10. Preview of “Portal Hypertension Imaging”

5/19/2018 10. Preview of Portal Hypertension Imaging

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9/8/14 11:00 AMPortal Hypertension Imaging

Page 1 of 28http://emedicine.medscape.com/article/372708-overview#a19

Portal Hypertension Imaging

Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR; Chief Editor: Kyung J Cho, MD, FACR more...

Updated: Aug 7, 2013

Overview

In portal hypertension imaging, ultrasound techniques such as duplex ultrasonography or spectral Doppler imagingand color Doppler imaging or power Doppler imaging are the modalities of choice, because they are noninvasive,rapid, and highly sensitive and specific.

Portal hypertension (PH) represents an increase of the hydrostatic pressure within the portal vein or its tributaries.It is defined as an increase in the pressure gradient between the portal vein and hepatic veins or the inferior venacava (IVC) (see the images below).

Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient withcirrhosis, these are suggestive of esophageal varices.

Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.

Most patients with venous PH have intrinsic liver disease. In PH, blood that normally flows through the liver isdiverted into systemic veins because of increased resistance to portal venous flow. This diversion of portal venous

blood occurs via exiting portosystemic communications (eg, the coronary vein) and the opening of embryonicchannels (eg, paraumbilical veins). The most common portosystemic anastomosis is via the coronary-gastroesophageal route; it occurs in 80-90% of patients and gives rise to lower esophageal and gastric varices.

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Hematemesis resulting from bleeding esophageal varices is the most common presentation in patients with PH,although some patients seek medical help because of decompensated liver disease. Findings from duplexultrasonography (US) and color Doppler imaging (CDI), MRI, CT, and endoscopy may support the diagnosis of PH.

Preferred examination

Plain radiographs are not often obtained in cases of portal hypertension, but because most hospitalized patientsundergo chest radiography, radiologists need to be aware of abnormalities that may be found in patients with PH.

The appearance of calcification in the distribution of the portal vein on a plain abdominal radiograph may indicatePH. An upper GI tract barium series is often performed for the detection of esophageal varices (see the imagesbelow).

Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal foldsand multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.

Endoscopic findings in a 47-year-old man with a history of polycythemia rubra vera who had a recent episode of hematemesis.Endoscopy showed a normal esophagus, but multiple polypoid submucosal lesions were seen in the fundus and body of the stomach).The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

Part of an upper gastrointestinal tract barium series (same patient as in the previous image) shows multiple polypoid filling defectswithin the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.

US techniques such as duplex US or spectral Doppler imaging and CDI or power Doppler imaging are themodalities of choice in the evaluation of the liver and PH. These techniques are noninvasive, rapid, and highlysensitive and specific.

Angiographic techniques such as splenosportography (SP), transhepatic portography, transumbilicalcatheterization, transjugular catheterization, wedge hepatic venography, and arterial portography are invasive.However, they are much more specific for the evaluation of PH hypertension; they are indicated when definitivesurgery or radiologic intervention is contemplated.

The use of angiographic techniques is declining because noninvasive imaging techniques such as US, CT,

computed tomographic angiography (CTA), and magnetic resonance angiography (MRA) are now available. Thesetechniques are quickly improving, and this will lead to further decline in the use of angiographic methods.

S leno orto ra h and transumbilical catheterization are rarel erformed. Arterial orto ra h indirect
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portography) and wedge hepatic venography with manometry is indicated before surgical portacaval shuntplacement.

Carbon dioxide wedge hepatic venography is the most commonly used method for visualizing the portal veinbefore portal vein puncture for a transjugular intrahepatic portosystemic shunt (TIPS) procedure. TIPS is aradiology-guided creation of a shunt between the portal and hepatic veins in the liver by use of a percutaneoustransjugular approach. Because of its proven safety and effectiveness, TIPS has largely replaced surgical

decompressive shunt procedures.[1, 2, 3]

Transient elastography (TE) is a new technique used as a noninvasive method to study portal hypertension inchronic liver disease, with variable results. Shi et al in a meta-analysis studied the performance of TE for detectionof significant portal hypertension, esophageal varices, and large esophageal varices. The analysis revealed thatTE could be used as a good screening tool for significant portal hypertension but had only moderate diagnostic

utility for the prediction of esophageal varices or large esophageal varices.[4]

Idiopathic portal hypertension (IPH) is frequently misdiagnosed as cryptogenic cirrhosis. Seijo et al studied 39patients retrospectively to determine whether hepatic vein catheterization and liver stiffness measurements candifferentiate IPH from noncirrhotic portal vein thrombosis. Patients with IPH frequently have hepatic vein-to-veincommunications, despite signs of portal hypertension, and lower mean hepatic venous pressure gradient and liverstiffness values much lower than the cut-off for clinical significant portal hypertension in those with cirrhosis. Thus,

when these signs occur, it is obligatory that IPH is ruled out.[5]

Limitations of techniques

Plain radiographs are usually not indicated for patients with portal hypertension. Most plain radiographs areobtained for other reasons, and signs of PH are detected incidentally. Therefore, plain radiographs are of limitedvalue.

Duplex US is a sensitive technique for the detection of PH in addition to other important features. When respiratoryvariation in the size of the portal, splenic, and superior mesenteric veins does not occur or when it is less than20%, PH may be diagnosed with a sensitivity of 80% and a specificity of 100%.

In cases involving bleeding varices that are unresponsive to endoscopic sclerotherapy or when intractable ascites

are present, a TIPS procedure is indicated. TIPS is performed after portal vein patency is documented at duplexUS.

Radiography

Plain radiographic findings

Calcification may be seen in the portal vein after prolonged portal hypertension and may occur within athrombosed portal vein. The calcification is linear or strandlike, and it typically lies transversely across the upperabdomen, or it slopes upward and obliquely toward the liver hilum.

Generalized increase in the liver opacity may be seen in patients with hemochromatosis. Although this may be

demonstrated by measuring the liver attenuation on CT scans, it rarely is demonstrable on plain abdominalradiographs.

Esophageal varices appear as lobulated posterior mediastinal masses in 58% of patients. Silhouetting of thedescending aorta and an abnormal convex contour of the azygos-esophageal recess are further signs of portalhypertension (PH) that may be shown on plain radiographs. Signs of underlying liver disease may be noted, suchas splenomegaly and ascites.

Portal hypertension is displayed in the radiographic images below.


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Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient withcirrhosis, these are suggestive of esophageal varices.

Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal foldsand multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.

Barium study findings of esophageal varices

Esophageal varices comprising dilated submucosal veins in the lower esophagus occur chiefly as a consequenceof PH, mostly in patients with cirrhosis. Varices appear as beaded or serpiginous translucent filling defects.

Barium study may depict 90% of esophageal varices; however, demonstration of esophageal varices on bariumexamination is highly dependent on technique. Important factors include the intravenous administration ofanticholinergic agents, use of barium paste, and examination of the esophagus in a relaxed state.

Esophageal peristalsis milks the blood out of the varices, whereas esophageal hypotonia allows the varices todistend with blood, making them easy to visualize.

A left anterior oblique projection with the patient recumbent or in the Trendelenburg position shows the varices tobest advantage. Images are obtained by use of the Valsalva maneuver and/or deep inspiration. The Valsalva

maneuver precludes swallowing and maintains the esophagus in a relaxed state. Exposure is made with theesophagus slightly underdistended. Overfilling produces distention, which may obliterate the varices.

After an acute episode of bleeding from esophageal varices, varices may collapse and become difficult to detectradiologically. Demonstration of varices in a patient with hematemesis does not necessarily establish the source asthe varices because in one third of patients, bleeding occurs from other causes, such as peptic ulcer.

Anticholinergic drugs are contraindicated in patients with a history of glaucoma, heart disease, or urinary retention.Glucagon is not useful for demonstrating esophageal varices because it lowers esophageal sphincter pressure anddoes not abolish peristalsis in the body of the esophagus.

Large esophageal varices are obvious and appear as nodular or vermiform changeable filling defects within theesophagus. Smaller varices appear as scalloped esophageal folds that are better seen on recumbent films

because they tend to disappear on upright films.

