Liver Sonography by Duplex and Color Doppler Author



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Liver Sonography by Duplex and Color Doppler


Author: Sharlene A. Teefey, M.D.


Objectives: Upon the completion of this CME article, the reader will be able to:

1. List the etiologies of portal hypertension and describe the Doppler sonographic findings associated with this disorder.

2. Describe the collateral vessels that may be seen sonographically in patients with portal hypertension.

3. List the etiologies of portal vein thrombosis and describe the Doppler sonographic findings associated with this disorder.

4. List the etiologies of Budd-Chiari Syndrome and describe the Doppler sonographic findings associated with this disorder.


Introduction

The liver is the largest intra-abdominal organ in the human body and it is unique in that it has a duel blood supply, the hepatic artery and the portal vein. On average, approximately two fifths of the blood flow into the liver is from the hepatic artery and three fifths is from the portal vein. The portal vein is the major venous return from the intestines (therefore, the venous blood from the intestines must pass through the liver before it enters the systemic circulation).

Upon entering the liver, both the hepatic artery and the portal vein branch into smaller vessels that eventually become capillaries. As the blood begins to exit the liver, these capillaries become venules and eventually form the hepatic veins that enter the inferior vena cava with blood flow back to the heart. In most circumstances, there are three main hepatic veins, the left, middle and right.


Liver Doppler Technique

Liver Doppler should be performed using a sector or curved array transducer with a frequency raging between 2 to 6 MHz, depending on the patient’s body habitus. The scan should also be performed after an overnight fast to limit the amount of bowel gas in the region of the porta hepatis. When evaluating the portal venous system, the main portal vein as well as the right and left portal veins and their respective branches should be evaluated for patency and flow direction. The right and main portal veins are imaged best through an intercostal approach with the patient turned slightly to the left. The transducer should be angled obliquely and placed slightly laterally along the axis of a lower rib. An attempt should also be made to visualize the right and main portal veins from a subcostal approach, but frequently, this approach cannot be used due to overlying bowel gas. Because the left portal vein runs in an anterior direction, it is best visualized with the patient supine and with deep inspiration. The probe should be oriented in a parasagittal plane in the sub-xiphoid region.

The hepatic venous system is best visualized with the patient supine or turned slightly to the left (at end-expiration if possible), especially if Doppler waveforms are to be obtained. Because of the superior location of the hepatic veins, deep inspiration may be necessary to improve visualization when using color Doppler. The left hepatic vein can best be visualized with the transducer in a sub-xiphoid location in a longitudinal plane. Transverse subcostal or slightly oblique images obtained more laterally or through an intercostal space will be useful when visualizing the middle and right hepatic veins. When visualizing the hepatic venous system, an effort should be made to show the communication of the hepatic veins with the inferior vena cava, especially in patients in whom the diagnosis of Budd-Chiari Syndrome is suspected.


Portal Hypertension

Cirrhosis is the most important cause of portal hypertension in the Western world. The best way to think of “portal hypertension” is to understand what creates portal pressure. Portal pressure is the product of portal venous flow and resistance to flow. The causes of portal hypertension can be categorized based on this formula. Etiologies causing primary increased flow include arterioportal fistula (which may be congenital, post-traumatic, atherosclerotic, or due to erosion of a hepatic artery aneurysm into the portal vein) and splenomegaly (for example, due to myelofibrosis). The better-known category of primary increased resistance is traditionally divided into pre-hepatic, intra-hepatic, and post-hepatic causes. Pre-hepatic causes include portal or splenic vein thrombosis and extrinsic compression of the portal vein. Intra-hepatic causes are based on the location of the increased resistance, that is, presinusoidal, sinusoidal/mixed, or post sinusoidal. Presinusoidal causes of portal hypertension include parasitic infections (such as schistosomiasis), sarcoidosis, myeloproliferative diseases, primary biliary cirrhosis, primary sclerosing cholangitis, and certain toxins. Sinusoidal causes include alcoholic hepatitis/cirrhosis and cryptogenic cirrhosis (cause unknown). Post-sinusoidal causes include veno-occlusive disease and hepatic vein obstruction (such as Budd-Chiari syndrome). Post-hepatic causes of portal hypertension include constrictive pericarditis, inferior vena cava obstruction, and severe right heart failure/tricuspid insufficiency.

