AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
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• References

Background

Portal vein thrombosis (PVT) is being recognized with increasing frequency with the use of ultrasonography. Reduced portal blood flow caused by hepatic parenchymal disease and abdominal sepsis (ie, infectious or ascending thrombophlebitis) are the major causes. Transient PVT is also being recognized with increasing frequency, partly because of the great increase in the use of ultrasonography in the evaluation of patients with abdominal inflammation such as appendicitis. Hypercoagulable syndromes can lead to portomesenteric and splenic vein thrombosis. Patients with these conditions may present with acute or subacute intestinal angina. In late stages, patients may have variceal bleeding.^{1, 2, 3}

Related Medscape topics:
Specialty Site Gastroenterology
Specialty Site Hematology-Oncology
Specialty Site Infectious Diseases
Portal Vein Thrombosis; Risk Factors, Clinical Presentation and Treatment

Pathophysiology

Cavernous transformation of the portal vein (ie, the development of periportal collaterals) occurs with long-standing PVT as a result of the development of multiple small vessels in and around the recanalizing or occluded main portal vein. A leash of fine or markedly enlarged serpiginous vessels is seen in place of the portal vein. The application of color and/or pulsed Doppler imaging shows blood flow in these periportal collaterals that form around the thrombosed portal vein or that replace the vein.⁴ The time-averaged mean velocity of blood flow in the recanalizing portal vein is usually 2-7 cm/s.

Cavernous transformation of the portal vein can appear as a subhepatic spongelike mass. This appearance has also been reported in cases of pancreatic hemangiosarcoma. Bile duct varices, also called the pseudocholangiocarcinoma sign, are occasionally observed with endoscopic retrograde cholangiopancreatography (ERCP) in patients with portal hypertension; this finding results from cavernous transformation of the portal vein (see Image 19).⁵ Bile duct varices may disappear after a transjugular intrahepatic portosystemic shunt (TIPS) procedure when the portal hypertension is reduced.

PVT occurs secondary to infection, surgical intervention, or abdominal malignancy (eg, pancreatic or hepatocellular carcinoma) or as a result of liver dysfunction.^{6, 7} PVT is a known complication of pyogenic cholangitis. Causes of PVT include the following:

• Idiopathic causes
• Causes secondary to tumor
• Hepatocellular carcinoma
• Cholangiocarcinoma
• Pancreatic carcinoma
• Gastric carcinoma
• Trauma
• Iatrogenic umbilical vein catheterization^{8, 9}
• Abdominal sepsis
• Pancreatitis
• Perinatal omphalitis
• Appendicitis
• Diverticulitis
• Ascending cholangitis
• Myeloproliferative disorders¹⁰
• Clotting disorders (hypercoagulable syndromes)
• Estrogen therapy
• Severe dehydration
• Cirrhosis, especially in the young
• Portal hypertension

Related eMedicine topics:
Portal Hypertension
Colon, Diverticulitis

Related Medscape topics:
CME The Surviving Sepsis Campaign: Clinical Practice Guideline Revisions for Improving Outcomes in Sepsis
CME Hepatocellular Carcinoma: An In-Depth Look at Local and Systemic Therapies
CME Promising New Treatment Approaches for Hepatocellular Carcinoma
CME Probiotics Should Not Be Given to Patients With Severe Acute Pancreatitis

Frequency

United States

The exact frequency of PVT is not known, but segmental or global PVT occurs in as many as 30% of patients with hepatocellular carcinoma. The incidence of PVT in patients with cirrhosis and portal hypertension is approximately 5%.

Mortality/Morbidity

Morbidity and mortality are related to the underlying disease that is exacerbated by PVT.

• PVT occurs slowly and silently. It usually is not discovered until gastrointestinal hemorrhage develops, unless the thrombosis is discovered during routine surveillance for an underlying disease process.
• Hypersplenism of acute onset is a known complication of PVT.
• In patients with hypercoagulable syndromes, mesenteric venous thrombosis often extends into the portal vein and results in mild to severe intestinal angina.