Gastric varices are seen in 278% of patients with PH. Gastric varices that occur in the absence of esophageal
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varices usually result from splenic vein thrombosis; bridging collaterals extend from the splenic hilum across thestomach to the coronary vein and then on to the portal vein.

A higher incidence of portosystemic encephalopathy is noted in patients with gastric varices. Varices in thestomach usually are confined to the gastric cardia and are difficult to recognize. The rate of detection on a bariumstudy has been reported to be 6589%.

Gastric varices usually present as a slight thickening or scalloping of the cardiac folds, but large gastric varices

presenting as large mucosal polypoid masses involving the fundus and cardia are sometimes encountered.Angiography is occasionally necessary to exclude gastric tumor. Gastric varices bleed less frequently thanesophageal varices, but when they do bleed, the hemorrhage is more severe.

Barium study findings of varices in other parts of the gastrointestinal tract

Gastric antral and duodenal varices are sometimes seen, usually in association with gastric fundal and esophagealvarices. Duodenal varices appear as lobulated filling defects on barium study and are demonstrated best with thepatient in a prone position. Internal hemorrhoids frequently are found in patients with severe PH.

In rare cases, varices involve the colon via portosystemic collaterals through the retroperitoneal veins or throughnewly formed collaterals in adhesions or scars from previous surgery. In addition, the demonstration of varices onbarium examination may include other features of PH, such as splenomegaly or ascites.

The enlarged spleen may compress the stomach and displace the splenic flexure of the colon downward. Ascitescauses a central location of the small bowel loops and separation of the colon from flank fat stripes.

Degree of confidence

Plain radiography is not sensitive in the diagnosis of portal hypertension. With good operator technique, bariumexamination may depict more than 90% of varices. The rate of detection with barium study has been reported tobe 6589%.

False positives/negatives

Other causes of calcification overlying the liver may mimic portal vein calcification. One example is hepatic arterialcalcification. Esophageal varices may occur with superior vena caval obstruction and may be seen as lobulatedposterior mediastinal masses.

An enlargement of mucosal folds may be seen with esophagitis on barium swallow, but the enlarged folds are notposition dependent and are seen equally well on upright films.

A rare neoplastic process that occasionally may be confused with varices is varicoid esophageal carcinoma.Primarily seen as a nodular fold thickening, it may be differentiated from varices by its lack of position dependence,the fact that the involvement does not extend to the lower esophagus, and the rigidity of the involved segment.

Downhill varices may occur as a result of collateral circulation extending from the superior vena cava through theesophageal plexus to the portal venous system. These varices are seen in patients with superior vena caval

obstruction usually distal to the entry of the azygos vein. They most commonly result from bronchogeniccarcinoma, mediastinal fibrosis, lymphoma, thymoma, or thyroid disease. Downhill varices may be seen only in theproximal part of the esophagus, or they may involve the entire esophagus.

Differentiation of gastric varices from gastric carcinoma may be difficult at times and may require angiography.

Computed Tomography

Computed tomography has been used to assess portal hypertension (see the images below).[6, 7, 8, 9, 10]


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CT scan through the spleen of a 43-year-old man with a known history of intravenous drug abuse and hepatitis C cirrhosis. The patientpresented to the emergency department with a sudden onset of a hypotensive episode and clinical features of hepatic encephalopathy.The scan shows splenomegaly with a dilated tortuous splenic vein/varices at the splenic hilum and free peritoneal fluid. The finaldiagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), andarterioportal shunting (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).

CT scan through the liver (same patient as in the previous image) was not of optimal quality because of patient movement, but theattenuation in the left lobe of the liver was patchy, suggestive of a mass lesion. The final diagnosis was hepatitis C cirrhosis,hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which haddeveloped inside the ruptured tumor, giving rise to severe portal hypertension).

A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum. CT wasperformed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (arrow), suggestive

of a dilated tortuous splenic vein or varices. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal veinthrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum (same patientas in the previous image). CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses atthe splenic hilum (solid arrow), suggestive of a dilated tortuous splenic vein or varices, and the origin of a large splenic vein (open
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. , ,spontaneous splenorenal shunt.

Contrast-enhanced axial CT (same patient as in the previous 2 images) shows a cavernous transformation at the porta hepatis (arrows)caused by portal vein thrombosis. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portalhypertension complicated by a spontaneous splenorenal shunt.

Contrast-enhanced axial CT scan shows a dilated left renal vein (arrow; same patient as in the previous 3 images). The final diagnosiswas hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenalshunt.

Splenomegaly and ascites are readily demonstrated. In some patients, the liver is of nonuniform attenuation. Low-attenuating components probably represent residual foci of infiltration. Often, the attenuation of a cirrhotic liver is

homogeneous and within the reference range.

In the absence of obvious abnormality of size and shape, the liver may appear entirely normal on CT scans.Nonenhanced CT is necessary for identification of confluent fibrosis when a cirrhotic liver is imaged. Confluentfibrosis is characteristically of low attenuation and tends to become isoattenuating or minimally hypoattenuatingafter the intravenous administration of contrast material. Thus, confluent fibrosis is frequently missed if onlycontrast-enhanced CT is used.

Collateral veins are occasionally seen in the peritoneal cavity, the retroperitoneum, the abdominal wall, and themediastinum. In the presence of hemochromatosis, liver attenuation is increased because of excessive iron load.As a result of poor inherent contrast between normal liver and many types of liver lesions, lesions are missed onplain CT.

The portal vein supplies 75% of blood flow to the liver; therefore, peak liver contrast enhancement occurs duringthe portal venous phase, approximately 60 seconds after the start of a bolus injection of contrast material. Withhelical CT, approximately 20 seconds is required to complete a liver examination; an image usually can beacquired in a single breath hold. The technique may be extended, and dual-phase contrast-enhanced CT scansmay be acquired. In this technique, the liver is imaged twice with a single bolus of contrast agent, first during thearterial phase and then through the portal venous phase.

Dual-phase CT is indicated for some patients with benign and malignant lesions in which vascular characteristicssuggest the correct diagnosis. Angiographically assisted CT may be used to achieve better delineation of theportal venous system and of the portal venous enhancement of the liver. An angiographic catheter is placed in thecommon celiac axis/hepatic/superior mesenteric artery by use of a modified Seldinger technique via the femoralartery.

CT scanning begins 35 seconds after the initiation of the contrast agent injection. The examination should becompleted as soon as possible, before the contrast material recirculates. To prevent significant artifacts related tothe contrast medium, 70 mL of dilute iodinated contrast agent (130%) is used, with an infusion rate of 2 mL/s.


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Although angiographically assisted CT scanning may produce elegant images, it is invasive, it is expensive, and ithas not gained widespread acceptance.

Portal vein thrombosis (PVT) may manifest as a hypoattenuating center in the portal vein surrounded by peripheralenhancement on contrast-enhanced CT. The attenuation of the portal vein is 2030 HU less than that of the aortaafter the administration of contrast material.

CT findings in BCS include inhomogeneous mottled-liver contrast enhancement with delayed enhancement in the

periphery of the liver and around the hepatic veins. The caudate lobe is enlarged and has increased contrastenhancement compared with the rest of the liver. Thrombosis within the hepatic veins and the inferior vena cava(IVC) may sometimes be identified.

CT angiography

CTA is an exciting new application of helical CT. The speed of helical CT allows the maintenance of a higherconcentration of intravenous contrast medium, particularly through the arterial enhancement phase, with thecapability of 3-dimensional reconstruction. Both peripheral intravenous injections of contrast material and CTarterial portography have been used as a basis for CTA.

CTA has shown great promise in the evaluation of hepatic vessels before liver resection. It provides preoperativesurgical information regarding the segmental location of liver tumors, the segmental venous anatomy, and

significant arterial anomalies if present. The value of CTA for patients with PH remains unclear.


A diagnosis of portal hypertension frequently is made on the basis of the demonstration of signs of cirrhosis.Splenomegaly and ascites are demonstrated readily on CT; however, CT findings in cases of cirrhosis are highlyvariable. In some patients, the liver is of nonuniform attenuation; hypoattenuating components probably representresidual foci of infiltration.

