension in liver diseases. Expert Rev Gastroenterol Hepatol. 7, 141-55.
    Pubmed CrossRef
  2. Bosch, J, Groszmann, RJ, and Shah, VH (2015). Evolution in the understanding of the pathophysiological basis of portal hypertension: how changes in paradigm are leading to successful new treatments. J Hepatol. 62, S121-30.
    Pubmed KoreaMed CrossRef
  3. Wachsberg, RH, Yaghmai, V, Javors, BR, Levine, CD, Simmons, MZ, and Maldjian, PD (1995). Cardiophrenic varices in portal hypertension: evaluation with CT. Radiology. 195, 553-6.
    Pubmed CrossRef
  4. Bosch, J, Abraldes, JG, Berzigotti, A, and García-Pagan, JC (2009). The clinical use of HVPG measurements in chronic liver disease. Nat Rev Gastroenterol Hepatol. 6, 573-82.
    Pubmed CrossRef
  5. Bosch, J, Abraldes, JG, Fernández, M, and García-Pagán, JC (2010). Hepatic endothelial dysfunction and abnormal angiogenesis: new targets in the treatment of portal hypertension. J Hepatol. 53, 558-67.
    Pubmed CrossRef
  6. Bosch, J, Navasa, M, Garcia-Pagán, JC, DeLacy, AM, and Rodés, J (1989). Portal hypertension. Med Clin North Am. 73, 931-53.
    Pubmed CrossRef
  7. Thabut, D, and Shah, V (2010). Intrahepatic angiogenesis and sinusoidal remodeling in chronic liver disease: new targets for the treatment of portal hypertension?. J Hepatol. 53, 976-80.
    Pubmed CrossRef
  8. Kim, YJ, Raman, SS, Yu, NC, To’o, KJ, Jutabha, R, and Lu, DS (2007). Esophageal varices in cirrhotic patients: evaluation with liver CT. AJR Am J Roentgenol. 188, 139-44.
  9. Lee, SJ, Lee, KS, Kim, SA, Kim, TS, Hwang, JH, and Lim, JH (1998). Computed radiography of the chest in patients with paraesophageal varices: diagnostic accuracy and characteristic findings. AJR Am J Roentgenol. 170, 1527-31.
    Pubmed CrossRef
  10. Arora, A, Rajesh, S, Meenakshi, YS, Sureka, B, Bansal, K, and Sarin, SK (2015). Spectrum of hepatofugal collateral pathways in portal hypertension: an illustrated radiological review. Insights Imaging. 6, 559-72.
    KoreaMed CrossRef
  11. Cho, KC, Patel, YD, Wachsberg, RH, and Seeff, J (1995). Varices in portal hypertension: evaluation with CT. RadioGraphics. 15, 609-22.
    Pubmed CrossRef
  12. Stankovic, Z, Csatari, Z, Deibert, P, Euringer, W, Blanke, P, and Kreisel, W (2012). Normal and altered three-dimensional portal venous hemodynamics in patients with liver cirrhosis. Radiology. 262, 862-73.
    Pubmed CrossRef
  13. Lafortune, M, Marleau, D, Breton, G, Viallet, A, Lavoie, P, and Huet, PM (1984). Portal venous system measurements in portal hypertension. Radiology. 151, 27-30.
    Pubmed CrossRef
  14. Subramanyam, BR, Balthazar, EJ, Madamba, MR, Raghavendra, BN, Horii, SC, and Lefleur, RS (1983). Sonography of portosystemic venous collaterals in portal hypertension. Radiology. 146, 161-6.
    Pubmed CrossRef
  15. Wachsberg, RH, and Simmons, MZ (1994). Coronary vein diameter and flow direction in patients with portal hypertension: evaluation with duplex sonography and correlation with variceal bleeding. AJR Am J Roentgenol. 162, 637-41.
    Pubmed CrossRef
  16. Garcia-Tsao, G (2001). Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. 120, 726-48.
    Pubmed CrossRef
  17. Takashi, M, Igarashi, M, Hino, S, Musha, H, Takayasu, K, and Arakawa, M (1985). Esophageal varices: correlation of left gastric venography and endoscopy in patients with portal hypertension. Radiology. 155, 327-31.
    Pubmed CrossRef
  18. Lin, CY, Lin, PW, Tsai, HM, Lin, XZ, Chang, TT, and Shin, JS (1994). Influence of paraesophageal venous collaterals on efficacy of endoscopic sclerotherapy for esophageal varices. Hepatology. 19, 602-8.
    Pubmed CrossRef
  19. Gluud, LL, Klingenberg, S, Nikolova, D, and Gluud, C (2007). Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials. Am J Gastroenterol. 102, 2842-8.
    Pubmed CrossRef
  20. Kirby, JM, Cho, KJ, and Midia, M (2013). Image-guided intervention in management of complications of portal hypertension: more than TIPS for success. Radiographics. 33, 1473-96.
    Pubmed CrossRef
  21. Zheng, M, Chen, Y, Bai, J, Zeng, Q, You, J, and Jin, R (2008). Transjugular intrahepatic portosystemic shunt versus endoscopic therapy in the secondary prophylaxis of variceal rebleeding in cirrhotic patients: meta-analysis update. J Clin Gastroenterol. 42, 507-16.
    Pubmed CrossRef
  22. Narahara, Y, Kanazawa, H, Fukuda, T, Matsushita, Y, Harimoto, H, and Kidokoro, H (2011). Transjugular intrahepatic portosystemic shunt versus paracentesis plus albumin in patients with refractory ascites who have good hepatic and renal function: a prospective randomized trial. J Gastroenterol. 46, 78-85.
  23. García-Pagán, JC, Caca, K, Bureau, C, Laleman, W, Appenrodt, B, and Luca, A (2010). Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 362, 2370-9.