Age

PVT predominantly affects young children, but it can occur in persons of any age.

Anatomy

The portal vein forms behind the neck of the pancreas with the union of the splenic and superior mesenteric veins. It courses to the porta hepatis in the free edge of the lesser omentum and receives the cystic, pyloric, accessory pancreatic, superior pancreaticoduodenal, and other veins that are too small to visualize.

Generally, the portal vein enters the porta hepatis and divides into the right and left main branches. The right main branch divides into anterior and posterior branches that supply the anterior and posterior segments of the right lobe. The left main branch courses horizontally to the left before turning vertically to form the medial and lateral segmental branches. Several variations of the portal venous anatomy have been described by using ultrasonography, CT, and cadaveric dissection.

Anatomic variants are possible. The normal origin of the left main portal vein branch and the horizontal part of the left main portal vein can be absent. A branch of the right anterior portal vein radical supplies the left lobe of liver. The right main portal trunk can also be absent. Immediately after it enters the porta hepatis, the portal vein turns to the left without giving rise to any of the normal right portal vein branches. The right hepatic lobe is smaller than usual, and small veins of varying sizes supply it. The right main portal vein trunk can be absent while its branches are present. Branches of the anterior and posterior right portal veins arise by means of trifurcation of the main portal vein trunk. The right posterior portal vein branch can arise from the main portal vein trunk. The main portal vein then continues into the liver and bifurcates.

Clinical Details

PVT is often not discovered until gastrointestinal hemorrhage develops, unless the thrombosis is discovered during routine surveillance for a known underlying pathologic condition. In most patients, PVT occurs slowly and silently. The signs and symptoms of PVT can be subtle or nonspecific, and they can be overshadowed by those of the underlying illness. The radiologist may be the first physician to suggest the diagnosis on the basis of imaging findings. The exceptions to this scenario are patients with hypercoagulation and portal and mesenteric venous thromboses who present with moderate or severe abdominal pain after acute or subacute development of the thrombosis.

Patients may present with abdominal pain; portal systemic encephalopathy; or gastrointestinal hemorrhage caused by esophageal varices, splenomegaly, and/or ascites. Symptoms of the underlying cause of the PVT, such as acute pancreatitis, intra-abdominal sepsis, or ascending cholangitis, may predominate.

Portal biliopathy is a recently described entity characterized by bile duct and gallbladder wall abnormalities in association with portal hypertension, particularly with extrahepatic portal vein obstruction.^{11, 12, 13} Cavernous transformation of the portal vein, choledochal varices, and ischemic injury of the bile duct have been postulated as causes. Portal cavernous transformation gives rise to many dilated pericholedochal and periportal collaterals that bypass the portal vein obstruction. Extrinsic compression of the common duct by dilated venous collaterals together with pericholedochal fibrosis from the inflammatory process causing portal thrombosis may lead to biliary stricture and dilatation of the proximal biliary tree. This condition sometimes causes the formation of secondary biliary stones and cholangitis. Most patients remain asymptomatic, but some present with raised alkaline phosphatase level, abdominal pain, fever, and cholangitis.¹⁴

Preferred Examination

Preferred examinations include duplex Doppler ultrasonography and/or color Doppler ultrasonography, CT, magnetic resonance angiography (MRA) (see Image 7), and arterial portography or splenoportography.¹⁵

Tumor in the portal vein may have an appearance identical to that of thrombosis, but this appearance is far less common than others. Tumor in the portal vein is most frequently related to hepatocellular carcinoma. The thrombus may be partial or complete. It may be mixed with bland thrombus as well.