Often, the attenuation of a cirrhotic liver is homogeneous and within the reference range. In the absence ofobvious abnormalities of size and shape, the liver may appear entirely normal on CT scans. Nonenhanced CT isnecessary when the cirrhotic liver is imaged for the identification of confluent fibrosis. Confluent fibrosis

characteristically demonstrates low attenuation, which tends to become isoattenuating or minimallyhypoattenuating on CT following intravenous contrast enhancement. Thus, confluent fibrosis is frequently missed ifonly contrast-enhanced CT is used.

Collateral veins are occasionally seen in the peritoneal cavity, retroperitoneum, abdominal wall, and mediastinum.CT lacks the dynamic capability of angiography in demonstrating the exact sites of portosystemic shunts and thefeeding vessels.

False positives/negatives

In patients with cirrhosis, CT scans may appear entirely normal. Other causes of diffuse liver disease, such assplenomegaly and ascites, must be considered.

Magnetic Resonance Imaging

The vascular anatomy of the liver may be outlined by use of spin-echo and gradient-recalled echo MRI, but thesetechniques cannot demonstrate the direction of portal flow. Time-of-flight MRI with bolus tracking has been foundto be successful in imaging portal hypertension and its sequelae.

Phase-contrast sequences may be used to evaluate the portal vein, and phase-contrast cine MRA may show thedirection of portal venous flow and the presence of portal vein thrombus.

MRI evaluation of the portal venous system is accurate in demonstrating thrombosis and collateral circulation;however, MRI remains an expensive tool with limited availability.

Standard MRI findings reported in BCS include hepatic vein thrombosis, hepatic vein occlusion and narrowing,hepatomegaly, atrophy of the right lobe of the liver, and enlargement of the caudate lobe. Liver parenchyma isinhomogeneous (64%). IVC abnormalities, as demonstrated on MRI, include diffuse narrowing or focal thrombosis.


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Venous collaterals are readily shown. Liver transplantation is regarded by many as the definitive treatment for PH.Although portal vein thrombosis is no longer considered as a contraindication to liver transplantation,demonstration of a portal vein thrombus is necessary for patient care. MR is an ideal noninvasive method fordetection of portal vein thrombus. Although it is not critical, visualization of venous collaterals is useful forassessing the severity of disease. All major portosystemic collaterals may be detected by using MRA.

Comma-shaped intrahepatic varices are a characteristic finding not appreciated by other modalities. Thesecollaterals are formed in an attempt to bypass the obstructed flow.

In patients with elevated creatinine levels who cannot undergo a CT scan with intravenous contrast enhancement,MRI with gadolinium enhancement may often be performed. These contrast-enhanced images are typically breath-hold fast spoiled gradient-echo sequences, which may be dynamically obtained in both the arterial and portal

venous phases.[11, 12, 13]

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine[MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linkedto the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). Thedisease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-basedcontrast agent to enhance MRI or MRA scans.

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; jointstiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; andmuscle weakness.


MRI does not offer an advantage over CT in the diagnosis of cirrhosis; however, morphologic changes identifiedon US or CT are clearly depicted on MRI. One advantage of MRI over CT is its capacity to characterizeregenerative nodules in a cirrhotic liver. MRA may offer a noninvasive, nonoperator dependent evaluation of theportal venous system; however, the exact sensitivity and specificity still need to be determined.

Ultrasonography

Flow studies of hepatic vessels may provide important information about the hemodynamic effects of hepatic

parenchymal disease (see the images below).[14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30]

Power Doppler sonogram through the spleen shows varices at the hilum of an enlarged spleen. The final diagnosis was hepatitis Ccirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which haddeveloped inside the ruptured tumor, giving rise to severe portal hypertension).

Duplex spectral Doppler sonogram of the portal vein (same patient as in the previous image) shows a bidirectional flow within the vein.The final dia nosis was he atitis C cirrhosis, he atocellular carcinoma of the left he atic lobe which had ru tured into the eritoneum ,


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and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).

Transverse sonogram of the liver in a patient with hepatitis B cirrhosis shows a coarse echo structure of the liver.

Sagittal oblique sonogram of the liver shows a small liver with an irregular surface, moderate ascites, and a dilated portal vein. Note thethick gallbladder wall.

Sagittal oblique sonogram of the liver shows a dilated portal vein (22 mm in transverse diameter) in a patient with portal hypertension.

End-stage liver cirrhosis showing a small liver, gross ascites, and a dilated portal vein


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Doppler sample volume in portal vein reveals continuous venous flow without evidence of respiratory variation, consistent with ahypertensive portal venous system. Note the coarse liver echo structure and ascites.

Doppler sample volume in portal vein reveals bidirectional flow in the portal vein associated with portal hypertension.

Sagittal oblique sonogram of the liver shows several tubular structures at the porta hepatis resulting from cavernous transformationsecondary to portal vein thrombosis.

Duplex power Doppler sonogram shows an enlarged spleen; varices are apparent at the splenic hilum.

Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.


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Spleen in portal hypertension, with a positive splenic interface sign.

Color Doppler ultrasound showing pericholecystic varices.

Color Doppler ultrasound showing pericholecystic varices.

Peripancreatic varices as shown on power Doppler.

Peripancreatic varices as shown on power Doppler.

Peripancreatic and perihilar varices as shown on real-time scanner.


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Periportal varices on power Doppler

Periportal varices on conventional Doppler and power Doppler

Periportal varices conventional Doppler and power Doppler.

Dilatation of umbilical vein as shown on color Doppler.

Examination results are not always straightforward because the liver may move during respiration, but breathholding may facilitate the demonstration of blood flow and hepatic waveforms, particularly in the hepatic veins.

Examination is undertaken with as small an angle as possible between the axis of the US beam and the long axisof the vessel. This approach is usually straightforward because the hepatic veins course posteriorly to the inferiorvena cava (IVC), whereas the portal vein curves forward as it passes through the porta hepatis. The blood flowwaveform from the left hepatic vein frequently shows artifact caused by cardiac pulsation. Thus, when the hepaticveins are examined, the middle and right hepatic veins are usually encountered. The hepatic artery is small, andusually, it must be examined on suspended respiration.

Doppler analysis of vascular flow patterns is a valuable adjunct to real-time 2-dimensional scanning. Color-flow

analysis is a valuable means of differentiating vessels from other fluid-filled structures. Power Doppler analysis isparticularly valuable for demonstrating low flow rates in small vessels.


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, , -

index. The pulsatility index is low if the vascular bed is of low resistance and can accommodate sudden pressurewaves. A high-resistance or low-compliance vascular bed shows a high pulsatility index.

Portal vein waveforms

The portal vein typically shows continuous forward flow with minor modulation caused by respiration andtransmitted arterial pulsation. The rate of blood flow is greatest at the center of the vessel and is least at its

margins; therefore, the average flow across a segment of the vessel is used to overcome the internal variationresulting from respiration and transmitted cardiac pulsation. The time-averaged velocity usually is on the order of1214 cm/s in adults.

Flow within the portal vein changes rapidly in response to eating. Blood flow to the small bowel begins to increasewithin 2 minutes of taking the first mouthful of food. The time-averaged blood flow velocity in the portal vein mayincrease to 25 cm/s after a meal, and with minor increase in vessel diameter, the flow volume may increase 45times.

Most patients with mild hepatic parenchymal disease have normal portal venous blood flow. As hepatic diseasebecomes more severe, the first detectable flow abnormality is a reduction in the level of increase in flow seen aftera meal. Then, the splenic and superior mesenteric veins may begin to distend, and the change in vessel caliberthat is seen normally with respiration is lost. In severe hepatic parenchymal disease, portal venous blood flow is

reduced, and a rough correlation is noted between the degree of reduction in portal flow velocity and the severityof hepatic parenchymal disease (providing that studies are performed in strictly fasting patients).

As portal venous flow is compromised further, forward flow may be seen only during systole, with reversed flowoccurring during diastole. Eventually, flow within the portal vein may be reversed continuously, but the rate anddirection of flow may vary from day to day, particularly in patients with acute exacerbation of chronic liver disease.Therefore, serial examinations provide a better picture than single scans. Clearly reduced portal flow velocity isassociated with an increase in the risk of thrombosis.

