1 5 4 : ) .('4 .2,la trombosis portal(tp) tiene dos formas de presentación, una aguda (tp...

Portal Vein Thrombosis (PVT) is the most fre-

quent cause of pre-sinusoidal Portal Hyperten-

sion (PH). In developing countries, it represents

30% of the causes of PH in adults and 75% in

children, even though it is regarded as an infre-

quent pathology.

From an anatomical point of view, thrombosis

can affect intra-hepatic small branches or the main

stem with or without involvement of its tributary

splenic and superior mesenteric veins. It can also

occlude the portal vein lumen completely or par-

tially with the thrombus in the central area.

Clinically, it is very important to differentiate bet-

ween acute and chronic thrombosis since the clini-

cal management and diagnosis would be different

in each case. In acute PVT the therapeutic objective

is the recanalization of the veins whereas in chronic

PVT the objective is the prevention of digestive he-

morrhages, recurring thrombosis and portal cholan-

giopathy (2). Even though acute and chronic PVT

are clinically different, they represent different sta-

ges of progress of the same disease and therefore,

they have similar causes. They have different ima-

ging characteristics.

Nowadays, non-invasive studies like Ultrasound,

Multidetector Computed Tomography (MDCT) and

Magentic Resonance Imaging (MRI) play an essen-

tial role in the diagnosis of PVT, in the detection of

local thrombosis risk factors and of possible com-

plications. The importance of this disease lies in its

high morbidity and mortality when not diagnosed

and treated efficiently. Being familiarized with ima-

ging findings will help to make an early diagnosis

and implement the appropriate treatment.

La trombosis portal(TP) tiene dos formas de presentación, unaaguda (TP aguda) y otra crónica (TP crónica o cavernomatosis por-tal). Ambas representan el estadio evolutivo de la misma enfermedadpero son consideradas clínicamente como entidades distintas ya quetienen diferente manejo médico ypronóstico.El diagnóstico clínicoes dificultoso debido a que los signos y síntomas no son específicos.La Tomografía Computada Multidetector (TCMD) y la ResonanciaMagnética (RM) permiten realizar su diagnóstico y diferenciar entrela forma aguda y la crónica. También permiten detectar factores deriesgo pro-trombóticos locales y posibles complicaciones.

Introduction

Key words: Portal vein thrombosis, MDCT, MRI. Palabras clave: Trombosis portal, TCMD, RM.

P V T: F MDCT MRI

Sebastián Rossini, Diego Haberman, Javier Pérez, Carlos Capiel, Sebastián Costantino, Matías Landi, Carlos Bouzas

Abstract Resumen

Revista Argentina de Diagnóstico por Imágenes

Case review

Portal vein thrombosis (PVT) can be acute PVT or chronic PVT (por-tal cavernoma). Both represent the stage of progress of the same di-sease, but they are clinically different since they have differentmanagement and diagnosis. Clinical diagnosis is often difficult asclinical signs and symptoms are nonspecific. Multidetector Compu-ted Tomography (MDCT) and Magnetic Resonance Imaging (MRI)allow for an accurate diagnosis and differentiation between the acuteor chronic condition. They may also detect local pro-thrombotic riskfactors and future complications.

Received: November 30, 2013 / Accepted: February 10, 2014Recibido: 30 de noviembre de 2013 / Aceptado: 10 de febrero de 2014

Contact information: Sebastián Rossini. Instituto Radiológico Mar del Plata - Mar del Plata, Bs. As.

e-mail: [email protected]

PVT can be caused by local or general risk fac-

tors. Local risk factors are identified in 30% of the

cases and they include cirrhosis, abdominal orga-

nic lesions, inflammatory or infectuous processes,

instrumental or surgical procedures and abdomi-

nal trauma. It is important to know these risk fac-

tors since non-invasive imaging studies such as

ultrasound, MDCT and MRI play an essential role

in their identification. General risk factors are pre-

sent in 70% of the cases and are related to birth

or acquired prothrombotic conditions. Myelopro-

liferative disorders are the most frequent in adult

population (1,3).

