Vascular imaging and interventional procedures in hepatic cirrhosis

Vascular imaging and interventional procedures in hepatic cirrhosis

Vascular Imaging and I n t e r v e n t i o n a l Procedures in Hepatic Cirrhosis Elena Lonjedo and Tomas Ripoll6s Changes in the vascularization of th...

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Vascular Imaging and I n t e r v e n t i o n a l Procedures in Hepatic Cirrhosis Elena Lonjedo and Tomas Ripoll6s Changes in the vascularization of the cirrhotic liver are related to the progression of the disease. Knowledge of normal hepatic vascular anatomy and anatomic is essential for understanding the altered hepatic circulation seen in cirrhosis. We analyze the changes in liver perfusion with special interest in the anatomic features that are important in interventional procedures. The indications, technical notes, and complications of transjugular liver biopsy, transjugular intrahepatic portosystemic shunt (TIPS), and embolization of hepatocellular carcinoma, are reviewed.

Copyright 2002, Elsevier Science (USA). All rights reserved.

HE OBJECTIVES of imaging techniques in hepatic cirrhosis are to detect portal hypertension, diagnose early hepatocellular carcinoma (HCC), and follow-up the results of different therapeutic options in cirrhotic patients. Radiologists must know the pathophysiology and the natural history of cirrhosis because several changes in vascularization caused by the progression of the disease have been described. TM The angiographic appearance in cirrhosis is related to the progressive fibrosis that accompanies this disorder, as well as increased blood flow through the hepatic artery. Cirrhosis produces a typical appearance of the peripheral hepatic artery branches. One must always be alert to the possibility of superimposed HCC in cirrhotic livers. These tumors are usually hypervascular lesions with arteriovenous shunting. 1 One of the first angiographic signs of portal hypertension is the development of extrahepatic portosystemic collaterals. Selective angiographic studies in the splanchnic circulation are the usual invasive methods for evaluating the portal venous system. Complementary morphologic and hemodynamic information can be provided by selective transhepatic catheterization of the portal vein.~'5'6 Noninvasive methods are commonly used in the diagnoses of morphologic changes related to cirrhosis. Invasive procedures are indicated in only those few instances in which interventional proce-

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From the Department of Radiology, Doctor Peset University Hospital, Valencia, Spain. Address reprint requests to Elena Lonjedo, MD, PhD, Secci6n de Radiologfa vascular e intervencionista, Servicio de Radiolog£a, Hospital Universitario Dr. Peset, C/Gaspar Aguilar, 90 46017 Valencia, Spain; e-mail: [email protected] Copyright 2002, Elsevier Science (USA). All rights"reserved. 0887-2171/02/2301-0008535.00/0 do# l O.lO53/sult.2002.29797 130

dures are required. Nevertheless, if we analyze the different aspects of the hepatic arterial and venous systems in normal and in cirrhotic patients, we can better understand the behavior of the liver in different imaging techniques. In this article we review the anatomy of the hepatic arterial and venous systems and the particular changes that occur with the progression of chronic liver disease. The role of the interventional radiologist in patients with cirrhosis is very important, not only for diagnostic purposes such as transjugular liver biopsy (TLB) or hemodynamic studies in portal hypertension, but especially for performing therapeutic options, such as the transjugular intrahepatic portosystemic shunt (TIPS), or the palliative treatment in HCC. HEPATIC VASCULARIZATION: ANATOMY, ANATOMIC VARIATIONS, AND CIRRHOTIC CHANGES

To understand the behavior of the liver as seen on different imaging techniques, and to properly perform interventional procedures, it is necessary to know the hepatic vascular anatomy and its normal variants. There is considerable normal variation in the size, morphology, and vascularization of the liver.

Hepatic Arteries The hepatic artery arises from the celiac trunk, which is an anterior main branch of the aorta located at the T 12-L1 interspace. The main hepatic artery divides intrahepatically into right and left branches. An accessory or replaced right hepatic artery is a variant that occurs in 12% to 25% of individuals. The replaced hepatic artery arises from either the celiac axis or the superior mesenteric artery (Fig 1) and passes posterior to the portal vein and posterolateral to the bile duct, within the hepatoduodenal ligament, to reach the liver hilium.

