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717

Review Article

CT of Portal Charles

S. Marn1

Thrombosis

Venous

and Issac

Occlusion

R. Francis

of a portion of the portal venous system can be

directly imaged by contrast-enhanced CT as a low-attenuation lesion within the involved portal venous segment with or without expansion of the vessel or enhancement at the margin of the thrombus. Collateral venous pathways are often evident, which provide supporting evidence of the occlusion. Alterations in portal venous blood flow lead to metabolic disturbances in the liver and to abnormalities in parenchymal enhancement during dynamic CT scanning, and these changes are manifested as abnormalities in hepatic parenchymal density. The detection of portal venous thrombosis or occlusion, collateral veins, or abnormal liver enhancement should initiate a search for the diseases that cause these abnormalities.

The portal

venous

system

can be affected

by a variety

of

Technique Much

emphasis

imaging amounts

has been placed

on the use of dynamic

CT

during the bolus administration of relatively large of contrast material for the detection of hepatic [1 ]. The detection and characterization of vascular

lesions

in the abdomen also are facilitated by similar techniques. At our institution, routine contrast-enhanced abdominal CT using 100-150 ml of 60% meglumine iothalamate is performed in the vast majority of cases. Contrast medium is given by a mechanical injector at a rate of 2 mI/sec through an 1 8-gauge catheter placed in the antecubital fossa. Contigabnormalities

uous

1 0-mm

time

and

patient’s

axial

sections

7- to 1 0-sec size. Scanning

are obtained

interscan is initiated

delay, 30-45

with

2-sec

scanning

depending on the sec (depending on

neoplastic, inflammatory, hematologic, and hypertensive disorders. In many cases, the portal venous abnormality reflects pathologic processes in the liver, spleen, pancreas, or gas-

age, 30 sec for patients less than 40 years old, owing to their better cardiac output) after the initiation of the bolus to ensure hepatic imaging in the portal venous phase of contrast en-

trointestinal

hancement.

tract.

Abdominal

CT is often

used

in the initial

evaluation of many abdominal disorders. Recent advances, such as faster scanning times, the rapid bolus administration of contrast medium using mechanical injectors, and scanning during the portal phase of intraarterial contrast injection into the superior mesenteric artery (CT arterial portography), have significantly increased our understanding of CT patterns of hepatic contrast enhancement in normal and diseased states. This article focuses on the portal venous system as a mirror of abdominal diseases, with emphasis on the pathophysiologic conditions that affect the portal and splenic veins. The CT imaging findings typically seen in some of these conditions

also are discussed

and illustrated.

routinely

limited

When

completed

repeated

this

technique

in 2-3

scanning

mm.

is used,

hepatic

If necessary,

during

tional bolus of 50 ml of contrast confirm or exclude an abnormality scanning.

imaging

single-level

administration medium can suspected

is

or

of an addibe used to on routine

Anatomy The portal venous system drains the stomach, spleen, pancreas, small bowel, and colon to the liver. Contrast-en-

hanced CT scans can show the central portions of the superior and inferior mesenteric veins, the splenic vein, main, right,

Received February 14, 1992; accepted after revision April 5, 1992. Both Arbor,

authors: Department

Ml 48109-0030.

AJR 159:717-726,

of Radiology,

Box 0030, University

Address reprint requests

October

1992 0361 -803X/92/1

of Michigan Medical Center, University of Michigan Hospitals,

to C. S. Mam. 594-0717

© American

Roentgen

Ray Society

1500 E. Medical Center Dr., Ann

MARN

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718

AND

and left portal veins, and central portions of the intrahepatic portal veins. Smaller branches of more peripheral portions of the superior or inferior mesenteric veins in the mesentery or portal vein branches within the liver are not consistently shown by CT unless they contain air. An understanding of normal and collateral venous drainage of the stomach is essential to diagnose portal venous abnormalities (Fig. 1). Small venous branches along the lesser curve drain into the coronary vein, traversing the gastrohepatic ligament, a triangular space between the lesser curve of the stomach and the left lobe of the liver. The coronary vein joins the portal venous system at or near the portal confluence [3]. If vessels larger than 6 mm are present in the gastrohepatic ligament, then varices are present [4]. The greater curve of the fundus is drained toward the splenic hilum, either directly by short gastric veins or by the left gastroepiploic vein. The greater curve of the antrum is drained by the right gastroepiploic vein, which