Adults who have acute PVT secondary to abdominal sepsis may completely recover, and the vessel may recanalize with successful treatment of the underlying sepsis.¹⁶ In children, the portal vein may recanalize with the development of multiple, small, collateral channels. These channels are seen as a partly echogenic band of small vessels extending to the porta hepatis (cavernous transformation). These have a reduced flow velocity of 2-7 cm/s. Nonvisualization of the portal vein is strongly suggestive of occlusion. The portal vein may then be seen as a band of high-level echoes at the porta hepatis.¹⁷

DIFFERENTIALS

Section 3 of 11  

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• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

RADIOGRAPH

Section 4 of 11  

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• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
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• References

Findings

Plain radiographs may reveal hepatosplenomegaly, an enlarged azygos vein, and paraspinal varices. Esophageal varices that consist of dilated submucosal veins in the lower esophagus occur chiefly as a consequence of portal hypertension, mostly in cirrhosis. The varices appear as beaded or serpiginous translucent filling defects. Large esophageal varices are obvious and appear as nodular or vermiform, changeable filling defects within the esophagus. Smaller varices appear as scalloped esophageal folds, which are better seen on recumbent radiographs, because they tend to disappear on upright images.

CT SCAN

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• Ultrasound
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Findings

The portal vein supplies 75% of the blood flow to the liver. Therefore, peak liver contrast enhancement occurs during the portal venous phase, about 60 seconds after the start of a bolus injection of contrast material. With helical CT, a liver examination requires about 20 seconds to complete; images can usually be acquired in one breath hold.¹⁸

This technique can be extended to acquire a dual-phase contrast-enhanced CT scan in which the liver is imaged twice with a single contrast agent bolus, first during the arterial phase and then through portal venous phase. Dual-phase CT is indicated in some cases involving benign or malignant lesions in which vascular characteristics suggest the correct diagnosis (see Images 4-6, 13, 14, 16-17).

Angiographically assisted CT, or CT arterial portography, can provide better delineation of the portal venous system and portal venous enhancement of the liver. An angiographic catheter is placed in the common celiac axis, hepatic artery, or superior mesenteric artery by using a modified Seldinger technique via the femoral artery. Image acquisition begins 3-5 seconds after injection of the contrast agent is initiated. The examination should be completed as soon as possible, before the contrast material recirculates. To prevent significant artifacts related to the density of the contrast material, 70 mL of dilute (1-30%) iodinated contrast agent is used with an infusion rate of 2 mL/s. Although angiographically assisted CT can produce elegant images, it is invasive, expensive, and not widely accepted.

On contrast-enhanced CT scans, PVT may be depicted as a low-attenuating center in the portal vein surrounded by peripheral enhancement. Portal vein attenuation is 20-30 HU less than that of the aorta.

CT angiography (CTA) is an application of helical CT. The rapidity of helical CT allows the maintenance of a higher concentration of intravenous contrast medium, particularly through the arterial enhancement phase, and it has the capability of 3-dimensional (3D) reconstruction. Both peripheral intravenous injections of contrast agent and CT arterial portography have been used as with CTA. CTA has shown great promise in the evaluation of hepatic vessels before liver resection. It provides preoperative surgical information about the segmental location of liver tumors, the segmental venous anatomy, and the presence of significant arterial anomalies. The value of CTA in the evaluation of portal hypertension is unclear, but CTA is likely to be useful because it may delineate the collateral vessels, varices, and other findings in patients with portal hypertension.

MRI

Section 6 of 11  

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Findings

The vascular anatomy of the liver may be outlined by using spin-echo and gradient-recalled-echo (GRE) techniques, but these techniques cannot demonstrate the direction of portal flow. Time-of-flight MRI with bolus tracking has been successful in the assessment of portal hypertension and its sequelae. Phase-contrast sequences can also be used to evaluate the portal vein, and phase-contrast cine MRA can show the direction of portal venous flow and the presence of portal vein thrombus. Magnetic resonance evaluation of the portal venous system accurately demonstrates thrombosis and the collateral circulation. Gadolinium enhancement is useful in this application (see Image 18).^{19, 20, 21}

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

As of late December 2006, the FDA had received reports of 90 such cases of NSF/NFD. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