    Pubmed CrossRef
  24. Rössle, M, Haag, K, Ochs, A, Sellinger, M, Nöldge, G, and Perarnau, JM (1994). The transjugular intrahepatic portosystemic stent-shunt procedure for variceal bleeding. N Engl J Med. 330, 165-71.
    Pubmed CrossRef
  25. Petersen, BD, and Clark, TW (2008). Direct intrahepatic portocaval shunt. Tech Vasc Interv Radiol. 11, 230-4.
  26. Feldman, M, and Feldman, MJ (1956). Gastric varices. Gastroenterology. 30, 318-21.
  27. Mitty, HA, Cohen, BA, Sprayregen, S, and Schwartz, K (1983). Adrenal pseudotumors on CT due to dilated portosystemic veins. AJR Am J Roentgenol. 141, 727-30.
    Pubmed CrossRef
  28. Sharma, M, and Rameshbabu, CS (2012). Collateral pathways in portal hypertension. J Clin Exp Hepatol. 2, 338-52.
    Pubmed KoreaMed CrossRef
  29. Irani, S, Kowdley, K, and Kozarek, R (2011). Gastric varices: an updated review of management. J Clin Gastroenterol. 45, 133-48.
  30. Saad, WE, Khaja, MS, and Hirota, S (2012). Balloon-occluded retrograde transvenous obliteration of gastric varices: conception, evolution, and history. Tech Vasc Interv Radiol. 15, 160-4.
    Pubmed CrossRef
  31. Cho, SK, Shin, SW, Lee, IH, Do, YS, Choo, SW, and Park, KB (2007). Balloon-occluded retrograde transvenous obliteration of gastric varices: outcomes and complications in 49 patients. AJR Am J Roentgenol. 189, W365-72.
    Pubmed CrossRef
  32. Fukuda, T, Hirota, S, and Sugimura, K (2001). Long-term results of balloon-occluded retrograde transvenous obliteration for the treatment of gastric varices and hepatic encephalopathy. J Vasc Interv Radiol. 12, 327-36.
  33. Ninoi, T, Nishida, N, Kaminou, T, Sakai, Y, Kitayama, T, and Hamuro, M (2005). Balloon-occluded retrograde transvenous obliteration of gastric varices with gastrorenal shunt: long-term follow-up in 78 patients. AJR Am J Roentgenol. 184, 1340-6.
    Pubmed CrossRef
  34. Lee, EW, Saab, S, Gomes, AS, Busuttil, R, McWilliams, J, and Durazo, F (2014). Coil-Assisted Retrograde Transvenous Obliteration (CARTO) for the treatment of portal hypertensive variceal bleeding: preliminary results. Clin Transl Gastroenterol. 5, e61.
    Pubmed KoreaMed CrossRef
  35. Gwon, DI, Kim, YH, Ko, GY, Kim, JW, Ko, HK, and Kim, JH (2015). Vascular plug-assisted retrograde transvenous obliteration for the treatment of gastric varices and hepatic encephalopathy: a prospective multicenter study. J Vasc Interv Radiol. 26, 1589-95.
    Pubmed CrossRef
  36. Morin, C, Lafortune, M, Pomier, G, Robin, M, and Breton, G (1992). Patent paraumbilical vein: anatomic and hemodynamic variants and their clinical importance. Radiology. 185, 253-6.
    Pubmed CrossRef
  37. Farghal, AS, Almansoori, TM, and Valenti, DA (2013). Embolization of spontaneous portosystemic shunt for treatment of refractory hepatic encephalopathy. J Vasc Interv Radiol. 24, S27-8.
  38. Laleman, W, Simon-Talero, M, Maleux, G, Perez, M, Ameloot, K, and Soriano, G (2013). Embolization of large spontaneous portosystemic shunts for refractory hepatic encephalopathy: a multicenter survey on safety and efficacy. Hepatology. 57, 2448-57.
    Pubmed CrossRef
  39. Spier, BJ, Fayyad, AA, Lucey, MR, Johnson, EA, Wojtowycz, M, and Rikkers, L (2008). Bleeding stomal varices: case series and systematic review of the literature. Clin Gastroenterol Hepatol. 6, 346-52.
    Pubmed CrossRef
  40. Saad, WE, Saad, NE, and Koizumi, J (2013). Stomal varices: management with decompression tips and transvenous obliteration or sclerosis. Tech Vasc Interv Radiol. 16, 176-84.
    Pubmed CrossRef
  41. Léauté, F, Frampas, E, Mathon, G, Leborgne, J, and Dupas, B (2002). Massive hemoperitoneum from rupture of an intra-peritoneal varix. J Radiol. 83, 1775-7.
  42. Bataille, L, Baillieux, J, Remy, P, Gustin, RM, and Denié, C (2004). Spontaneous rupture of omental varices: an uncommon cause of hypovolemic shock in cirrhosis. Acta Gastroenterol Belg. 67, 351-4.
  43. Okuda, K, and Matsutani, S (1991). Portal-systemic collaterals: anatomy and clinical implications. Portal hypertension: clinical and physiological aspects, Okuda, K, and Benhamou, JP, ed. Tokyo: Springer Japan, pp. 51-62
  44. Malde, H, Nagral, A, Shah, P, Joshi, MS, Bhatia, SJ, and Abraham, P (1993). Detection of rectal and pararectal varices in patients with portal hypertension: efficacy of transvaginal sonography. AJR Am J Roentgenol. 161, 335-7.
    Pubmed CrossRef
  45. Kim, M, Mitchell, DG, and Ito, K (2000). Portosystemic collaterals of the upper abdomen: review of anatomy and demonstration on MR imaging. Abdom Imaging. 25, 462-70.
    Pubmed CrossRef

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