drains

into

the

superior

mesenteric

vein

at the

level

of

the inferior aspect of the head of the pancreas by means of the gastrocolic trunk. Portions of the right or left gastroepiploic vein are evident in many cases, and the mean size of this vessel is 3 mm, with 6 mm or more representing pathologic enlargement [2, 5-7]. A diameter of 5 mm has been reported as a threshold value for abnormality of the gastrocolic trunk [8]. Although large vascular structures are usually present in the splenic hilum, vessels greater than 4 mm in diameter at the margin of the spleen are suggestive of short gastric varices [2].

FRANCIS

AJR:159,

CT Appearance

of Thrombosed

October

1992

Veins

The CT appearance of thrombosed portions of the portal venous system has been well described [7-1 2]. Thrombi are identified readily on contrast-enhanced CT scans by the presence of a low-attenuation intraluminal filling defect (Fig. 2). Frequently, a high-attenuation rim representing contrast enhancement of the vessel wall is seen (Fig. 3). It has been suggested that this enhancement is a pathophysiologic response to proliferation of the vasa vasorum [7, 1 3]. Others have noted that vessel wall enhancement is most likely always present, but obscured by the intraluminal contrast [1 0]. In either case, rim enhancement accentuates the presence of intraluminal

clot.

This

finding

is much

more

apparent

in por-

tions of the portal venous system surrounded by mesenteric fat than in segments surrounded by enhancing pancreatic or liver tissue [1 0]. Unenhanced CT scans are usually noncontributory.

In one study,

only

four of 1 22 patients

with

portal

venous thrombosis had clot identified on the unenhanced study [1 4]. These cases had intraluminal masses that were of increased attenuation when compared with flowing blood or soft tissue (Fig. 4). It is known that hematomas change over time, with the highest density clot seen in the first 72 hr after bleeding [15]. This observation about hyperdense fresh hematoma has been extended to thrombosis to suggest that a hyperdense intraluminal abnormality represents fresh thrombus [9, 11, 14]. Enlargement of the occluded portal vein segment also has been reported in portal venous thrombosis

Lt. GE V

B

A Fig. 1.-Portal

venous drainage of stomach and spleen.

A, Normal venous drainage. Left gastric (coronary) and right gastric veins drain lesser curve of stomach. Short gastric veins drain fundus. Greater curve Is drained either toward splenic hilum via left gastroepiplolc vein or toward superior mesenteric vein via right gastroepiploic vein and gastrocolic

trunk. B, Occlusion of splenic vein. Increased flow occurs through short gastric varices around fundus to coronary and right gastric veins, and along greater curve via gastroeplplolc vein. 50 = short gastric veins, LGV = left gastric vein, RGV = right gastric vein, GCT = gastrocolic trunk, Rt GEV = right gastroeplplolc veIn, Lt 0EV = left gastroeplplolc vein. Reprinted with permission from Mam et al (2].

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AJR:159,

October

CT OF PORTAL

1992

VENOUS

OCCLUSION

719

Fig. 2.-Portal venous thrombosis from diverticulitis. A and B, Contrast-enhanced CT scans through level of main portal vein (A) and midportion of liver (B) show low-attenuation thrornbus (T) filling central portions of portal veln A band of low attenuation (arrows in B) representing decreased portal perfusion or fatty Infiltration extends to dome of liver.

Fig. 3.-Hepatoma with portal venous thrombosis. Contrast-enhanced CT scans through level of main portal vein (A)and, more superiorly, through level of ascending segment of left portal vein (B) show a hepatoma (H) with an extensive tumor thrombus (1), which has spread from tumor Into main and left portal veins. A band of Increased contrast enhancement at periphery of lesion (arrows) is due to compensatory hepatic arterial flow In response to decreased portal flow.