MRCP coupled with dynamic 3D gradient-echo imaging can not only detect portal vein occlusion, cavernous transformation, and gallbladder varices but also depict bile duct abnormalities associated with portal biliopathy.^{22, 23, 24}

False Positives/Negatives

Lin and associates compared surgery and X-ray portography with 3D CE MRA in patients with portal vein involvement from hepatocellular carcinoma.²⁵ The overall sensitivity with 3D CE MRA was 99%; the specificity was 96%; the positive predictive value was 91%; and the negative predictive value was 99%. The accuracy in diagnosis of the main portal vein was 100%. 3D CE MRA resulted in 7 false-positive interpretations involving 6 left portal veins and 1 right portal vein. One false-negative diagnosis was made with right portal vein involvement.

Shah and associates compared MRI with intraoperative findings in the diagnosis of portal vein thrombosis in transplantation candidates. In this study, the sensitivity and specificity of MRI for detecting main PVT were 100% and 98%, respectively. The cause of discordance between findings on MRI and at transplantation in 2 cases was a diminutive caliber of the main portal vein that was interpreted as recanalized chronic thrombosis on MRI. The major reason for a false-positive MRI is a diminutive but patent portal vein.²¹

An extremely slow portal venous flow is considered to be the cause of false-positive findings with unenhanced MRI and sonography.²⁶

ULTRASOUND

Section 7 of 11  

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• Ultrasound
• Angiography
• Intervention
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Findings

PVT is being recognized with increasing frequency at ultrasonography. Abdominal sepsis and reduced portal blood flow resulting from hepatic parenchymal disease are the major causes. Transient PVT is also being recognized with increasing frequency, partly because of the great increase in the use of ultrasonography in the evaluation of patients with abdominal inflammation, such as appendicitis. Tumor in the portal vein may have an appearance identical to that of thrombosis, but this appearance is far less common than others (see Images 1-3, 8-12, 15, 17).

On sonograms, echogenic lesions may be present in the portal vein. Clot with variable echogenicity may be depicted. The clot usually has moderate echogenicity, but if it is recently formed, it may be hypoechoic. Patent vessels may have increased intraluminal echogenicity because of erythrocyte rouleaux formation, which makes slow-flowing blood slightly echogenic. Increased or decreased echogenicity may be observed in the lumen of the portal vein. In isolation, this finding is not sufficient to diagnose or exclude PVT.

PVT eliminates the usual venous flow signal from the lumen of the portal vein during either pulsed or color flow Doppler imaging. Color flow Doppler images can show flow around a thrombus that partially blocks the vein. However, if flow is sluggish, the Doppler signal may not be detected. Color flow may be present in other small collateral vessels.²⁷

Incomplete occlusion may occur. This is common with neoplastic invasion. Alternatively, thrombolytic recanalization may occur. The 2 cannot be differentiated on sonograms. Cavernous malformation, spontaneous shunts, and splenorenal and portosystemic collaterals may be seen. The underlying cause (eg, hepatocellular carcinoma, metastases, cirrhosis, pancreatic neoplasms) may be evident. The incidence of PVT is reported to be low in portal hypertension.

The string sign—that is, thickening of the portal vein with narrowing of its lumen—is assumed to be caused by portal phlebitis. This is considered a precursor of PVT in patients with acute pancreatitis. The portal vein thrombus may be calcified. The diameter of the portal vein is larger than 15 mm in 38% of the cases of PVT.²⁸

ANGIOGRAPHY

Section 8 of 11  

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• Angiography
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Findings

Among catheter-directed techniques, arterial portography is now the preferred method for evaluating the portal venous system because it is less invasive and has a lower complication rate than the other methods (eg, splenoportography). The method involves the indirect opacification of the portal venous system with an injection of contrast material into the splenic vein to outline the splenic and portal veins or superior artery to outline the superior mesenteric and portal veins.