The double blood flow of the liver goes through

the portal vein and the hepatic artery. The portal

vein supplies 75-80% of the total hepatic blood to

the liver, while the hepatic artery only supplies 20-

25%. That is why during the arterial phase in MDCT

and MRI there is almost no evidence of hepatic pa-

renchymal enhancement, while the greatest enhan-

cement is identified in the portal phase within

approximately 70 seconds after the contrast injec-

tion (Fig. 1). Both systems present a compensating

relation where the arterial flow increases if the por-

tal flow decreases in such a way that the total he-

patic flow tends to remain unaltered (4).

Vol. / Nº - Mayo

Portal Vein Thrombosis: Findings in MDCT and MRI Rossini S. et al.

Etiology Pathophysiology

Fig. : Normal Dynamic MDCT. The liver shows a double blood flow through the por-tal vein (supplying 75 - 80%) and the hepatic artery(20 - 25%). During arterial phase MDCT or MRI showalmost no hepatic parenchymal enhancement. A grea-ter enhancement is identified in the portal phase(70"). During the portal phase, the splenic-portal-me-senteric venous system has a complete and homoge-neous enhancement.

a cb



When there is obstruction of the portal flow be-

cause of thrombosis or any other cause there will

be a decrease in the hepatic perfusion in the portal

phase with a compensating increase of the perfu-

sion in the arterial phase. In acute obstructions, the

greatest arterial blood flow can cause hepatic pa-

renchyma edemas in the affected area (Fig. 2). This

could be related to the greater vascular pressure

that the arterial system has as opposed to the portal

system. The obstruction of the main portal stem will

also produce an increase in the pressure of the en-

tire portal system (presinusoidal portal hyperten-

sion), splenomegaly and a redistribution of the flow

through porto-systemic and mainly porto-portal co-

llaterals (4,5). Generally, the presence of ascites in

patients with PH due to thrombosis is not frequent

and it could be related to the redistribution through

accessory circulation.

MDCT and MRI permit diagnosis of PVT and diffe-

rentiation between acute and chronic PVT since

they have different imaging presentation. MDCT

with intravenous contrast is the study that the Ame-

rican Association for the Study of Liver Diseases

(AASLD) recommends when evaluating patients

suspected to suffer from PVT (Class 1 Level B re-

commendation) (1). When compared to MRI,

MDCT has the advantage of being a faster study

available, with multiplanar isovolumetric capacity

and greater spatial resolution.

Both MDCT and MRI have to be performed with

intravenous contrast and preferably through a dyna-

mic hepatic study (phase without contrast, arterial

phase and portal phase). It is recommended to per-

form a late arterial phase (30 seconds) where in

normal conditions there is a minimum hepatic pa-

renchymal enhancement, a complete enhancement

of the hepatic artery and a general heterogeneous

enhancement of the portal venous system. During

the portal phase (70-75 seconds) there is a greater

hepatic parenchymal enhancement and the portal

vein normally presents a complete and homogene-

ous enhancement (Fig. 1) (6).

During the late arterial phase there might be a fi-

lling defect in the main portal stem simulating

thrombosis, which is known as pseudothrombosis(Fig. 3). This flow phenomenon is produced when

the contrasted blood from the splenic vein is mixed

with non-contrasted blood from the superior me-

senteric vein. Since it has less viscocity, non-con-

trasted blood adopts a central laminar flow that can

be wrongly interpreted as thrombosis (7). To avoid

a wrong diagnosis of PVT it is important to observe

if that image disappears during the portal phase.

Fig. :

Portal Obstruction. The obstruction of the portal flow causes a de-crease in hepatic portal perfusion with a com-pensating increase of the arterial perfusion. A)MDCT without intravenous contrast with anarea of parenchymal edema. B) In the arterialphase there is compensating hyperperfusion. C)The portal phase shows hypoperfusion, but it isnot always present. D) The cause of the obstruc-tion is the infiltration of a portal branch due tometastasis (arrow) in a patient with pancreaticcancer.

a bc d

Imaging interpretation

Acute Portal Vein ThrombosisThe portal phase is the most important phase to de-

tect thrombosis of this vessel and collateral circula-

tion (1). In this phase, acute thrombosis is seen as

an intravascular filling defect that could occlude the

lumen in a partial or a complete way. In the partial

PVT, the thrombus is generally located in the center

of the vein and it is surrounded by a thin contrast

halo (Fig. 4). Generally, the partial PVT does not

produce significant changes in the hepatic perfu-

sion nor signs of portal hypertension. The complete

PVT occludes the venous lumen; however, in some

cases, there is an annular enhancement of the

thrombosed vein wall, probably corresponding to

the dilation of the vasa vasorum (Fig. 5).