Before discussing the sonographic findings in patients with portal hypertension, it is important to recall the gross and histopathologic changes that occur in patients with cirrhosis. Using alcoholic cirrhosis as a model, classic changes include hepatocyte necrosis, nodular regeneration, and the formation of fibrotic septae. Alcohol can also induce hepatocyte enlargement by stimulating intracellular fat and protein deposition that compresses the sinusoids and obstructs flow. Likewise, collagen deposition occurs in the sinusoids, which also increases resistance to portal venous flow. An abnormal imbalance of vasodilators and vasoconstrictors also contributes to portal hypertension. When resistance to portal venous flow increases beyond a pressure gradient of ≥ 12 mm of Hg, portosystemic collaterals develop, which diverts some of the portal venous blood flow. In an effort to compensate for the decreased portal venous flow, hepatic artery flow increases. In patients with advanced end-stage liver disease, hepatic artery flow may be diverted through the sinusoids to the portal vein producing hepatofugal flow (which is flow retrograde through the portal venous system).

There are several sonographic changes that can be detected in the portal vein, hepatic artery, and hepatic veins in patients with portal hypertension. Within the portal vein, flow may be hepatofugal (either within the right or left branch or the main portal vein), bi-directional (alternating hepatopetal or flow toward the liver and hepatofugal or flow away from the liver), or static in which the flow is too slow to be detected with color Doppler sonography (figure 1). In cases where no flow is detected, it is important not to misdiagnose portal vein thrombosis. The hepatic artery is often enlarged and tortuous with high peak systolic and diastolic velocities. This occurs in the setting of advanced cirrhosis and decreased portal vein flow. There are also changes within the hepatic veins. The waveform frequently has a monophasic appearance with loss of the “a” wave, and low amplitude “D” and “S” waves. This is thought to be due to increased resistance to transmission of right atrial pressure changes secondary to focal hepatic vein stenoses.

An important and specific sonographic finding in patients with portal hypertension is the presence of portosystemic collaterals. Collaterals may be classified as either tributary collaterals, that is, normally existing collaterals or developed collaterals, which are normally closed channels that open in the setting of portal hypertension. Normally existing collaterals include the coronary (left gastric), short gastric, superior mesenteric, and inferior mesenteric veins (figure 2). Because of improvements in technology, the coronary vein can be seen in some normal patients, however, its diameter should be  6 mm and flow should be hepatopetal (towards the liver). When flow is hepatofugal (away from the liver) patients are at increased risk for a variceal bleed.

Normally closed portosystemic collaterals that may open in the setting of portal hypertension include the paraumbilical vein, spleno-renal collaterals, and spleno-retroperitoneal collaterals. In patients with portal hypertension, a re-canalized paraumbilical vein will extend beyond the anterior liver surface and show hepatofugal venous flow. Spleno-renal shunts can often be identified with the patient in a right lateral decubitus position. If the shunt itself cannot be visualized, high velocities in the left renal vein would be an indirect sign of such a shunt.


Portal Vein Thrombosis

There are many causes of portal vein thrombosis including hypercoagulable states (such as anti-phospholipid antibody syndrome, protein S deficiency, protein C deficiency, and antithrombin II deficiency), myeloproliferative diseases, birth control pill usage, polycythemia vera, and sickle cell anemia. Inflammatory causes include inflammatory bowel disease, Behcet’s disease, and pancreatitis. Infectious diseases such as appendicitis and diverticulitis can rarely cause portal vein thrombosis. Medical or surgical interventions to treat neoplasms of the liver also have been shown to cause portal vein thrombosis such as chemo-embolization, alcohol injection, and partial hepatectomy. Portal vein thrombosis also occurs in patients undergoing liver transplant, sclerotherapy, and transjugular intrahepatic portosystemic shunting (TIPS) placement. Miscellaneous causes include cirrhosis, hepatocellular carcinoma, and trauma.

At sonography, portal vein thrombus may appear echogenic, isoechoic, or anechoic, and may be obstructive or non-obstructive (figure 3). At color Doppler, there will be no detectable flow or partial flow if the thrombus is non-occlusive. It is important to always examine the vessels with gray scale before performing color Doppler so as not to miss a subtle non-occlusive thrombus.

When a portal vein thrombus is present, it is important to distinguish benign from malignant thrombosis. The presence of a hepatofugal arterial signal within the thrombus is very specific for a malignant thrombus and is due to tumor vessels growing into the portal vein. However, this finding is not always seen.