The 3 major indications for arterial portography are the following: (1) to examine patients with portal hypertension and its sequelae, particularly when surgical treatment is planned; (2) to determine the resectability of hepatic and pancreatic tumors when both the arterial- and venous-phase angiographic findings make a significant contribution; and (3) to perform transcatheter embolization, in cases of metastases of islet cell tumors or carcinoid metastases, or chemoembolization, in cases of hepatocellular carcinoma. (A widely or partly patent portal vein is a prerequisite for such treatment.)

Patient preparation and contraindications are the same as those of conventional angiography. Selective catheters are used to cannulate the appropriate vessel. In a superior mesenteric artery injection, the tip of the catheter is placed to enable opacification of all the branches with contrast material. Before the delivery of the contrast agent, a vasodilator (tolazoline [Priscoline], papaverine,  or prostaglandin E) is administered to improve opacification of the portal vein.

Manual or digital subtraction is necessary. If digital subtraction is used, the administration of an anticholinergic drug (eg, glucagon) before imaging reduces bowel motion. Selective injection of the superior mesenteric artery can be used to outline the superior mesenteric and portal veins. For splenic and/or portal vein delineation, splenic artery catheterization is chosen. Injection of the left gastric artery consistently demonstrates esophageal varices.

For details about splenoportography, see Portal Hypertension.

Another technique for opacifying the portal system is wedged hepatic venous injections of carbon dioxide.²⁹ The low viscosity of the gas allows it to readily float across the hepatic sinusoids, successfully opacifying the portal vein in most cases. See Carbon Dioxide Angiography for details and images.

Degree of Confidence

Diagnostic modalities such as ultrasonography, CT, and MRI have reduced the diagnostic importance of arteriography in the diagnosis of liver tumors. The role of liver angiography seems to be limited to the occasional mapping of the vascular anatomy before surgery (now largely performed with MRA or CTA) and the transcatheter treatment of liver tumors. Venous-phase imaging in the celiac axis and superior angiography provide sufficient detail to make direct portography unnecessary in most cases.

INTERVENTION

Section 9 of 11  

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The development of PVT can precipitate the need for emergency endoscopy for sclerotherapy of varices, transjugular intrahepatic portosystemic shunt (TIPS) creation, surgical portocaval shunt creation, transjugular or transhepatic portomesenteric thrombolysis and thrombectomy, or even resection of ischemic bowel or liver transplantation.³⁰ However, PVT may complicate sclerotherapy. Fine-needle aspiration biopsy of PVT can be performed with color Doppler sonographic guidance to assess therapeutic effectiveness.

Early complications of TIPS creation that are detectable with ultrasonography include the following: intraperitoneal hemorrhage, shunt thrombosis, neck hematoma, compromise of hepatic blood supply, PVT, hepatic artery occlusion, hepatic infarction, failed stent deployment, inadequate stent expansion, stent retraction, stent fracture, and biliary obstruction.³¹

Delayed complications of TIPS creation that are detectable with ultrasonography include shunt stenosis caused by pseudointimal hyperplasia and hepatic vein stenosis.^{32, 33}

Medical/Legal Pitfalls

• With PVT, patients are sick, and most percutaneous procedures are associated with high risk.^{34, 35}
• This concern must be explained to the patients and/or their guardians.

MULTIMEDIA

Section 10 of 11  

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• Ultrasound
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• Intervention
• Multimedia
• References

Media file 1:  Portal vein thrombosis. Longitudinal oblique sonogram was obtained through the liver in a 36-year-old woman with a known history of Leber optic atrophy (hereditary optic neuroretinopathy) and alcohol abuse who presented with nonspecific complaints of ill health and vague abdominal pain. Image shows ascites and a bright liver (fatty). The portal vein has a linear echogenic structure running the length of the portal vein (solid arrow). A complex cystic mass is present within the liver (open arrow).
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Media file 2:  Portal vein thrombosis. Power Doppler sonogram of the liver, obtained in the same patient as in Image 1, shows blood flow around an intraluminal filling defect in the portal vein (P).
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Media file 3:  Portal vein thrombosis. Spectral Doppler sonogram of the liver, obtained in the same patient as in Images 1-2, shows the portal vein (cursor), which demonstrates no blood flow.
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Media type:  Image