Portal venous shunts

Percutaneous creation of a shunt between the portal and hepatic veins with TIPS is becoming increasinglycommon as a treatment for PH. Doppler US may be used to assess patency and show the direction of flow withinthe portal vein and shunt. If the walls of an artificial shunt prevent direct analysis of blood flow within it, an analysisof flow at the ends of the shunt usually allows adequate assessment of shunt function.

Surgically created shunts include portocaval (end or side of main portal vein to IVC), mesocaval, and splenorenalshunts (Warren shunt). Mesocaval and splenorenal shunts are used more frequently to maintain portal venouspatency for transport than for other purposes. Color Doppler imaging is valuable for the evaluation of shunts.

US evaluation of PH

The diameter of the portal vein is measured with the patient in a supine position, in quiet respiration, and havingfasted for a minimum of 4 hours. Measurements are made at the point at which the portal vein crosses the IVC. Inan individual without portal hypertension (PH), the diameter of the portal vein is 13 mm or 16 mm during deep

inspiration.

Under standard conditions, measurements greater than 13 mm indicate PH with a specificity of 100% but a lowsensitivity of 4550%. Sensitivity may be increased to 81% by measuring splenic vein and superior mesentericvein diameters. An increase of 20100% in diameter during deep inspiration is normal. An increase of less than20% is associated with PH.

The differential diagnosis of a dilated portal vein includes PH splenomegaly (whatever the cause), acute portal veinthrombosis (PVT), and postprandial increase in portal vein diameter.

Portal flow direction and velocity

Usually, blood flow in the portal vein is hepatopetal (toward the liver) during the entire cardiac cycle. The mean

velocity is 1518 cm/s and varies with cardiac cycle. In PH, velocity fluctuations disappear, resulting in continuousflow. With a further increase in portal venous pressure, the blood flow direction becomes to-and-fro (biphasic), andfinally, the direction is reversed (hepatofugal).


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Differential diagnosis of hepatofugal portal venous flow includes PH, Budd-Chiari syndrome (BCS), side-to-sideportocaval shunts, surgical or spontaneous splenorenal shunts with cirrhosis, and tricuspid regurgitation (tricuspidflow reversal). Differential diagnosis of portal venous flow reversal includes severe PH, tricuspid regurgitation, andcongestive heart failure.

The differential diagnosis of reversal of hepatofugal-to-hepatopetal portal flow includes eating and the use of drugsthat increase portal flow. Static flow without Doppler signal occurs occasionally.

Pulsatile portal vein flow

A pattern similar to that seen in patients with impaired right heart function occasionally is seen in patients withcirrhosis and/or PH. Patients with right-sided cardiac dysfunction with pulsatile portal venous flow invariably haveabnormal liver function.

The differential diagnosis of pulsatile portal venous flow includes tricuspid regurgitation, aorticright atrial fistula,fistula between the portal vein and hepatic vein, PH, and congestive heart failure. Rarely, it is a false-positivefinding.

Decreased volume flow in the portal vein

In mild to moderate PH, the volume of flow in the portal vein is maintained. A reduction in volume flow occurs withadvanced cirrhosis when intrahepatic obstruction to portal flow is severe, as indicated by hepatofugal flow andextensive portosystemic collaterals.

Congestive Index

PH may be recognized by use of the congestive index, in which the ratio of the portal vein (in units of squarecentimeter) is divided by the mean portal flow velocity (in units of centimeter per second). This ratio reflects thephysiologic changes that occur in PH (ie, portal vein dilatation associated with diminished flow velocity). Inindividuals without PH, the ratio should not exceed 0.7.

Splenomegaly

The size of the spleen is not well correlated with the level of PH; however, if splenomegaly is absent, PH isunlikely. The spleen is best measured in the coronal plane. In the midaxillary line, a cephalocaudal measurementgreater than 13 cm suggests enlargement.

Splenic interface sign

Linear reflective channels are observed in the splenic parenchyma in a variable number of patients with PH.Channels may be explained by dilatation of intrasplenic venous sinuses with increased collagen in the walls and byperiarterial fibrosis. The pathologic changes are known to occur in PH. The splenic interface sign seldom is foundin patients with splenomegaly that is unrelated to PH. The vascular nature of channels is readily confirmed byusing CDI.

Ascites

Uncomplicated PH usually does not cause ascites. Usually, ascites occurs secondary to underlying liver diseaseswith liver cell failure.

Arterialization of hepatic blood supply

Hepatic arteries are enlarged and usually have aliased frequency shifts compared with those of normal hepaticarteries. The arteries also appear tortuous. As portal venous flow to the liver decreases, arterial flow increases.Increased arterial flow occurs with the development of large collaterals and hepatopetal flow.

The differential diagnosis of an enlarged hepatic artery includes an occluded or interrupted portal vein, a surgical

portosystemic shunt, reversal of flow in the portal vein, parenteral feedings in newborns, hereditary hemorrhagictelangiectasia, cirrhosis or hepatic diseases associated with alcohol, vascular hepatic tumors, and primary hepaticartery dissection.


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Portosystemic venous collaterals

The demonstration of portosystemic venous collaterals (PVCs) is diagnostic of PH.

Umbilical venous collateral flow is an important feature of PH because it has a specificity of 100%. Typically, anartery or vein with a diameter of 2 mm may be present within the ligamentum teres. Thus, the demonstration of ablood vessel in the ligamentum teres does not equate with the presence of a PVC. The diagnosis of PVCs requires

the demonstration of venous flow away from the liver. The enlarged umbilical vein is usually solitary, originating inthe left portal vein, which courses inferiorly through the falciform ligament and along the anterior abdominal wall tothe umbilicus, seen on longitudinal or transverse scans.

The diameter of a typical coronary vein is 4 mm; a diameter greater than 7 mm is evidence of an abnormalportosystemic gradient (>10 mm Hg). Because the coronary vein may be seen in some individuals without PH, itspresence does not indicate PH. A coronary vein appears as a prominent cephalic-directed vessel that joins theportal vein near the termination of the superior mesenteric vein.

Splenosystemic collaterals may form as a result of splenic venous occlusion as well as PH. Demonstration ofsplenic venous occlusion with US is straightforward because in most patients, it is possible to trace the splenicvein to the portal vein. With splenic vein occlusion, collaterals may be identified in the pancreatic bed or thegastroesophageal area.

Tortuous short gastric and gastroesophageal veins near the upper pole of the spleen and gastroesophagealjunction are seen primarily on coronal images. Large portosystemic collaterals at the esophagogastric junction maybe mistaken for neoplastic masses if Doppler examination is omitted. Right gastric veins are cephalically directedand are seen along the inferior border of the left lobe of the liver on longitudinal scans.

Splenorenal veins are demonstrated as tortuous, inferiorly directed vessels from the splenic hilum to the leftkidney; they are primarily seen on coronal images. The left renal vein may be dilated. Retroperitonealportosystemic collaterals (varices) may mimic other masses (eg, pancreatic carcinoma or other retroperitonealtumors) on both CT and US images. CDI may show the mass to be full of flow colors; other signs of PH are oftenpresent.

Banti syndrome

Banti syndrome, or noncirrhotic idiopathic PH, is a common cause of PH in India and Japan but is rare in theUnited States and Europe. The syndrome is characterized by signs of PH, but liver function test results tend toremain normal. Hepatic wedge pressure readings are usually normal or slightly elevated. Signs of hypersplenismare often present. US shows a normal-appearing liver; patent hepatic veins; and a patent portal vein, which maybe associated with multiple portosystemic collaterals.

Portal venous thrombosis

PVT is being recognized with increasing frequency on US images. Reduced portal blood flow resulting fromhepatic parenchymal disease and abdominal sepsis are the primary causes. Transient PVT is also beingrecognized with increasing frequency, in part because of the large increase in the use of US in evaluating patients

with abdominal inflammation, such as appendicitis. Tumor within the portal vein may appear identical tothrombosis, but it is far less common. Tumor within the portal vein is most frequently related to a hepatocellularcarcinoma, which gives rise to serpiginous filling defects in the portal venous luminal flow, but it usually persistsaround the tumor without complete occlusion.