Seminars in Ultrasound, CT, and MR/, Vol 23, No 1 (February), 2002: pp 130-140

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Fig 1. Hepatic and portal angiogram. (A) Superior mesenteric artery injection showing the hepatic artery (arrow) during the arterial phase. (B) The portal vein (arrow) is visualized during the venous phase.

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A replaced left hepatic artery occurs in approximately 10% of individuals. This vessel arises from the left gastric artery, courses to the gastrohepatic ligament through the fissure for ligament venosum, and then into the umbilical fissure to supply the left lobe of the liver] The arteriographic appearance of the cirrhotic liver depends on the amount of liver volume loss. The balance between arterial and portal blood flow to the liver is altered in cirrhosis, with an increase in hepatic arterial perfusion and decreased portal blood flow. In the fibrotic, contracted, cirrhotic liver, the intrahepatic branches of the hepatic artery exhibit a characteristic corkscrew tortuosity (Fig 2). There is a correlation between the disorganization of the parenchymal architecture and distortion of the vascular tree. Hepatic arterial-venous shunting is present in cirrhosis and is shown during hepatic arteriography. 1

Hepatic Venous System Three main hepatic veins, right, middle, and left, flow into the inferior vena cava (IVC) within 1 cm of the diaphragm and 2 cm below the right atrium. Additional hepatic veins, variable in number, may drain into the lower aspect of the intrahepatic vena cava. The right hepatic vein drains directly into the

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Fig 3. Right hepatic venogram obtained after transjugular liver biopsy.The needle tract (arrow) is visible, but there is no extravasation of contrast.

vena cava, whereas the middle and left hepatic veins usually form a common trunk before entering the vena cava. The right hepatic vein is the largest of the three and is the most commonly used for interventional procedures, such as TIPS and TLB (Fig 3). Variations of hepatic artery anatomy occur in more than 30% of individuals, s The most common variant consists of multiple or supernumerary large branches of the main hepatic veins. In cirrhosis, there are several changes in the hepatic vein appearance. As a result of fibrosis, there is attenuation of the peripheral branches and enlargement of the central trunks, resulting in a characteristic pruned-tree appearance (Fig 4). As the right lobe atrophies, the angle with which the right hepatic vein intersects the IVC becomes more acute, making its catheterization difficult. Intrahepatic venous collaterals communicating with the hepatic veins can be observed in cirrhosis, but may also be associated with other pathologic processes, such as the Budd-Chiari syndrome and IVC obstruction. 3

Portal Venous System

Fig 2. Hepatic artery angiogram showing the characteristic corkscrew pattern of advanced cirrhosis.

The main portal vein arises from the union of the superior mesenteric vein and the splenic vein at about the TI2 or L1 level (Fig 5). The portal vein courses to the right and enters the liver at the porta hepatis, together with the hepatic artery and the common bile duct (Fig 1). All three structures are surrounded by a layer of fascia and, just distal to the porta hepatis, they are covered by the liver parenchyma. The main portal vein divides into

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Fig 4. Narrowing of the peripheral hepatic vein branches typical of cirrhosis. (Selective right hepatic venogram,)

fight and left branches to supply the corresponding lobes of the liver. Knowledge of the location of the portal vein bifurcation relative to the liver capsule is essential in performing the TIPS procedure. The