[91. This sign must

be used

with

caution,

,,#{248}!;’ 1

however,

because

a wide range of normal values for size of various segments of the portal vein has been reported. Measurements of the portal vein change with position, respiration, and fasting, and portal hypertension alone without thrombosis can enlarge the portal vein [16]. Dilatation can be so great as to mimic other mass lesions, such as pancreatic pseudocysts [17]. The true sensitivity of contrast-enhanced CT scans for the detection of portal venous thrombosis is unknown. Igawa and colleagues [1 8] performed a study using drip infusion and reported a sensitivity of only 1 1 % in 1 8 cases of thrombosis related to hepatocellular carcinoma (HCC). Another study from 1 984, in which the presence of a positive imaging test was used to select patients for a comparison of sonography and CT in this disease, reported a CT sensitivity of 76% [7]. Other studies have properly avoided any attempt at calculation of sensitivity because of variable methods of selecting patients, small study size, or limitations in pathologic proof [12, 13, 19]. A larger study using current equipment and techniques is needed to fully address the issue of sensitivity. The specificity of contrast-enhanced CT for portal venous

thrombosis is probably quite high. Numerous studies have made no reference to false-positive examinations [1 2, 13, 19]. One case of innumerable tiny calculi in the biliary system mimicking a calcified clot in the portal vein has been reported [1 7]. The

same

study

reports

a case

of intrahepatic

venous thrombosis mimicking biliary dilatation, have observed one such case (Fig. 5). Collateral

Pathways

in Segmental

portal

and we also

Occlusion

When segmental occlusion of the portal venous system occurs, local collateral pathways of flow arise spontaneously to bypass an obstruction. Two specific circumstances doserve mention: (a) cavernous transformation of the portal vein in response perigastric

to thrombosis collateral flow

in the main portal vein in response to occlusion

and (b) of the

splenic vein. Both these entities have specific appearances on contrast-enhanced CT scans. Recognition of these particular collateral patterns provides supporting evidence of the segmental occlusion and allows a more complete understanding of the patient’s clinical status.

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720

MARN

AND

FRANCIS

AJR:159,

Fig. 4.-Acute thrombosis of aneurysm In portal vein. A, Unenhanced CT scan shows high-attenuation thrombus (T), Indicative of acute thrombosis. B, CT scan during bolus administration of contrast medium shows flow at margin of thrombus (arrowheads).

October

1992

Fig. 5.-Contrast-enhanced CT scan In patient with pancreatic cancer wIth portal venous thrombosis mimickIng billary dilatation. Branching areas of decreased attenuation In liver were Initially misinterpreted as representing dilated bile ducts.

However, thrombosed portal venous system Is not as low In attenuation as expected for fluid (bile), and that observation should lead to correct diagnosis

Cavernous transformation of the portal vein (portal cavernoma) is defined as a masslike network of intertwined veins in the hepatoduodenal ligament and porta hepatis that provides an alternative pathway around a stenosed or occluded segment of the main portal vein or lobar branches [1 2, 20] (Fig. 6). Flow is maintained in the hepatopedal direction unless preexistent liver disease had already caused reversed flow [20]. The thrombosed portal segment is usually not seen, but is replaced by multiple enhancing smaller veins. This mass of abnormal vessels usually involves the main portal vein, but can extend into or be isolated to intrahepatic lobar branches [20]. Splenic venous known perigastric

occlusion leads to the development of wellcollateral venous pathways first defined by angiography [21 22] (Fig. 1B). The diagnosis of splenic venous occlusion by angiography is made when all or a portion of the splenic vein is not visualized during the portal phase of a high-dose celiac injection despite the visualization of intrasplenic or splenic hilar veins and collateral vessels. These collateral vessels include gastric fundal (short gastric and coronary) varices, increased flow along the greater curve of the stomach via the gastroepiploic vein and the omental and inferior mesenteric veins [21 22]. These same principles have been applied to CT scans in patients with splenic venous occlusion [2, 5, 6]. In most cases, the direct observation of dense contrast enhancement of the splenic vein during bolus contrast administration excludes the diagnosis of occlusion. As the splenic vein runs either parallel or slightly oblique to the axial scanning plane, occasionally a portion of the splenic vein is not well seen because of slice misregistration, motion, or distortion of the splenic vein by an adjacent mass. A careful search for the expected collateral vessels in splenic venous occlusion should then be performed. Fundal varices drain the ,

,

of portal

venous

thrombosis.

splenic hilum with flow to the main portal vein through the coronary vein. The spleen is also drained by increased flow along the greater curve via a dilated gastroepiploic vein terminating superior

in the gastrocolic mesenteric vein

trunk, which then drains into the below the head of the pancreas.