MDCT without intravenous contrast can show a

spontaneously hyperdense intravascular image, co-

rresponding to acute clot and vein dilation (Fig. 6).

In MRI, acute clot can be spontaneously hyper-

dense in T1 sequences and present restrictions in

the diffusion sequences (Fig. 7). In the arterial

phase, as an indirect sign of PVT there is an incre-

ase in the parenchymal enhancement due to a gre-

ater compensating arterial perfusion, known as

transitory elevation of the attenuation (Fig. 8). Less

parenchymal enhancement is not always present

and it is probably due to compensatory arterial flow

and venous flow coming from the porto-portal co-

Vol. / Nº - Mayo


A) MDCT in late arterial phase shows a central filling defect in the main portal vein that may simulate a thrombus. B) MDCT inportal phase shows a complete and homogeneous enhancement of the main portal vein. The key to make an accurate diag-nosis is to detect if the pseudo-thrombus vanishes during the portal phase. The false image is produced when the contrastedblood from the splenic vein is mixed with non-contrasted blood from the superior mesenteric vein.

Fig. :a-b

Portal Pseudo-thrombosis.

Fig. :a-b

Partial Portal Vein Thrombosis. A-B) Axial and sagittal view MDCT with intravenous contrast inportal phase. There is a central intravascular filling defect(arrows) with a peripheral contrast halo in the left portal vein.



llateral circulation (1,5,8).

Generally, when PVT is completed there are in-

direct signs of portal hypertension, such as spleno-

megaly and collateral circulation. The number, size

and type of collateral circulation are variable from

patient to patient and there is probably a relation

to constitutional factors and to the obstruction site

in the splenoportal axis (9). If the obstruction oc-

curs in the splenic vein or in the spleono-portal

confluence, usually there is porto-portal collateral

circulation, whereas if the thrombosis affects the

portal intrahepatic branches, the accessory circula-

tion is generally porto-systemic.

Chronic Portal Vein ThrombosisChronic portal vein thrombosis, also known as por-

tal cavernoma, is characterized by irreversible fibro-

sis of the portal system associated to a porto-portal

circulation through peri-choledochic veins located

in the hepatoduodenal omentum. Accessory peri-

choledochic veins try to replace the obstructed por-

tal blood flow (1,5,10).

With MDCT as well as with MRI in portal phase,

there are multiple serpiginous vascular structures

in the hepatic portal, with absence of the portal

stem or its main brnaches (Fig. 9). It is important

to point out that the portal vein is not visualized

in chronic PVT, probably due to fibrosis, and that

it has to be differentiated from acute PVT with

porto-portal circulation where it is possible to

identify the thrombosed portal vein with small ad-

jacent serpiginous vascular structures (Fig. 10).

The importance of such differentiation lies in the

fact that both entities need different treatment and

prognosis. As already stated, patients with acute

PVT receive anti-clotting drugs to canalize the

obstructed vein (Table 1).

Portal cavernoma produces morphological chan-

ges in the liver, with an atrophy of the peripheral

area (mainly the right lobe and the lateral segment

of the left lobe) and hypertrophia of the central

area (caudate lobe and medial segment of the left

lobe) (Fig. 11). This is probably due to the fact that

accessory venous circulation coming through the

portal can correctly supply the central region of the

liver while the peripheral area receives less venous

flow (11). There is also an increase of the compen-

sating arterial flow in the peripheral region with a

greater enhancement during arterial phase. The he-

patic artery is generally increased in size.