Adults with acute PVT secondary to abdominal sepsis completely recover with vessel recanalization aftersuccessful treatment of underlying sepsis. In children, the portal vein may recanalize by developing multiple smallcollateral channels, which are seen as a partly echogenic band of small vessels running to the porta hepatis.These show reduced flow velocity of 27 cm/s. Nonvisualization of the portal vein is strongly suggestive ofocclusion. Then, the portal vein may be seen as a band of high-level echoes at the porta hepatis.

Causes of PVT include idiopathic causes, malignancy (hepatocellular carcinoma, cholangiocarcinoma, pancreaticcarcinoma, and stomach carcinoma), trauma (which may be iatrogenic, such as umbilical vein catheterization), and

abdominal sepsis (pancreatitis, perinatal sepsis, omphalitis, appendicitis, diverticulitis, cirrhosis), especially inyounger individuals.


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, .

Conversely, patent vessels may show increased intraluminal echogenicity because of artifact or erythrocyterouleaux formation. In isolation, increased or decreased echogenicity in the lumen of the portal vein is not sufficientto make a diagnosis of PVT or to exclude PVT. In patients with PVT, the venous flow signal that is typicallyobtained from the lumen of the portal vein during pulsed or color-flow Doppler imaging is absent, and flow may beseen around a thrombus that partially occludes the vein. However, if flow is sluggish, the Doppler signal may notbe detected. Color flow may be demonstrated in other small collaterals.

Incomplete occlusion (common in neoplastic invasion) or thrombolytic recanalization may occur. These cannot bedifferentiated by use of US. Hepatopetal flow may be demonstrated, and spontaneous shunts may be visualized(splenorenal).

US may demonstrate portosystemic collaterals, and the cause may be identified, such as hepatocellularcarcinoma, metastases, cirrhosis, and pancreatic neoplasms. The incidence of PVT is reported to be low inpatients with PH, but it is associated with sclerotherapy. The string sign, or thickening of the portal vein withnarrowing of its lumen, which is interpreted as a portal phlebitis, is considered a precursor of PVT in patients withacute pancreatitis. The portal vein thrombus may become calcified.

Cavernous transformation of the portal vein

Cavernous transformation occurs in patients with long-standing PVT (19%) when numerous multiple collateral

vessels develop around the occluded portal vein; these collateral vessels appear as vermiform tubular structuresat the porta hepatis. Application of color-pulsed Doppler imaging shows blood flow in the periportal collateralsaround the thrombosed portal vein. Cavernous transformation of the portal vein has been reported to appear as asubhepatic spongelike mass. This appearance also has been reported in patients with pancreatichemangiosarcoma.

Bile duct varices, also called the pseudocholangiocarcinoma sign, are not infrequently observed during endoscopicretrograde cholangiopancreatography. In patients with PH, they result from cavernous transformation of the portalvein. Studies report that the sign may disappear after a TIPS procedure.

Assessment of TIPS

TIPS involves the percutaneous placement of a shunt via the jugular vein. TIPS is becoming popular as a definitiveprocedure for decompressing the portal venous system or as a prelude to liver transplantation.

Doppler US is a sensitive and relatively specific means of evaluating TIPS malfunction. US evaluation of the shuntis usually performed within 24 hours after shunt placement to establish baseline velocities within the portal vein,hepatic vein, and shunt. Follow-up studies are usually performed at 3-month intervals unless the clinical settingdictates a more emergent examination. The primary object of Doppler study of a TIPS is to document flow in theshunt and to demonstrate stenosis. The accuracy of Doppler US in shunt malfunction depends on several USparameters, which include the peak shunt velocity, distal shunt velocity, and antegrade flow in the left and rightportal veins.

Flow velocities in the portal vein may double in comparison with the preoperative velocities in a successful TIPSplacement. Direct observation of shunt thrombosis is possible with duplex or color Doppler US. Echo-enhanced

color Doppler US may also be helpful in the assessment of TIPS.

Complications of TIPS that are detectable with US include early complications and delayed complications.

Early complications

Intraperitoneal hemorrhageShunt thrombosisNeck hematomaCompromise of hepatic blood supply: PVT, hepatic artery occlusion, hepatic infarctionFailed stent deployment: inadequate stent expansion, stent migration, stent fractureBiliary obstruction

Delayed complications

Shunt stenosis: pseudointimal hyperplasia, hepatic vein stenosis


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The demonstration of portosystemic shunts is a specific sign of portal hypertension. Umbilical vein collateral flow isan important feature of PH because it has a specificity of 100%. In individuals without PH, the caliber of portal,splenic, and superior mesenteric veins shows significant variation during respiration. When respiratory variationdoes not occur or when it is slight (< 20%), PH may be diagnosed with a sensitivity of 80% and a specificity of100%. A portal vein diameter greater than 13 mm is specific for PH, but it is not a sensitive indicator of PH.

False positive and negatives include the following:

The differential diagnosis of a dilated portal vein includes PH splenomegaly (of any cause), acute PVT, andpostprandial increase in portal vein diameter.The differential diagnosis of portal vein flow reversal includes severe PH, tricuspid regurgitation, andcongestive heart failure.The differential diagnosis of reversal of hepatofugal-to-hepatopetal portal flow includes eating and the useof drugs that increase portal flow. Static flow without Doppler signal occurs occasionally.The differential diagnosis of pulsatile portal vein flow includes tricuspid regurgitation, aorticright atrialfistula, fistula between the portal vein and hepatic vein, PH, and congestive heart failure. Rarely, it may be afalse-positive finding.Uncomplicated PH usually does not cause ascites. Usually, ascites occurs secondary to underlying liver

diseases with liver cell failure.The differential diagnosis of an enlarged hepatic artery includes an occluded or interrupted portal vein; asurgical portosystemic shunt; reversal of flow in the portal vein; parenteral feeding in newborns; hereditaryhemorrhagic telangiectasia; cirrhosis or hepatic diseases associated with alcohol; vascular hepatic tumors;and primary hepatic artery dissection.

Angiography

Angiographic evaluation of the portal venous system may be performed (see the images below).

Venous phase of a digital subtraction celiac-axis angiogram shows no splenic vein, but multiple collateral venous pathways are seenthrough the stomach wall (straight arrows), which feed a normal portal vein (curved arrows). Several varices are noted within the body

of the stomach. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

Venous phase of a digital subtraction superior mesenteric angiogram (same patient as in the previous image) shows a normal portalvein (PV) with no streaming effect from splenic venous flow (arrow), suggestive of splenic vein thrombosis. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.


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Digital subtraction selective common hepatic artery angiogram shows immediate filling of the portal venous radicles in the left lobe ofthe liver (straight arrow) and early filling of portal vein (curved arrow), suggestive of hepatic arterial-portal vein fistula. The finaldiagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), andportoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).

Delayed venous phase of a selective common hepatic angiogram (same patient as in the previous image) shows the portal vein (P),with filling of the coronary vein caused by retrograde flow feeding gastric and lower esophageal varices (arrows). Retrograde flow inenlarged umbilical veins also is seen. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe(which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severeportal hypertension).

Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in the previous 2 images) showsretrograde flow into the coronary vein (curved arrow) and the inferior mesenteric vein (straight arrow). Note the flow defect of the distalportal vein caused by retrograde flow (open arrowhead). The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of theleft hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor,giving rise to severe portal hypertension).


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Conventional angiogram of the superior mesenteric artery shows a replaced hepatic artery in the right lobe of the liver in a patient with aprevious history of abdominal tuberculosis and a recent history of hematemesis. Note the multiple calcific foci in the splenic region as aresult of old healed tuberculous granulomas. Two previous liver biopsies had not revealed the changes of cirrhosis. The final diagnosiswas tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, andesophageal and gastric varices.

Venous phase of a superior mesenteric angiogram shows a stenosis of the portal vein near the porta hepatis with poststenoticaneurysmal dilatation of the portal vein. Filling of the gastric varices and the splenic vein are seen as a result of retrograde flow (samepatient as in the previous image). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal veinstenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow(same patient as in the previous 2 images). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causingportal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

Line diagram of findings on portal venous phase angiogram (same patient as in the previous 3 images). The superior mesenteric veinhas been added for anatomic clarity. The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal veinstenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.