These observations require careful mapping over many images (Fig. 7), but can often be made with confidence unless the fat around the stomach is obliterated by pancreatitis or because of cachexia. This pattern is unique, and differentiating isolated

splenic

hypertension

is usually possible

vein

occlusion

from

generalized

portal

[2]. A recent report indicates

that acute pancreatic disease initially dilates only the gastroepiploic vein, while other collateral veins (short gastric, left

gastric, [5].

or omental

Alterations Obstruction

veins) tend to dilate in a chronic

in Hepatic

Attenuation

setting

Due to Portal Venous

The normal liver derives 70-80% of its blood supply from the portal vein, with the remainder coming from the hepatic artery [23]. These two sources of blood differ in pressure and in content of oxygen and nutrients. Additionally, when contrast material is administered in a bolus during dynamic scanning,

contrast-laden

hepatic

arterial

blood

directly

from

the

aorta reaches the liver before contrast-laden portal venous blood, which must first pass through the capillary bed of the intestines and the sinusoids of the spleen. Therefore, a complex set of metabolic and vascular circumstances affect the density of the liver before, during, and after contrast administration. Metabolic disturbances in the liver can alter the baseline hepatic attenuation before the administration of contrast me-

AJR:159,

October

CT OF PORTAL

1992

VENOUS

OCCLUSION

721

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Fig. 6.-A and B, contrast-enhanced CT scans obtained at (A) and immediately above (B) main portal vein in patient with cavernous transformation of portal vein. In this case, a thrombosed segment of main portal vein (T) is surrounded by collateral veins (arrows).

4

Fig. 7.-Perigastric collateral veins venous occlusion. Four noncontiguous

in splenic contrast-

enhanced CT scans show a large gastroepiploic vein (arrowheads) coursing along greater curve of stomach, terminating at superior mesenteric vein via gastrocolic trunk (arrow). See Fig. lB for comparison.

dium. Because portal blood supplies absorbed nutrients to the liver, reduction of portal blood flow can alter liver density. In an animal experiment in which hepatic metabolism was altered through cant attenuation

manipulations differences

of diet and hormones, signifithroughout the entire liver were

reported between times when the liver was glycogen depleted and times when the liver was glycogen enriched [24]. The

well-nourished, is acutely

glycogen-rich depleted

of

liver is denser

glycogen.

When

than the liver that chronic,

glycogen

depletion

leads to increased deposition of fat within hepatocytes, and this effect further lowers the attenuation of nutrient-depleted liver [24]. These observations have been ex-

tended to explain unenhanced

low-attenuation,

CT scans

of patients

wedge-shaped with

segmental

defects

on

portal

ye-

MARN

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722

AND

nous occlusion, because decreased portal flow might decrease glycogen storage in involved segments [25, 26]. These fixed, metabolic alterations provide a background against which transient changes in density during bolus contrast administration occur. A mechanical model has been advanced that explains the relationship of portal to arterial blood flow using the analogy of the interposition of a slower flowing stream (portal flow) in the path of a faster flowing stream (arterial flow) [27]. When the flow in the slower stream decreases, an increase in the flow of the faster stream occurs immediately. In patients with portal thrombosis [9] and cayernous transformation [20], increased arterial flow to portions of the liver deprived of portal venous flow can be seen in scans obtained early in the bolus administration of contrast material (Figs. 3B and 8). In the case of cavernous transformation,

this enhancement

occurs

on the periphery

of the liver,

because the cavernoma most likely provides adequate flow only to the central portions of the liver [9]. More recent work with

CT

segmental

arterial portal

portography ischemia

provides in

patients

further with

evidence focal

of

hepatic

masses [28]. In this technique, a catheter is placed via the transfemoral route into the superior mesenteric artery, and CT scans are obtained while contrast material injected in the superior mesenteric artery provides purely portal enhancement of the hepatic parenchyma. This procedure is used in limited circumstances for patients with potentially resectable

FRANCIS

AJR:159,

October

1992

liver lesions, usually colon cancer metastases or hepatoma, and is superior to routine contrast-enhanced CT in depicting the number of lesions and the relationship between the lesion

and major hepatic blood vessels [29]. In more than one third of cases, a wedge-shaped defect with straight margins was evident, with tumor present at the apex of the defect (Fig. 9). Angiographic

correlation

proved

that in most

cases,

stoppage

of portal flow was responsible for this finding [27]. It is important to note that not every focal or segmental alteration in hepatic density or perfusion is due to an abnormality

of the

portal

vein.