Cavernous transformation is a sequela of portal vein thrombosis and implies the formation of porto-portal collaterals in the setting of acquired, benign portal vein thrombosis (figure 4). It seldom occurs in patients with hepatocellular carcinoma. It can develop as early as 6 to 20 days after the thrombotic event. Collateral vessels are thought to originate from paracholedochal (bile duct wall) veins, periportal veins originating from around the pancreatic head, the blood vessels of the portal vein wall, or re-canalization of the portal vein itself. Color Doppler findings include non-visualization of the extrahepatic portal vein and/or its branches with the formation of innumerable periportal collateral vessels. These vessels frequently extend intrahepatically around the thrombosed portal vein branches. Doppler analysis shows a portal vein-like waveform. Patients with portal vein thrombosis and cavernous transformation not only develop portosystemic collaterals, (most commonly a left coronary vein or perisplenic veins), but also develop porto-portal collaterals. Reversed flow may also develop in a patent portal vein branch to supply an area with portal vein thrombosis. Pericholecystic veins may also develop to supply the posterior aspect of the right lobe of the liver.


Budd-Chiari Syndrome

Budd-Chiari syndrome (thrombosis of the hepatic veins) has multiple etiologies, but recently, has been classified into primary and secondary types. The primary type has further been divided into two categories, intrahepatic hepatic vein thrombosis and inferior vena cava thrombosis (hepatic portion). This latter category was previously referred to as membranous obstruction of the inferior vena cava. Recently, researchers have suggested that membranous obstruction of the inferior vena cava is an acquired rather than a congenital phenomenon, thought to be due to the formation of thrombus within the intrahepatic portion of the inferior vena cava. These two categories of Budd-Chiari syndrome are distinctly different from one another. Hepatic vein thrombosis is common in developed Western countries but inferior vena cava thrombosis is more common in underdeveloped countries such as Nepal, China, South Africa, India, and Japan.

Common etiologies for intrahepatic hepatic vein thrombosis include hypercoagulable states (such as anti-phospholipid antibody syndrome, protein S deficiency, protein C deficiency, and antithrombin III deficiency) and myeloproliferative diseases. Inflammatory diseases such as Behcet’s syndrome or inflammatory bowel disease may also cause Budd- Chiari Syndrome. Inferior vena cava thrombosis, which may be caused by hypercoagulable states in many cases, is as yet of unknown cause. One recent theory proposes that compression of the inferior vena cava during diaphragm motion induces thrombus formation.

Secondary causes of Budd-Chiari Syndrome include compression or mechanical obstruction of the hepatic veins from a neoplasm (hepatocellular, adrenal, and renal cell carcinoma), an abscess, or hydatid cyst.

At sonography in the acute setting, a thrombus may be visible in the hepatic veins and may be obstructive or non-obstructive (figure 5). Again, it is important to examine the hepatic veins initially with gray scale sonography. Stenoses may also be observed, but typically, no collateral vessels are seen. When chronic, the hepatic veins may not be visualized and multiple intrahepatic collateral vessels may be seen (between a patent and an occluded hepatic vein, or between an occluded vein and a tortuous, developed collateral). Subcapsular and extrahepatic collaterals can also develop in the setting of chronic Budd-Chiari syndrome. It is also important to examine the caudate lobe of the liver, which frequently has enlarged veins that drain directly to the inferior vena cava in an attempt to decompress the liver. At color Doppler, there may be no detectable flow within the hepatic vein, or reversed flow when a proximal obstruction is present. The waveform is also monophasic.


Figures

1 Portal hypertension with slow hepatofugal flow in the main portal vein

2 Portal hypertension with coronary vein showing hepatofugal flow

3 Non-occlusive thrombus with porto-splenic confluence

4 Cavernous transformation of the main portal vein

5 Budd Chiari Syndrome with thrombosis of the right hepatic vein


References or Suggested Reading:

1. Teefey SA, Hildeboldt CC, Dehdashti F, et al. Detection of primary hepatic malignancy in liver transplant candidates: prospective comparisonof CT, MR imaging US, and PET. Radiology. 2003;226:533-42.

2. Rydzewski B, Dehdashti F, Gordon BA, Teefey SA, et al. Usefulness of intraoperative sonography for revealing hepatic metastases from colorectal cancer in patients selected for surgery after undergoing FDG PET. Am J Roentgenol 2002;178:353-8.