Media file 4:  Portal vein thrombosis. Portal venous–phase enhanced axial CT scan, obtained in the same patient as in Images 1-3, shows no flow in the portal vein. Note the multiple low-attenuating masses at the periphery of the right lobe of the liver.
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Media type:  CT

Media file 5:  Portal vein thrombosis. Portal venous–phase enhanced axial CT scan, obtained in the same patient as in Images 1-4, shows a low-attenuating mass in the termination of the splenic vein (arrow). Note the multiple low-attenuating masses at the periphery of the right lobe of the liver.
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Media type:  CT

Media file 6:  Portal vein thrombosis. Portal venous–phase enhanced axial CT scan, obtained in the same patient as in Images 1-5, shows an enlarged left gastric vein associated with a low-attenuating mass in the vein. No contrast enhancement is seen in the vein; this finding is suggestive of thrombosis (arrow).
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Media type:  CT

Media file 7:  Portal vein thrombosis. Digital subtraction portal venous–phase superior mesenteric angiogram, obtained in the same patient as in Images 1-6, shows collateral vessels at the porta hepatis but no patent portal vein. Note that the liver is displaced away from the thoracic cage as a result of ascites. This patient had severe hepatic failure and died within 72 hours after the imaging examination. Postmortem examination showed early cirrhosis, fulminant pyogenic cholangitis, multiple liver abscesses, and portal vein and splenic and left gastric vein thrombosis.
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Media type:  X-RAY

Media file 8:  Portal vein thrombosis. Longitudinal oblique sonogram was obtained in a 28-year-old woman who was referred for gallbladder ultrasonography. On questioning, she gave a history of an episode of severe pyrexial illness and dehydration during childhood. The image shows several vascular tubular structures at the porta hepatis, which are suggestive of a cavernous transformation.
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Media file 9:  Portal vein thrombosis. Color Doppler sonogram, obtained in the same patient as in Image 8, shows flow in the cavernous transformation.
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Media type:  Image

Media file 10:  Portal vein thrombosis. Color Doppler sonogram of the spleen, obtained in the same patient as in Images 8-9, shows moderate splenomegaly with varices at the splenic hilum. Endoscopic findings confirmed the presence of esophageal varices.
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Media type:  Image

Media file 11:  Color Doppler ultrasonography depicts a vascularized HCC portal venous thrombus.
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Media file 12:  Color Doppler ultrasonography depicts a vascularized HCC portal venous thrombus.
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Media file 13:  Contrast-enhanced axial CT depicts cavernous transformation following portal venous thrombosis. The portal venous thrombus is extending from the superior mesenteric vein (right image-arrow). Note the small ascites.
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Media file 14:  Coronal reconstruction of contrast-enhanced CT depicts cavernous transformation following portal venous thrombosis. Note the gallbladder varices (red arrow) and a dilated bile duct (white arrow). The appearances suggest portal biliopathy.
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Media file 15:  Ultrasound reveals an echogenic partially recanalized portal vein thrombus. The patient was a 36-year-old woman with idiopathic chronic portal vein thrombosis of 2 years' duration. She presented with cholestatic jaundice (same patient as in Images 14-19).
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Media file 16:  Axial contrast-enhanced CT images of the liver depicting dilated ducts (white arrow) and portal vein thrombus (red arrow) Note the varices around the spleen (same patient as in Images 14-19).
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Media file 17:  MRCP showing intrahepatic dilatation of the right lobe bile ducts and a long stricture of the common bile duct (same patient as in Images 14-19).
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Media file 18:  T1-contrast-enhanced coronal MR images showing thrombus within the main portal vein and a cavernous transformation of portal vein at the porta hepatis (same patient as in Images 14-19).
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Media file 19:  ERCP and PTC confirming the biliary abnormalities. The appearances are those of portal biliopathy (same patient as in Images 14-19).
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