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Venous phase of digital subtraction superior mesenteric angiogram shows the portal vein to be reduced to a threadlike structure(arrow). Retrograde flow into the splenic vein (S) is seen. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal veinthrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

Venous phase of a digital subtraction superior mesenteric angiogram shows a shunt between the splenic vein (S) and the left renal vein(R), and the IVC (V) is outlined with contrast material. Arrows mark the tiny threadlike portal vein (same patient as in the previousimage). The final diagnosis was hepatocellular carcinoma (not shown), cirrhosis, and portal vein thrombosis/portal hypertensioncomplicated by a spontaneous splenorenal shunt.

Splenoportography

Because of the use of alternative imaging methods, the use of splenoportography (SP) has declined considerablyafter having played a primary role in the investigation of cirrhosis and PH for several years. However, restrictedindications remain for the procedure. Even with the available methods of direct or indirect visualization of the portalvein, much of the information necessary to evaluate cirrhosis or PH may be obtained by use of SP (see the imagesbelow).

Splenoportogram in a patient with known alcoholic cirrhosis and two episodes of variceal bleeding in the past. The procedure wasperformed as a prelude to surgical portosystemic shunt placement. The splenoportogram shows a dilated coronary vein (CV) feedingthe lower esophageal and gastric varices (arrows). Retrograde filling of the inferior mesenteric vein (I) is present, but the main portalvein flow is hepatopetal in direction.


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Digital subtraction splenoportogram in a patient with portal hypertension shows a subcapsular contrast leak (arrows), which is a knowncomplication of splenoportography.

Splenoportogram in a 3-year-old child with a history of serious febrile illness in infancy and recent hematemesis. Splenoportogramshows a thrombosed distal portal vein and a cavernous malformation at the porta hepatis (C). The arrow marks gastric and esophagealvarices. The inferior mesenteric vein is outlined because of reverse flow (I).

Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow(same patient as in the previous 2 images). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causingportal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

Splenic pulp measurement provides an accurate reflection of the portal venous pressure, both in hepatic andprehepatic causes of PH. An intravenous injection of radiographic contrast medium into the splenic pulp outlinesthe portosystemic collaterals (ie, splenic and portal veins); it demonstrates well the intrahepatic portal radicles andenables an assessment of the rapidity of washout of the vessels in a hepatopetal direction. With reversal of flowwithin the portal vein resulting from severe PH, the splenic and portal veins are not visualized; the contrast outflowtract is via gastroesophageal collaterals. With splenic thrombosis/PVT, not only is the site of the obstructionevident but also portal-portal collateral veins, which regularly develop, are demonstrated as well.

Contraindications to SP include coagulation defects, platelet count less than 50,000, ascites, an uncooperative

patient, and splenic pathology (splenic mass lesions). To perform SP, the skin over the left side of the thorax andabdomen overlaying the spleen is prepared with an antiseptic after the spleen is localized. Historically, the spleenwas localized by use of fluoroscopy and palpation and percussion, but currently, localization is more commonly


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. ,

tissues are infiltrated with local anesthetic down to the peritoneum.

The entry site of the needle usually is the 9th or 10th intercostal space in the midaxillary line. The needle isdirected in a cephalic direction toward the splenic hilum. A nick is made at the site of the needle puncture, and atrack is made into the soft tissues with a 12-gauge needle, which facilitates the placement of the SP needle. TheSP needle is a 14-gauge, 6-inch-long polyethylene sheathed needle. With patient breath hold in mid respiration,the sheathed needle is introduced toward the direction of the splenic hilum, and the stilette is withdrawn, leaving

the sheath in place. The patient is instructed to take shallow respirations during the examination.

If the spleen has been entered accurately, blood flows back via the sheath. Then, the sheath is connected to aspinal pressure manometer filled with saline, and the splenic pulp pressure is measured. The sheath is taped tothe patient's side, and a test injection is made using 5 mL of contrast medium. When a sheath is placed correctly,contrast medium spreads into the splenic parenchyma, providing an uneven splenogram that rapidly drains into thesplenic vein. With a subcapsular placement, the contrast agent is viewed as a homogeneous collection thatspreads slightly as the agent is injected.

With subcapsular injection, the needle is withdrawn completely, and a fresh attempt is made to place the needlecorrectly. With the sheath correctly placed, a pump injection is performed using 40 mL of 75% contrast at a rate of10 mL/s. The injection is usually painless; discomfort and shoulder pain may occur with subcapsular injection. Afterthe procedure is complete, the needle tract is plugged with thromboembolic material, such as Gelfoam or Ivalon.

Complications of the procedure include hemorrhage, contrast agent extravasation, puncture of other organs,splenic hematomas, and capsular rupture. Capsular rupture may require emergency laparotomy and splenectomy.In addition to splenectomy, splenic artery embolization may be used to stop bleeding.

Indications for SP include the following:

Patency of the splenic vein is uncertain.Arterioportography has been unsuccessful.Portal pressure is required and other techniques have failed.A more accurate imaging of the intrahepatic portal veins is required (eg, when phlebosclerosis issuggested).

In PH, the following findings may be noted with SP:

Tributary collaterals usually feed into the portal venous system and develop hepatofugal flow associatedwith elongation, tortuosity, and an increase in lumen size. The coronary and short gastric veins lead to thegastroesophageal plexus and then to the hemiazygos and azygos systems and into the superior vena cava.The dilated veins in the esophageal submucosa that form varices may be outlined by contrastenhancement. The inferior mesenteric vein serves as another collateral, which may be demonstrated byreverse flow. Outflow is through the superior mesenteric vein via the retroperitoneum into the IVC.Abdominal surgery promotes the development of portosystemic shunts via adhesions.Embryonic collaterals are no longer used under normal conditions, but they retain a potential lumen. Inresponse to PH, these vessels open, dilate, and become elongated, tortuous, and beaded. They directportal centrifugal flow. The paraumbilical collaterals are the only vessels in this group that commonly

participate in the centrifugal flow. They communicate with the inferior or superior epigastric veins.Watershed collaterals are usually tiny vessels that form communications between the portal and systemiccirculations. They have virtually no blood flow. With an increase in the pressure gradient on either side, asoccurs with PH or as a temporary result of the injection of contrast medium, significant flow occurs in thedirection of the pressure gradient. With prolonged PH, the channels open permanently, dilate, elongate, andbecome tortuous. Splenorenal collaterals are the most common watershed collaterals; they may opacifywith left adrenal and renal vein injections. Gastrorenal collaterals that also connect the splenic vein with theleft adrenal and renal veins may opacify on rare occasions. Rarely, communications between the spleen,inferior phrenic vein, and left adrenal and renal veins are seen. Splenoretroperitoneal collaterals feed intothe lumbar venous plexus and may communicate with intercostal veins. Unnamed collaterals frequently areobserved.Bridging collaterals with extrahepatic portal/splenic venous obstruction occur to preserve hepatopetal flow.With occlusion of the splenic vein, hepatopetal flow occurs via the short gastric veins into the coronary vein

and then on to the portal vein. Some flow also occurs via the gastroepiploic vein into the superiormesenteric vein. When the portal vein is occluded close to the hilum, bridging collaterals form a cavernomaor run parallel to the occluded portal vein. Numerous capsular vessels opacify the liver surface and feed the


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per p era por a ranc es.

Intrahepatic portal vein changes depend on the severity of the cirrhotic process. Transit time of the contrastagent through the liver is diminished. In the early stages of cirrhosis, portal vein branches appear crowdedbut later are reduced in number. Portal radicles appear tortuous with abrupt caliber changes.Occlusion/thrombosis of the portal vein is well demonstrated. A thrombotic plaque may be seen within theportal vein; this plaque should not be confused with nonopacified blood flowing in from the superiormesenteric vein. Note that nonopacification of the portal vein on SP does not necessarily mean that theportal vein is occluded; in severe hepatofugal flow, the portal vein may fail to opacify.

Carbon dioxide SP

Carbon dioxide has been employed as a contrast agent for SP; a 22- or 25-gauge needle is used (therebyexploiting the low viscosity of the gas). This technique is less traumatic than others, and it has been effective invisualizing the portal venous system. The hope is that the difference in the collateral venous filling patterns issignificant, because carbon dioxide fills veins in the nondependent sites, whereas contrast material flows along thedependent sites. Contrast-enhanced SP has been infrequently used in the United States.