Fig 5. Portography after selective injection of contrast in the superior mesenteric artery. Arrow shows portal vein,

puncture of the portal vein in an extrahepatic location could lead to catastrophic intraperitoneai bleeding. In a recent study by Schultz et al, 9 an extrahepatic bifurcation was present in 48% of cadavers. It is important to prevent this complication by making the portal vein puncture 2 to 3 cm peripheral to the bifurcation. The umbilical vein is the terminal branch of the left portal vein. It is obliterated in normal adults and can be recanalized in patients with portal hypertension. The recanalized umbilical vein courses along the falciform ligament to the anterior abdominal wall. Variations in the intrahepatic portal venous branches occur in approximately 20% of individuals. 5 The most common variations are trifurcation of the main portal vein (10.8%), fight posterior segment arising from the main portal vein (4.7%), and right anterior segment from the left portal vein (4.3%). Portal vein variants may occur in cirrhotic patients who are pathologic in origin. The increased incidence of portal thrombosis in cirrhosis and its relation with hepatocellular carcinoma is well documented, a°

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The spatial relationships of the hepatic vessels is important in the performance of interventional procedures, and our colleagues who use other imaging techniques must be informed of every variation. In general, the right portal vein is located anterior and medial to the fight hepatic vein and is posterior and lateral to the middle hepatic vein. The main left portal vein is located inferior and medial to the left hepatic vein. 11-x3 Based on these normal anatomic features, the following three recommendations can be made: • When puncturing from the right hepatic vein to the right portal branch, the needle should be directed ventrally; • When puncturing from the fight hepatic vein to the right portal vein, the needle should be directed dorsally; and • When puncturing from the middle or the left hepatic vein to the left portal vein, ultrasound guidance may be needed. CIRRHOTIC LIVER AND PORTAL HYPERTENSION

In cirrhosis, there is destruction of the normal hepatic architecture by fibrous septa, which encompass regenerative nodules made of hepatocytes. Regenerative nodules impinge on, and deform, the hepatic veins, resulting in blood flow obstruction distal to the nodules. The small portal veins and venules are trapped, narrowed, and often obliterated by scarring of the portal tracts, causing an increase in portal outflow resistance. Moreover, blood flow through the hepatic artery is increased as small arteriovenous communications become functional. By this mechanism, portal hypertension (caused by obstruction of blood flow distal to the sinusoid) is augmented by an increase in splanchnic arterial blood flow. These two pathogenic factors, the increase of the resistance to flow within the liver, and the increase in splanchnic blood flow, maintain and worsen the increased pressure in the portal vein in patients with chronic liver dis-

venous system with the superior and inferior vena c a v a . 15,16

Spontaneous Portosystemic Shunts Portosystemic collaterals can be divided into two general groups according to the area of drainage: (1) shunting toward the superior vena cava through gastroesophageal varices, which are responsible for bleeding; and (2) shunting toward the inferior vena cava along wide-bore vessels, which can produce encephalopathy. 2'4'6'17'18 The principle portosystemic collaterals shunting toward the inferior vena cava are the following: 1. Paraumbilical vein. The umbilical vein originates from the left portal vein, connects (generally at the umbilicus) with veins in the abdominal wall, and drains into the external iliac vein. Angiography is not very sensitive for the depiction of paraumbilical shunts. 2. Splenorenal and splenoretroperitoneal shunts. These collaterals both originate from the splenic vein and drain either into the left renal vein, through the splenorenal ligament, or into the lumbar veins, along the phrenicocolic ligament (Fig 6). 3. Collaterals originating from the superior mesenteric vein. Peripancreatic or mesenteric collaterals arise from superior mesenteric vein branches and drain directly into the IVC or indirectly through retroperitoneal branches to the IVC.

e a s e 2,14-16

Increased portal pressure is accompanied by the formation of collaterals, and blood flow that normally passes through the liver is diverted toward the low-pressure systemic venous circulation via the collaterals pathways. These spontaneous portosystemic collaterals include both preexisting veins that dilate, as well as closed embryonic vascular channels that reopen to connect the portal