Alterations

in venous

drainage

caused by occlusion of hepatic veins (Budd-Chiari syndrome) [30] or alterations in hepatic arterial flow due to tumors [13, 31 32] or simply focal fatty infiltration [33, 34] can produce ,

segmental or subsegmental uation. In studies performed

areas of decreased liver attenwith CT arterial portography, it

has been shown that not all perfusion defects are related to portal venous thrombosis or mass effect by tumor. Defects in contrast enhancement during arterial portography can be due to cirrhosis, nodular regeneration, siphoning of blood supply by vascular tumors, compression or may occur with no known cause

of vessels by tumor, (Fig. 1 0) [35]. A well-

defined oval or bandlike area of decreased attenuation in the posterior aspect of the medial segment of the left lobe is present in 14% of CT arterial portographic studies (Fig. 11) [36]. As this area is sometimes spared in fatty infiltration, it is

Fig. 8.-colon cancer metastasis with portal venous thrombosis. Four contiguous T scans show large metastasis (M) with an associated portal venous thrombus (t) that has a peripheral area of increased enhancement (arrowheads) eariy in bolus phase of study owing to compensatory increase in arterial flow.

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AJR:159,

October

Fig. 9.-CT metastases

right lobe margins,

CT OF PORTAL

1992

arterial portogram from colon

cancer.

of liver. Posterior most

likely

because

In patient with Two lesions are in

lesion has straight of interruption

Fig. 10.-A enhancement,

VENOUS

OCCLUSION

723

and B, CT arterial portograms show patchy Irregular areas of increased and decreased which were artifactual in this case. Palpation and intraoperative sonography showed

no lesions.

of

portal venous flow.

Fig. 11.-CT arterial portogram shows a welldefined ovoid pseudolesion (arrowheads) in posterior aspect of medial segment of left hepatic lobe, along with two small metastatic deposits (arrows).

postulated that some local variance for this abnormality [26, 35, 36].

Diseases Causing Venous System

Segmental

Fig. 12.-Pancreatic

vein (P)

of main

portal vein without occlusion.

in blood

Occlusions

cancer.

A, CT scan shows vascular encasement with no collateral veins. A portion of main portal is enhanced. B, Angiogram of portal phase of superior mesenteric artery injection shows narrowing

flow accounts

of the Portal

Thrombi generally originate in the portion of the portal venous system nearest the diseased organ. HCC invades the portal venous system in the hepatic parenchyma, but often extends centrally into the main portal vein. Pancreatitis or pancreatic cancer often occludes the splenic vein along the

pancreatic body, but thrombosis may propagate into the main portal vein or inferiorly into the superior mesenteric vein. These abnormalities therefore are grouped according to the portion of the portal venous system that they most commonly involve. Intrahepatic and main portal venous occlusions are usually caused by HCC, metastatic disease, and hepatic venocclusive disease (Budd-Chiari syndrome), and these are discussed first. Pancreatic cancer, pancreatitis, and splenectomy tend to predominate as causes of splenic venous occlusion, and these are discussed second. Septic thrombosis and coagulopathy can involve any portion of the portal venous system, and these are discussed last.

724

MARN

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Hepatocellular

AND

Carcinoma

portal

As the vast majority of HCCs are unresectable at the time of presentation, a careful preoperative clinical and imaging evaluation is necessary to select those patients who should undergo resection in the hope of surgical cure. The distribution of tumor within the liver must be carefully documented. Infiltrative or multifocal lesions are almost always unresecta-

ble, and any planned resection must not only be anatomically possible but also must leave the patient with adequate hepatic function.

Extrahepatic

metastatic

disease

with

spread

to no-

dal or peritoneal sites is common and also precludes resection. Clinical factors such as ascites, jaundice, cirrhosis, or liver failure also weigh in the decision to attempt resection. Invasion of the portal vein by tumor is a well-known manifestation of HCC, occurring in up to 70% of cases [1 3, 18, 19], and precludes surgery in two ways. First, involvement of the main portal vein by tumor makes resection impossible because no surgical technique allows for bypass of this critical structure

[1 9].