Transhepatic portography

With percutaneous transhepatic portography (PTP), the same technique is used as with percutaneous

cholangiography. The portal vein is punctured directly and is replaced by a guidewire/catheter, and contrastmaterial is injected into the splenic vein and/or the superior mesenteric vein, depending on the clinical setting. PTPis an easy and quick procedure. As a result of the straight course of the catheter through the liver substance,catheterization of several tributaries is possible, but the distance between the cutaneous entrance of the catheterand the liver makes catheter manipulation difficult. The few reported complications mostly result from nontargetorgan puncture (gallbladder, pleura) and intra-abdominal hemorrhage. With US guidance, the incidence ofnontarget organ puncture is expected to decrease.

Transcatheter obliteration of esophageal varices with various embolic agents is possible via transhepatic catheterplacement, but this is not a procedure to be followed by suitable surgical procedure. Transcatheter obliterationshould not be used as an elective procedure; even in an acute setting, hemostasis is best attempted with othermethods.

Transumbilical catheterization

Transumbilical catheterization requires a surgical procedure in which a transverse incision is made 35 cm abovethe umbilicus, and the umbilical vein is catheterized. Complications are few, but the procedure is difficult and timeconsuming. With so many noninvasive procedures currently available, the procedure is seldom indicated.

Transjugular catheterization

The transjugular approach to the portal vein first was described by Rsch et al in 1969. Since then, the techniquehas improved; currently, it is used more for therapeutic applications, such as the establishment of a TIPS.

Wedged hepatic venography

When a catheter is placed in a small hepatic vein via the inferior vena cava (IVC) or jugular vein, pressures may bemeasured either with a transducer or with a saline manometer. In patients with sinusoidal or postsinusoidal portalvenous obstruction, as occurs in cases of cirrhosis, pressure measured in this way accurately reflects the totalportal pressure. The wedged hepatic venous pressure is the same as the splenic pulp pressure measured by useof SP. Normal portal pressure levels measured in this way are 40150 mm of saline. Pressures above 150 mm ofsaline indicate PH.

Two components contribute to PH. The first is intrahepatic resistance to portal venous flow, and the second istransmitted pressure from the IVC. In addition, IVC pressures are measured, and the corrected sinusoidal pressureis derived by subtracting the IVC pressure from the wedged hepatic pressure. The corrected sinusoidal pressure isuseful clinically because it reflects the true status of the liver disease responsible for development of portosystemic

shunts and variceal bleeding. Corrected sinusoidal pressure readings of as high as 100 mm of saline areconsidered normal.

Although corrected sinusoidal pressure makes the most significant contribution to variceal bleeding in patients with


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c rr os s, t e tota pressure usua y contr utes to ee ng rom esop agea var ces. us, a pat ent w t ot

cirrhosis and congestive heart failure may bleed from esophageal varices because of a temporary increase incentral venous pressure; conversely, esophageal bleeding may cease when the central venous pressuredecreases. Typically, patients with cirrhosis do not bleed from varices with portal venous pressures of 200250mm of saline. Patients with cirrhosis who bleed at pressures lower than 200 mm of saline almost always bleedfrom an alternative source.

Arterial portography

Arterial portography (AP) is currently the preferred method of evaluating the portal venous system because it isless invasive and has a lower complication rate. AP involves the indirect opacification of the portal venous systemwith the injection of contrast material into the celiac axis (delayed images outline the splenic, gastric, and portalveins) or into the superior mesenteric artery (outlining superior mesenteric and portal veins).

The 3 major indications for AP include the following:

To perform workup in patients with PH and its sequelae, particularly when surgical treatment is planned.To determine the resectability of hepatic and pancreatic tumors when both arterial- and venous-phaseangiograms make significant contributions.To perform transcatheter embolization, as in islet cell tumor metastases and carcinoid metastases, or to

perform chemoembolization, as in hepatocellular carcinoma (demonstration of a patent portal vein is aprerequisite for these treatments).

Preparation and contraindications for AP are identical to those of standard conventional angiography. Selectivecatheters are used to cannulate the appropriate artery. In a superior mesenteric artery injection, the tip of thecatheter is placed such that it opacifies all the branches with contrast medium. Before delivery of the contrastagent, administration of a vasodilator (tolazoline, papaverine, nitroglycerin) improves opacification of the portalvein. Manual or digital subtraction imaging improves resolution. If digital subtraction is used, administration of ananticholinergic drug before filming reduces bowel movement. Left gastric artery injection consistently demonstratesesophageal varices.

AP findings in PH include the following:

Arterial-phase findings: pancreatic carcinoma, hepatocellular carcinoma, pancreatitisVenous-phase findings: splenic vein thrombosis, superior mesenteric vein thrombosis, portal veinthrombosis, collateral channels


Splenoportography (SP) is a fairly accurate method of outlining the portal venous system and the portosystemiccommunications for patients with portal hypertension; for this, SP remains the criterion standard. Diagnosticmodalities such as US, CT, and MRI have reduced the diagnostic importance of arteriography. The major role ofangiography is in mapping the vascular anatomy before surgery and in guiding the transcatheter treatment of livertumors. In celiac-axis and superior angiography, the venous phase provides sufficient detail to render directportography unnecessary in most patients.

Contributor Information and DisclosuresAuthorAli Nawaz Khan, MBBS, FRCS, FRCP, FRCR Consultant Radiologist and Honorary Professor, NorthManchester General Hospital Pennine Acute NHS Trust, UK

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR is a member of the following medical societies:AmericanAssociation for the Advancement of Science,American Institute of Ultrasound in Medicine, British MedicalAssociation, British Society of Interventional Radiology, Royal College of Physicians, Royal College ofPhysicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons ofEngland

Disclosure: Nothing to disclose.

Coauthor(s)Murad Ali, MBBS, PhD, DTCD Consulting Radiologist, Department of Radiology, Postgraduate Medical
http://www.rcseng.ac.uk/http://www.rcr.ac.uk/http://www.rcpsus.com/http://www.rcplondon.ac.uk/http://www.bma.org.uk/ap.nsf/content/splashpagehttp://www.aium.org/http://www.aaas.org/


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nst tute, a y ea ng osp ta , a stan


Specialty Editor BoardEric P Weinberg, MD Associate Professor, Department of Radiology, University of Rochester Medical Center,Strong Memorial Hospital

Eric P Weinberg, MD is a member of the following medical societies:American College of Radiology,AmericanRoentgen Ray Society, and Radiological Society of North America


Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, HuttValley District Health Board, New Zealand


George Hartnell, MBChB Professor of Radiology, Tufts University School of Medicine; Director ofCardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center

George Hartnell, MBChB is a member of the following medical societies:American College of Cardiology,American College of Radiology,American Heart Association,Association of University Radiologists, BritishInstitute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society ofNorth America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular andInterventional Radiology


Robert M Krasny, MD Resolution Imaging Medical Corporation

Robert M Krasny, MD is a member of the following medical societies:American Roentgen Ray SocietyandRadiological Society of North America


Chief EditorKyung J Cho, MD, FACR William Martel Professor of Radiology, Interventional Radiology Fellowship Director,University of Michigan Health System

Kyung J Cho, MD, FACR is a member of the following medical societies:American College of Radiology,American Heart Association,American Medical Association,American Roentgen Ray Society,Association ofUniversity Radiologists, and Radiological Society of North America


Additional ContributorsThe authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authorsSumaira MacDonald, MBChB, PhD, MRCP, FRCR, and David Sherlock, MBBS, FRCS,to the development andwriting of this article.

References

1. Mergo PJ, Ros PR. Imaging of diffuse liver disease. Radiol Clin North Am. Mar 1998;36(2):365-75.[Medline].

2. Murakami T, Mochizuki K, Nakamura H. Imaging evaluation of the cirrhotic liver. Semin Liver Dis. May2001;21(2):213-24. [Medline].