Portal cavernoma can present itself as a solid

mass in the hepatic portal with enhancement in a

progressive way where accessory veins can not be

individualizaed. This entity known as tumor-like ca-

vernoma is rare and it consists of fibrous tissue with

multiple collateral veins (Fig. 12) (1).

Generally, tumoral thrombosis is present in pa-

tients suffering from cirrhosis with Hepatocellular

Carcinoma (HCC). HCC frequently permeates and

is disseminated through the portal system causing

an occlusion in the venous system. Tumoral throm-

bosis is characterized by presenting enhancement

of the thrombus with the intravenous contrast in-

jection and it is usually hypertense in T2 sequences.

On the other hand, clot thrombi are never enhan-

ced and are hypointense in T2 sequences. Both tu-

moral thrombosis and acute thrombosis can have

restrictions in MRI diffusion sequences, so it is not

a specific sign of tumoral thrombosis (Fig. 13)

(12,13,14).

Fig. :a-b

Complete Portal Vein Thrombosis. A-B) Axial view MDCT with intrave-nous contrast in portal phase showscomplete thrombosis of the portalsystem and splenic vein in a patientafter splenectomy (*). There is annularenhancement of walls of the comple-tely thrombosed veins probably due todilation of vasa vasorum. The hepaticparenchyma has areas of hypoperfu-sion with low collateral circulation atthe level of the hepatic portal.

Vol. / Nº - Mayo


Complete obstruction of the superior mesenteric vein (SMV). A) MDCT without intravenous contrast shows dilation of theSMV with an intravascular spontaneously hyperdense image corresponding to acute clot. B) MDCT in portal phase evidencescomplete thrombosis of the SMV.

Fig. :a-b

Acute Thrombosis at MDCT.

Fig. : Acute Thrombosis at MRI. Partial thrombosis of the main portal vein. A) Fat-satT1 sequence MRI in portal phase: intravascular centralfilling defect in the main portal vein. B) T1 sequenceMRI: Acute thrombus characterized as being sponta-neously hyperintense. C) Diffusion weighted imaging(DWI) sequence MRI: The thrombus shows restrictionsin diffusion sequence.

a bc



Fig. :a-b

Hepatic Arterial Hyperperfusion.A) MDCT in arterial phase shows great increase of hepatic pa-renchyma enhancement, similar to splenic enhancement dueto a compensating increase of the arterial flow. It is associa-ted to an increase in the size of the hepatic artery. B) MDCTin portal phase shows complete portal and splenic thrombo-sis with porto-portal collateral circulation. Note multiple he-patic metastases in a patient with a history of colon cancer.

Fig. :a-b

Chronic Portal Vein Thrombosis (Portal Caver-noma). A-B) Axial and sagittal view MDCT with intravenous con-trast where the portal branch is not seen probably due to fi-brosis. Instead, there are multiple serpiginous structureswith accessory porto-portal circulation through peri-chole-dochal veins located in the hepatoduodenal ligament.

Tab. : Relevant characteristics of acute and chronic PT.

Vol. / Nº - Mayo


Fig. :a-b

Dysmorphism due to portal cavernoma. A) Axial view MDCT in portal phase shows atrophy of theperipheral area of the hepatic parenchyma with hyper-trophy of the central area. B) Coronal view MDCT showsportal cavernoma. Portal cavernoma produces atrophy ofthe peripheral area of the hepatic parenchyma with hyper-trophy of the central area. One reason may be that peri-choledochal accessory vein circulation can supply thecentral area while the peripheral area receives less bloodflow.

Fig. :a-b

Acute vs Chronic PVT.Acute PVT may have peri-choledochal collateral cir-culation, similar to portal cavernoma. The differenceis that in chronic PVT the portal vein disappears dueto fibrosis, while in acute PVT the portal vein isthrombosed and often distended.

A) T2 sequence coronal view MRI shows a mass in the hepatic portal with heterogeneous signal and low mass effect. B)Fat-sat T1 sequence MRI in portal phase: A mass present an intense and homogeneous enhancement. A less frequenttumor-like form of presentation of portal cavernoma is a solid mass in the hepatic portal where accessory veins cannot beindividualized.