3. Ralls PW. Color Doppler Sonography of the Hepatic Artery and Portal Venous System. Radiology 1990; 155: 517-525.

4. Lorenz J, Winsberg F. Focal Hepatic Vein Stenoses in Diffuse Liver Disease. JUM 1996; 15: 313-316.

5. Wachsberg RH, Simmons MA. Coronary Vein Diameter and Flow Direction in Patients with Portal Hypertension: Evaluation with Duplex Sonography and Correlation with Variceal Bleeding. AJR 1994; 162: 637-641.

6. Wachsberg RH, Obolevich AT. Blood Flow Characteristics of Vessels in the Ligamentum Teres Fissure at Color Doppler Sonography: Findings in Healthy Volunteers and in Patients with Portal Hypertension. AJR 1995; 164: 1403-1405

7. Pozniak M; Baus K. Hepatofugal Arterial Signal in the Main Portal Vein: An Indicator of Intravascular tumor Spreas. Radiology 1991; 180: 663-666.

8. Dodd GD; Memel DS, Baron RL, Eichner L, Santiguida LA. Portal Vein Thrombosis in Patients with Cirrhosis: Does Sonographic Detection of Intrathrombus Flow Allow Differentiation of Benign and Malignant Thrombus? AJR 1995; 165: 573-577.

9. DeGaetano AM, Lafortune M, Patriquin H, De Franco A, Aubin B, Paradis K. Cavernous Transformation of the Portal Vein: Paterns of Intrahepatic and Splanchnic Collateral Circulation Dertected with Doppler Sonography. AJR 1995; 165: 1151-1155.

10. Okuda K, Kage M, Shrestha SM. Proposal of a New Nomenclature for Budd-Chiari Syndrome: Hepatic Vein Thrombosis Versus Thrombosis of the Inferior Vena Cava at Its Hepatic Portion. Hepatology 1998; 28: 1191-1198.

11. Hosoki T; Kuroda C, Tokunaga K, Marukawa T, Masuike M, Kozuka T. Hepatic Venous Outflow Obstruction: Evaluation with Pulsed Duplex Sonography. Radiology 1989; 170: 733-737.

12. Kane R, Eustace S. Diagnosis of Budd-Chiari Syndrome: Comparison between Sonography and MR Angiography. Radiology 1995; 195: 117-121.

13. Lin EC. Peri-stent vascular channels after transjugular intrahepatic portosystemic shunt placement for Budd-Chiari syndrome: CT and US findings. Abdom Imaging 2001;26:191-3.

14. Killi RM. Doppler sonography of the native liver. Eur J Radiol 1999;32:21-35.

15. Chawla Y, Kumar S, Dhiman RK, et al. Duplex Doppler sonography in patients with Budd-Chiari syndrome. J Gastroenterol Hepatol 1999;14:904-7.

16. Naganuma H, Ishida H, Konno K, et al. Intrahepatic venous collaterals. Abdom Imaging 1998;23:166-71.


About the Author

Sharlene A. Teefey, M.D. is currently an Associate Professor of Radiology at the Mallinckrodt Institute of Radiology at Washington University School of Medicine in St. Louis Missouri. She is a member of numerous societies and organizations including the American College of Radiology, the Society of Radiologists in Ultrasound, and the American Institute of Ultrasound in Medicine.

She is a reviewer of manuscripts for Radiology, the American Journal of Roentgenology, and Radiographics. She has more than 45 publications in peer review medical journals and has been a speaker at numerous institutions and conferences across the country.


Examination:

1. On average, approximately ______ of the blood flow into the liver is from the from the portal vein.

A. one fifth

B. one third

C. two fifths

D. three fifths

E. three fourths


2. When evaluating the portal venous system, the right and main portal veins are imaged best through

A. a subcostal approach with the patient supine

B. a subcostal approach with the patient turned slightly to the right

C. the sub-xiphoid region with the patient turned slightly to the left

D. the sub-xiphoid region with the patient supine

E. an intercostal approach with the patient turned slightly to the left


3. When evaluating the hepatic venous system, the left hepatic vein can best be visualized with the transducer in

A. an intercostal location with the patient turned slightly to the left

B. a subcostal location with the patient turned slightly to the left

C. a sub-xiphoid location in a longitudinal plane

D. an intercostal location with the patient turned slightly to the right

E. a subcostal location with the patient turned slightly to the right


4. _______ is the most important cause of portal hypertension in the Western world.