3. Parvey HR, Raval B, Sandler CM. Portal vein thrombosis: imaging findings.AJR Am J Roentgenol. Jan1994;162(1):77-81. [Medline].
http://reference.medscape.com/medline/abstract/8273695http://reference.medscape.com/medline/abstract/11436573http://reference.medscape.com/medline/abstract/9520988http://www.rsna.org/http://www.aur.org/http://www.arrs.org/http://www.ama-assn.org/http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.acr.org/http://www.rsna.org/http://www.arrs.org/http://www.scvir.org/http://www.rcr.ac.uk/http://www.rcplondon.ac.uk/http://www.rsna.org/http://www.massmed.org/AM/Template.cfm?Section=Homehttp://www.bma.org.uk/ap.nsf/content/splashpagehttp://www.bir.org.uk/http://www.aur.org/http://www.americanheart.org/presenter.jhtml?identifier=1200000http://www.acr.org/http://www.acc.org/http://www.rsna.org/http://www.arrs.org/http://www.acr.org/


27/28



4. Shi KQ, Fan YC, Pan ZZ, Lin XF, Liu WY, Chen YP, et al. Transient elastography: a meta-analysis of

diagnostic accuracy in evaluation of portal hypertension in chronic liver disease. Liver Int. Jan2013;33(1):62-71. [Medline].

5. Seijo S, Reverter E, Miquel R, Berzigotti A, Abraldes JG, Bosch J, et al. Role of hepatic veincatheterisation and transient elastography in the diagnosis of idiopathic portal hypertension. Dig Liver Dis.Oct 2012;44(10):855-60. [Medline].

6. Henseler KP, Pozniak MA, Lee FT Jr, Winter TC 3rd. Three-dimensional CT angiography of spontaneousportosystemic shunts. Radiographics. May-Jun 2001;21(3):691-704. [Medline].

7. Mitchell DG, Nazarian LN. Hepatic vascular diseases: CT and MRI. Semin Ultrasound CT MR. Feb1995;16(1):49-68. [Medline].

8. Winter TC 3rd, Nghiem HV, Schmiedl UP, Freeny PC. CT angiography of the visceral vessels. SeminUltrasound CT MR. Aug 1996;17(4):339-51. [Medline].

9. Zhao LQ, He W, Chen G. Characteristics of paraesophageal varices: A study with 64-row multidetectorcomputed tomograghy portal venography. World J Gastroenterol. Sep 14 2008;14(34):5331-5. [Medline].

10. Ulu EM, Kirbas I, Emiroglu FK, Cakir B, Harman A, Bakar C, et al. Multidetector CT findings of splenic

artery aneurysm in children with chronic liver disease. Pediatr Radiol. Oct 2008;38(10):1095-8. [Medline].

11. Kim M, Mitchell DG, Ito K. Portosystemic collaterals of the upper abdomen: review of anatomy anddemonstration on MR imaging.Abdom Imaging. Sep-Oct 2000;25(5):462-70. [Medline].

12. Nghiem HV, Winter TC, Schmiedl UP, Freeny PC. MR angiography of the portal venous system. SeminUltrasound CT MR. Aug 1996;17(4):360-73. [Medline].

13. Spritzer CE. Vascular diseases and MR angiography of the liver. Magn Reson Imaging Clin N Am. May1997;5(2):377-96. [Medline].

14. Bolognesi M, Sacerdoti D, Merkel C, et al. Noninvasive grading of the severity of portal hypertension incirrhotic patients by echo-color-Doppler. Ultrasound Med Biol. Jul 2001;27(7):901-7. [Medline].

15. Colli A, Cocciolo M, Riva C, et al. Abnormalities of Doppler waveform of the hepatic veins in patients withchronic liver disease: correlation with histologic findings.AJR Am J Roentgenol. Apr 1994;162(4):833-7.[Medline].

16. Grant EG. Doppler imaging of the liver. Ultrasound Q. 1992;10:117-54.

17. Kedar RP, Merchant SA, Malde HH, Patel VH. Multiple reflective channels in the spleen: a sonographicsign of portal hypertension.Abdom Imaging. Sep-Oct 1994;19(5):453-8. [Medline].

18. Koslin DB, Mulligan SA, Berland LL. Duplex assessment of the portal venous system. Semin UltrasoundCT MR. Feb 1992;13(1):22-33. [Medline].

19. Millener P, Grant EG, Rose S, et al. Color Doppler imaging findings in patients with Budd-Chiarisyndrome: correlation with venographic findings.AJR Am J Roentgenol. Aug 1993;161(2):307-12.[Medline].

20. Nelson RC, Sherbourne GM, Spencer HB, Chezmar JL. Splenic venous flow exceeding portal venousflow at Doppler sonography: relationship to portosystemic varices.AJR Am J Roentgenol. Sep1993;161(3):563-7. [Medline].

21. Piscaglia F, Donati G, Serra C, et al. Value of splanchnic Doppler ultrasound in the diagnosis of portalhypertension. Ultrasound Med Biol. Jul 2001;27(7):893-9. [Medline].

22. Ralls PW. Color Doppler sonography of the hepatic artery and portal venous system.AJR Am JRoentgenol. Sep 1990;155(3):517-25. [Medline].

23. Ralls PW, Mack LA. Spectral and color Doppler sonography. Semin Ultrasound CT MR. Oct1992;13(5):355-66. [Medline].
http://reference.medscape.com/medline/abstract/1419140http://reference.medscape.com/medline/abstract/2117348http://reference.medscape.com/medline/abstract/11476921http://reference.medscape.com/medline/abstract/8352105http://reference.medscape.com/medline/abstract/8333368http://reference.medscape.com/medline/abstract/1562346http://reference.medscape.com/medline/abstract/7950827http://reference.medscape.com/medline/abstract/8141001http://reference.medscape.com/medline/abstract/11476922http://reference.medscape.com/medline/abstract/9113681http://reference.medscape.com/medline/abstract/8858775http://reference.medscape.com/medline/abstract/10931979http://reference.medscape.com/medline/abstract/18712376http://reference.medscape.com/medline/abstract/18785288http://reference.medscape.com/medline/abstract/8858773http://reference.medscape.com/medline/abstract/7718282http://reference.medscape.com/medline/abstract/11353116http://reference.medscape.com/medline/abstract/22721839http://reference.medscape.com/medline/abstract/22973991


28/28



. - , , - , .blood flow detected by color Doppler sonography in two patients with hematologic diseases and

splenomegaly. J Clin Ultrasound. Jun 2001;29(5):294-7. [Medline].

25. Tessler FN, Mitchell E, Siskin T. Sonography of the transjugular intrahepatic portosystemic shunt.Ultrasound Q. 1998;14(3):165-70.

26. Zwiebel WJ. Sonographic diagnosis of hepatic vascular disorders. Semin Ultrasound CT MR. Feb1995;16(1):34-48. [Medline].

27. McKiernan PJ, Sharif K, Gupte GL. The role of endoscopic ultrasound for evaluating portal hypertensionin children being assessed for intestinal transplantation. Transplantation. Nov 27 2008;86(10):1470-3.[Medline].

28. Pan JJ, Chen C, Geller B, Firpi R, Machicao VI, Caridi JG, et al. Is sonographic surveillance ofpolytetrafluoroethylene-covered transjugular intrahepatic portosystemic shunts (TIPS) necessary? Asingle centre experience comparing both types of stents. Clin Radiol. Oct 2008;63(10):1142-8. [Medline].

29. Morgan J, Sadler MA, Siegel S. US, CT, and MR imaging of hepatic masses in Alstrm syndrome: a casereport. Clin Imaging. Sep-Oct 2008;32(5):393-5. [Medline].

30. Goyal AK, Pokharna DS, Sharma SK. Ultrasonic measurements of portal vasculature in diagnosis of

portal hypertension. A controversial subject reviewed. J Ultrasound Med. Jan 1990;9(1):45-8. [Medline].

Medscape Reference 2011 WebMD, LLC
http://reference.medscape.com/medline/abstract/2404133http://reference.medscape.com/medline/abstract/18760729http://reference.medscape.com/medline/abstract/18774362http://reference.medscape.com/medline/abstract/19034020http://reference.medscape.com/medline/abstract/7718281http://reference.medscape.com/medline/abstract/11486325

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