Second,

involvement

of

first

or

second

branches of the portal vein adversely affects prognosis because of an increased risk of intrahepatic metastases (Fig. 3) [18]. The signs of portal venous involvement by HCC include an intraluminal

filling

defect,

enlargement

of the occluded

sag-

ment, and the formation of a portal cavemoma, as stated earlier [1 3, 19]. Most thrombi in the portal venous system in patients with HCC are tumor thrombi and not bland thrombi [37]. In some instances, abnormal enhancement at the margin of the thrombus (“rail sign”) or linear enhancement within the thrombus (corresponding to the angiographic “thread and streak” sign) provides further evidence of tumor thrombus [1 3]. The absence of these signs, however, does not mean that the thrombus is necessarily bland. Large central thrombi in HCC are not the only manifestation of venous invasion by this tumor. The inferior vena cava and hepatic vein are sometimes invaded, but this occurs much less frequently. Smaller branches of the portal vein also can be involved and are imaged as punctate or linear low-attenuation

foci

adjacent

to the

lesion.

These

thrombi

may

be

associated with rapid tumor growth and a poor clinical outcome if they occur in portal branches proximal to the tumor [38]. Abnormalities

contrast sion

of liver

administration

is altered

attenuation

both

are common

by arteriovenous

before

in HCC. Hepatic

shunts

within

perfu-

the tumor

or

,

and the detection

of a thrombosed

AJR:159,

vein does

not necessarily

malignant

tumor

Metastatic

Disease

thrombi

the presence

of a

[10, 14].

Although hepatic metastatic than HCC in Western countries,

is rarely however,

imply

1992

October

disease is far more common involvement of the portal vein

shown by contrast-enhanced CT [39]. There a report of the Doppler sonographic identification in the main,

right,

or left

portal

veins

in eight

is, of of a

series of 100 consecutive patients with hepatic metastatic disease [40]. Gastric and colonic cancers are the most common primary sources of hepatic metastases causing portal venous thrombosis, but cases of breast, ovarian, and bladder cancer also have been reported [39, 40].

Budd-Chiari

Syndrome

Hepatic venous occlusion common and typically occurs

abdominal

pain. Jaundice,

ing, and hepatic

failure

(Budd-Chiari with ascites,

syndrome) hepatomegaly,

portal hypertension,

also are features

is unand

variceal bleed-

of this disorder

[41].

The causes of hepatic venous thrombosis include hypercoagulable states (polycythemia, leukemia, malignant tumors, or use of oral contraceptive pills) and mechanical obstruction (tumors or congenital webs), but up to two thirds of cases have no known cause [41 ]. The diagnosis is difficult to confirm and usually requires some combination of scintigraphy, CT, sonography,

MR imaging,

angiography,

and biopsy

for proof.

The CT descriptions of this disorder have largely focused on the markedly abnormal pattern of hepatic enhancement, with dense early enhancement of the caudate lobe and portions of the left lobe [30, 41 42]. In one report of four cases, three patients had thrombosis of intrahepatic branches of the portal ,

vein, and one of those

patients

had extensive

thrombosis

of

the main portal, splenic, and superior mesenteric veins [30]. As hepatic transplantation is now offered as one therapeutic option

in these

excluded cates

patients,

because

or precludes

Pancreatic

portal

occlusion

venous

thrombosis

must

be

of the main portal vein compli-

transplantation

[43].

Cancer

and during

shunts due to cirrhosis, along with portal venous compression or thrombosis. Abnormalities seen on unenhanced scans reflect local changes due to edema, glycogen depletion, and fatty infiltration, whereas abnormal enhancement during the bolus phase of contrast enhancement reflects changes in both arterial and portal flow (Fig. 3) [1 3, 25, 31 32]. It is important to recognize these flow abnormalities, because they may lead to an overestimation of the size of the tumor and to selection of an inappropriate location for biopsy. Finally, it must be stressed that patients with cirrhosis and portal hypertension without hepatoma may have portal venous thrombosis,

FRANCIS

portion

of the

Pancreatic

cancer

frequently

becomes

clinically

apparent

at

an advanced, sion,

unresectable stage owing to local tumor extencontiguous organ invasion, metastases to lymph nodes

or liver, peritoneal carcinomatosis, In a series of 1 59 patients with

and vascular involvement. proved pancreatic cancer

[44], obstruction of the splenic vein with associated varices was present in 54 patients, and the superior mesenteric vein was obstructed

in 1 5 cases.