A. Alcoholism

B. Renal Failure

C. Cirrhosis

D. Sarcoidosis

E. Diabetes


5. All of the following are etiologies that cause a primary increased flow due to an arterioportal fistula EXCEPT

A. post-traumatic

B. splenomegaly

C. congenital

D. erosion of a hepatic artery aneurysm into the portal vein

E. atherosclerotic


6. An example of a pre-hepatic cause for portal hypertension is

A. splenic vein thrombosis

B. schistosomiasis

C. right heart failure

D. alcoholic hepatitis/cirrhosis

E. sarcoidosis


7. Regarding intra-hepatic causes for portal hypertension, an example of a sinusoidal cause is

A. parasitic infections (such as schistosomiasis)

B. sarcoidosis

C. hepatic vein obstruction

D. primary sclerosing cholangitis

E. alcoholic hepatitis/cirrhosis


8. An example of a post-hepatic cause for portal hypertension is

A. myeloproliferative diseases

B. alcoholic hepatitis/cirrhosis

C. primary sclerosing cholangitis

D. right heart failure

E. splenic vein thrombosis


9. When resistance to portal venous flow increases beyond a pressure gradient of _____, portosystemic collaterals develop.

A. > 8 mmHg

B. > 12 mmHg

C. > 16 mmHg

D. > 20 mmHg

E. > 24 mmHg


10. When imaging patients that have portal hypertension, in cases where no flow is detected by color Doppler sonography, it is important not to misdiagnose

A. portal vein thrombosis

B. metastatic cancer within the liver

C. hepatocellular carcinoma

D. hepatic vein thrombosis

E. renal vein thrombosis


11. An important and specific sonographic finding in patients with portal hypertension is the presence of

A. coronary vein thrombosis

B. hepatofugal flow in the hepatic artery

C. portosystemic collaterals

D. hepatopetal flow in the splenic vein

E. portal vein thrombosis


12. In patients with portal hypertension, normally existing collaterals include all of the following veins EXCEPT

A. coronary

B. paraumbilical

C. inferior mesenteric

D. short gastric

E. superior mesenteric


13. Because of improvements in technology, the coronary vein can be seen in some normal patients, however, its diameter should be

A.  6 mm and flow should be hepatofugal

B.  6 mm and flow should be hepatopetal

C.  6 mm and flow should be bi-directional

D. > 6 mm and flow should be hepatofugal

E. > 6 mm and flow should be hepatopetal


14. In patients with portal hypertension, high velocities in the left renal vein would be an indirect sign of which of the following shunts

A. porto-portal

B. spleno-retroperitoneal

C. paraumbilical

D. spleno-renal

E. hepato-adrenal


15. An example of an inflammatory cause of portal vein thrombosis would be

A. anti-phospholipid antibody syndrome

B. antithrombin II deficiency

C. hepatocellular carcinoma

D. polycythemia vera

E. pancreatitis


16. If a thrombus is identified within the portal vein, the presence of ________ within the thrombus is very specific for a malignant thrombus.

A. a monophasic waveform

B. a bi-directional flow

C. an absence of flow

D. low amplitude “D” and “S” waves

E. a hepatofugal arterial signal


17. Patients with portal vein thrombosis and cavernous transformation not only develop portosystemic collaterals, but also develop ________ collaterals.

A. porto-portal

B. hepato-adrenal

C. paracholedochal

D. spleno-renal

E. paraumbilical


18. The type of Budd-Chiari syndrome that is more common in underdeveloped countries such as Nepal, China, South Africa, India, and Japan is

A. inferior vena cava thrombosis

B. compression of the hepatic veins from a neoplasm

C. mechanical obstruction of the hepatic veins

D. compression of the hepatic veins from an abscess

E. hepatic vein thrombosis


19. All of the following are examples of secondary causes of Budd-Chiari Syndrome EXCEPT

A. compression of the hepatic veins by hepatocellular carcinoma

B. mechanical obstruction of the hepatic veins by an abscess

C. hepatic vein thrombosis caused by protein S deficiency

D. compression of the hepatic veins by renal cell carcinoma

E. mechanical obstruction of the hepatic veins from a hydatid cyst.


20. When scanning a patient in the setting of chronic Budd-Chiari syndrome, it is also important to examine the ________ of the liver, which frequently has enlarged veins that drain directly to the inferior vena cava.

A. portal vein portion

B. left lobe

C. right lobe

D. caudate lobe

E. hepatic artery portion



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