Fig 6. Splenorenal shunt seen during direct portography during a TIPS procedure,

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4. The portosystemic collaterals shunting blood toward the superior vena cava can be observed as follows: (A) The coronary vein drains blood to the stomach, then to the venous plexus in the lower portion of the esophagus, and then to paraesophageal vessels; (B) The short gastric veins, situated in the gastroesplenic ligament, connect the splenic vein with the venous plexus around the stomach (Fig 7). The portal venous system is examined during the venous phase of celiac and superior mesenteric angiography (Fig 1), or after direct injection of contrast into the portal venous system via a splenic or transhepatic route. Angiography has long been considered the gold standard in assessing the portal vein, but its invasiveness precludes its use for screening or follow-up examinations. Ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) can show the portal venous system accurately, and the direction and velocity of flow can be assessed with ultrasound and MRI. 19 In some cases, these techniques can give more information than angiography because vascular opacification on indirect splenoportography can be compromised by dilution effects in patients with large portosystemic collaterals, or when the portal vein fails to opacify because of hepatofugal flow. z° Presently, we only use portography in the venous

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phase of arteriography in preparation for hepatic tumor embolization.

Transjugular Intrahepatic Portosystemic Shunt: Indications, Technical Notes, and Patency Evaluation The main role of interventional radiologists in patients with cirrhosis is to perform diagnostic biopsies and TIPS in portal hypertension management. The first introduction of portosystemic shunts into clinical practice was in the 1940s, with the surgical approach to decrease portal hypertension in cirrhotic patients. However, these surgical patients had a high level of mortality and morbidity and a percutaneous alternative was sought. The performance of TIPS was described in dogs by Rrsch in 1969. 21 The procedure consisted of creating a bridge between the systemic circulation, the hepatic veins, and the portal system by using a jugular approach and local anesthesia. The first clinical TIPS using a metallic stent was created by Richter in 1989. za The present technical challenge concerning TIPS is the development of methods to prevent shunt stenoses and occlusions. Currently, TIPS is a common procedure in clinical practice. TIPS is an alternative technique for treatment of portal hypertension, gastrointestinal bleeding, and ascites in cases in which clinical

Fig 7. (A and B) Short gastric veins (arrows) seen in 2 patients with gastrointestinal bleeding. (Direct portography during emergency TIPS procedure,)

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management is not sufficient, or as a temporizing measure before liver transplantation. The first TIPS procedures performed clinically were performed in desperate circumstances, in patients with severe liver disease or massive variceal bleeding. Since then, the indications have been expanded and refined (Table 1). The performance of the TIPS procedure is not the first step in the treatment of gastrointestinal bleeding in most cases. In approximately 80% of cases, medical and endoscopic treatment control bleeding, but when there is no success after somatostatine infusion or sclerotherapy, the indication for TIPS is clear. The possibility of liver transplantation has expanded the indications for TIPS. Even patients with severe hepatic failure with bleeding and those with a hepatic neoplasm are candidates for TIPS when liver transplantation is anticipated. Although the TIPS procedure has been shown to be safe and effective with minimal morbidity and mortality, several contraindications exist (Table 2). A variety of TIPS techniques have been described, and interventional radiologists can use several approaches as well as different types of stents. The transjugular approach, using the right internal jugular vein, is the most common. The Cope-Ring set (William Cook Europe, Bjaeverskov, Denmark) is the most frequently used system. After canalization of the right hepatic vein, a 10 F introducer set is advanced into the vein. A 21 G needle is passed through the introducer and the assembly is used to puncture the liver centrally and anteriorly in an attempt to find the right portal vein. After the needle is removed, contrast media can be injected to verify that the portal system has been entered, and a stiff guidewire is advanced through the catheter into the portal vein. Contrast is again injected to confirm the intrahepatic location of the portal bifurcation. Once the bridge is made between the hepatic and portal veins, it is necessary to dilate the tract with a balloon catheter. We used 8-ram and 10-mm diameter balloons. Because di-

Table 1. Indications for TIPS Procedure

Uncontrolled acute variceal bleeding Recurrent variceal bleeding Refractory or recurrent ascites Budd-Chiari syndrome Cirrhotic hydrothorax Hepatorenal syndrome