Fig. :a-b

Pseudo-tumoral Cavernoma.



Complications are more frequent in patients with

chronic PVT. Gastrointestinal bleeding due to eso-

phageal varices from portal hypertension is the

most frequent complication (Fig. 14), followed by

recurring thrombosis of the superior mesenteric

vein and cholangiopathy associated to portal ca-

vernoma (1).

Intestinal ischemia or infarction is produced by

the impairment of the superior mesenteric vein in

patients with acute PVT or by recurrent thrombo-

sis in patients with chronic PVT. MDCT with intra-

venous contrast is more useful than ultrasound

and MRI to evaluate patients suspected to have in-

testinal vascular involvement. Evidenced by less

parietal enhancement, the lack of intestinal perfu-

sion is a specific sign of intestinal infarction (Fig.15). Tomographic findings of intestinal ischemia

are parietal thickening, neumatosis and an incre-

ase in the density of the adipose tissue, adjacent

to the affected loop (15).

Patients with portal cavernoma can present dis-

placement and stenosis of the intra and extra-he-

patic biliary tract. This is produced by a

compression due to peri-choledochic collateral cir-

culation over the biliary tree and is called cholan-

giopathy or portal biliopathy. MR cholangiography

plays an essential role in the evaluation of these pa-

tients since it is a non-invasive study. Findings in

MR cholangiography are very similar to Primary

Sclerosing Cholangitis with multiple strictured bi-

liary trees (Fig. 16) and are present in 70% to 100%

of patients with Chronic PVT. Although most pa-

tients do not have symptoms, 50% can present al-

terations of the hepatogram and some have clinical

features of cholestasis (16).

Fig. : Tumoral Portal Thrombosis. A) Fat-sat T1 sequence MRI in arte-rial phase: Segmentary portalthrombosis with hepatic hyperper-fusion. B) Fat-sat T1 sequence MRIin portal phase: Tumoral thrombusis enhanced after the contrast in-jection. C) DWI MRI: The thrombusshows restrictions in diffusion se-quence. D) Coronal view T2 se-quence MRI: There is an HCC overthe porto-tumoral thrombosis.Restriction in diffusion may be pre-sent in tumoral thrombosis oracute thrombosis. Clot thrombus isnot enhanced after contrast injec-tion.

a bc d

Portal Vein Thrombosis Complications

Vol. / Nº - Mayo


Fig. :a-b

Intestinal Infarction. A) MDCT without contrast shows acute thrombosis(hyperdense thrombus) of the superior mesentericvein (SMV). B) MDCT in portal phase shows com-plete thrombosis of the SMV and partial thrombosisof the main portal vein. Associated to thickening ofthe intestinal loops with hypoperfusion compatiblewith intestinal infarction.

Fig. :a-b

Portal Biliopathy. A) Fat-sat T1 sequence MI in portal phase shows portal caver-noma. B) Cholangio-MRI: There are several biliary stenosis.Portal cavernoma may cause compression and deformationof the biliary tree that, when serious, can cause biliopathy orportal cholangiopathy.

A) Contrast MDCT shows multiple venous peri-esophageal structures in a patient with recurring symptomatology of melena.B) Axial view MDCT shows portal cavernoma. PVT produces portal hypertension with porto-systemic collateral circulationand esophageal varices causing gastrointestinal bleeding.

Fig. :a-b

Esophageal Varices.

MDCT and MRI play an essential role in the eva-

luation of patients suspected of having portal vein

thrombosis. They allow for diagnosis and differen-

tiation between acute and chronic PVT, identifica-

tion of pro-thrombotic local risk factors and

detection of potential complications, such as eso-

phageal varices, superior mesenteric vein throm-

bosis and portal cholangiopathy. Both MDCT and

MRI have to be performed with intravenous con-

trast and preferably through a dynamic hepatic

study (phase without contrast, arterial phase and

portal phase).

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Conclusion

Bibliography

1 5 4 : ) .('4 .2,la trombosis portal(tp) tiene dos formas de presentación, una aguda (tp...

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