1. Patel N, Haskal ZJ, Kerlan RK. Portal Hypertension: Diagnosis and Interventions. 2nd ed. Society of Cardiovascular and Interventional Radiology;. 2001.
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3. Sheen CL, Lamparelli H, Milne A. Clinical features, diagnosis and outcome of acute portal vein thrombosis. QJM. Aug 2000;93(8):531-4. [Medline].
4. Ricci P, Cantisani V, Biancari F. Contrast-enhanced color Doppler US in malignant portal vein thrombosis. Acta Radiol. Sep 2000;41(5):470-3. [Medline].
5. Vleggaar FP, Van Buuren HR, Laméris JS. [Bile duct lesions in portal vein thrombosis]. Ned Tijdschr Geneeskd. Oct 9 1999;143(41):2057-62. [Medline].
6. Maalouf M, Papasavas P, Goitein D, Caushaj PF, Gagne D. Portal vein thrombosis after laparoscopic splenectomy for systemic mastocytosis: a case report and review of the literature. Surg Laparosc Endosc Percutan Tech. Apr 2008;18(2):219-21. [Medline].
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8. Sakha SH, Rafeey M, Tarzamani MK. Portal venous thrombosis after umbilical vein catheterization. Indian J Gastroenterol. Nov-Dec 2007;26(6):283-4. [Medline].
9. Rubabaza P, Persadie RJ. Two Cases of Umbilical Vein Thrombosis, One With Associated Portal Vein Thrombosis. J Obstet Gynaecol Can. Apr 2008;30(4):338-343. [Medline].
10. de Suray N, Pranger D, Brenard R. Portal vein thrombosis as the first sign of a primary myeloproliferative disorder: diagnostic interest of the V617F JAK-2 mutation. A report of 2 cases. Acta Gastroenterol Belg. Jan-Mar 2008;71(1):39-41. [Medline].
11. El-Matary W, Roberts EA, Kim P, Temple M, Cutz E, Ling SC. Portal hypertensive biliopathy: a rare cause of childhood cholestasis. Eur J Pediatr. Feb 13 2008;[Medline].
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13. Chandra R, Kapoor D, Tharakan A, Chaudhary A, Sarin SK. Portal biliopathy. J Gastroenterol Hepatol. Oct 2001;16(10):1086-92. [Medline].
14. Colle I, Van Vlierberghe H, Pattyn P, Troisi R, Vogelaers D, de Hemptinne B, et al. Cholestasis as presenting symptom of portal cavernoma. Hepatol Res. Jan 2003;25(1):32-37. [Medline].
15. von Herbay A, Frieling T, Haussinger D. Color Doppler sonographic evaluation of spontaneous portosystemic shunts and inversion of portal venous flow in patients with cirrhosis. J Clin Ultrasound. Sep 2000;28(7):332-9. [Medline].
16. Stein M, Link DP. Symptomatic spleno-mesenteric-portal venous thrombosis: recanalization and reconstruction with endovascular stents. J Vasc Interv Radiol. Mar 1999;10(3):363-71. [Medline].
17. Parvey HR, Raval B, Sandler CM. Portal vein thrombosis: imaging findings. AJR Am J Roentgenol. Jan 1994;162(1):77-81. [Medline].
18. Novick SL, Fishman EK. Portal vein thrombosis: spectrum of helical CT and CT angiographic findings. Abdom Imaging. Sep-Oct 1998;23(5):505-10. [Medline].
19. Glockner JF, Forauer AR, Solomon H. Three-dimensional gadolinium-enhanced MR angiography of vascular complications after liver transplantation. AJR Am J Roentgenol. May 2000;174(5):1447-53. [Medline].
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Article Last Updated: May 27, 2008