In this study,

CT and angiography

produced similar results in a vessel-to-vessel analysis for vascular encasement or occlusion. When all indicators of unresectability (arterial and venous involvement, local extension, and hepatic metastases) were used, 42 cases deemed unresectable by CT were proved unresectable at the time of surgery, whereas only three of nine cases judged resectable

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AJR:159,

October

CT OF PORTAL

1992

by CT were found to be resectable at surgery. Palliative biliary bypass did not improve the length of survival of patients with unresectable lesions. The authors conclude that angiography is not necessary for preoperative assessment and that CT alone is adequate for selecting patients for attempted resection [44]. CT can show extension of splenic or portal venous thrombosis from the pancreatic tumor with or without cavernous transformation (Fig. 6) or arterial and portal venous encasement without thrombosis (Fig. 12).

Pancreatitis Pancreatitis in any form (acute, chronic, or complicated by abscess or pseudocyst) can have vascular complications, including portal, superior mesenteric, or splenic venous occlusion and formation of a pseudoaneurysm [2, 5, 10, 21 22, 45, 46]. Venous occlusions are most likely due to spasm, stasis, intimal damage, and mass effect [2]. The splenic vein is very vulnerable to the effects of pancreatic inflammation because it is in direct contact with the body and tail of the pancreas over much of its course. In patients with pancreatitis, the direct visualization of a thrombosed splenic vein by CT may be difficult because of obliteration of retroperitoneal soft-tissue planes by inflammation, but the indirect evidence of splenic venous occlusion provided by the recognition of collateral flow through short gastric and gastroepiploic collateral vessels may be helpful [2]. Splenic venous occlusion can lead to bleeding gastric varices, and the differentiation of splenic venous occlusion from portal hypertension as the ,

underlying cause is critical for selecting the appropriate surgical procedure to stop bleeding. Splenectomy usually cures bleeding from splenic venous occlusion, while a more complex

procedure required

such as the formation of a portosystemic bleeding due to portal hypertension

to stop

shunt is [2].

VENOUS

OCCLUSION

Miscellaneous

725

Disorders

A wide variety of entities are occasionally seen in association with portal, splenic, or superior mesenteric venous thrombosis. Various forms of coagulopathy, including protein C deficiency, excessive factor VIII administration, and oral contraceptive use have been reported as causes of portal thrombosis [10, 49]. Although portal venous thrombosis can complicate any abdominal surgery, it is most commonly seen after splenectomy [7-9]. Hepatic arterial thrombosis is more common than portal venous thrombosis after liver transplantation [43].

Conclusions Imaging of portal venous occlusions has been discussed in terms of the appearance of the occluded segment, the manifestations of occlusion in the development of collateral venous pathways, and the diseases that commonly lead to portal venous obstruction. The liver is affected by variations in portal venous flow, and CT scans in such patients reflect both metabolic changes and alterations in contrast enhancement. CT arterial portography is a sensitive method to show abnormalities in hepatic enhancement because this technique delivers contrast medium solely through the portal vein. Currently, Doppler sonography and CT are the main noninvasive imaging tools used for the detection of thrombosis of the mesenteric vasculature. However, MR is being used more often for this purpose [52-55] and also has been shown to be sensitive to hepatic parenchymal changes due to portal blood flow [56]. MR techniques are being developed to allow quantitative as well as qualitative assessment of portal venous flow.

REFERENCES 1 . Foley WD. Dynamic hepatic CT. Radiology 1989;170:617-622 2. Mam CS, Glazer GM, Williams DM, Francis IR. CT-angiographic

Septic

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a sign of intrahepatic

portal

CT of portal venous occlusion.

Thrombosis of a portion of the portal venous system can be directly imaged by contrast-enhanced CT as a low-attenuation lesion within the involved por...
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