Table 2. TIPS Contraindications

Absolute

Relative

Severe hepatic failure Severe right heart failure

Hepatic malignancy Policystic liver disease Severe hepatic encephalopathy Portal vein thrombosis

latation of the tract causes considerable discomfort, additional analgesics are given before this point. Localized narrowing of the balloon shows the location of the hepatic and portal vein walls, which in turn permits the accurate positioning of a stent of proper length. We generally used either a 10-mm or a 12-mm × 8-ram Wallstent (Boston Scientific Corporation, Meditech, Natick, MA). Right atrium, hepatic vein, and portal manometrics must be performed before and after the procedure. On the follow-up portogram, there should be minimal or no tilling of the intrahepatic portal veins, as well as minimal tilling of any residual varices (Fig 8A). Ideally, the portal systemic gradient should drop to 12 mm Hg. If there has been inadequate decompression of the portal system, further dilatation of the stent can be performed. 22 The advantage of the TIPS procedure is not only the intrahepatic location of the shunt, but also the entirely percutaneous method by which the shunt is created. Elective portocaval shunt surgery may have a mortality rate of up to 15%, and emergency shunt surgery may have a mortality rate from 60% to 100 %.23 In contrast, TIPS procedural mortality is 1.4% to 3%. TIPS mortality is directly related to the number of punctures made through the liver and is inversely related to the experience of the interventionalist. Fatal complications included hemorrhage into the peritoneum, retroperitoneum, and mediastinum; lacerations of the hepatic artery, portal vein, and liver capsule; and right heart failure. One of the most critical steps in the TIPS procedure is the creation of the parenchymal tract before stent placement. A portagram must always be obtained before tract dilitation. The tract must clearly be intraparenchymal to avoid dilatation of the extrahepatic portion of the portal vein. This can have disastrous results; namely, free portal vein rupture and exsanguination. These warnings notwithstanding, it is possible to puncture the extrahepatic portion of the portal vein if a covered stent is used. 22 TIPS may be complicated by portal vein

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Fig 8. TIPS. (A) Blood flow goes mainly from the portal system through the stented intrahepatic tract (arrows) to the IVC. No variceal filling is seen. (B) The same patient 6 months later, with endothelial hyperplasia and narrowing (arrows) of the stent lumen.

injury, dissection, or thrombosis. In these cases, another stent can be installed, or we can dilate the stent with balloon catheters. Thrombus embolized to the lungs in the course of this procedure undergoes spontaneous autolysis. 24 Acute liver failure (4% to 9%) and portal-systemic encephalopathy (12% to 34%) are additional complications reported after TIPS. We can reduce these complications with proper selection of patients referred for TIPS .25 It has been shown that TIPS can be performed with extremely high success rates (92%-99%). 24'25 Although there is a high initial success rate with TIPS in controlling acute variceal hemorrhage (91%), rebleeding from varices after TIPS is a problem. At 3 months, 1 year, and 2 years, the recurrence of bleeding is 5.6%, 16.6%, and 20.7%, respectively. Good results have also been obtained with TIPS in the control of intractable ascites (38% to 90% of cases). Follow-up of TIPS is a very important component of the procedure and can be divided into the routine follow-up in asymptomatic patients and the follow-up in patients with recurrent symptomsY Clinical survey, ultrasound, and portal venography are the methods used to ensure TIPS patency. Stenosis of occlusion after TIPS is common, occurring in 35% to 85% of patients. 2a-25 The incidence of stenosis is progressive in the first year and increases slowly thereafter (Fig 8B). Fortunately, TIPS malfunctions responded well to reinterven-

tion, including balloon dilatation or insertion of a new stent, and assisted patency can be maintained with good shunt function in 95% of patients. The noninvasive ultrasound evaluation of TIPS is well documented in this journal and elsewhereY

Transjugular Liver Biopsy Liver biopsy is the most specific test to assess the nature and severity of liver diseases, and is mandatory in the diagnosis and management of diffuse liver disease. At the present time, ultrasound-guided percutaneous liver biopsy remains the method of choice to obtain histologic samples (easy, safe, and inexpensive), and is standard practice in most hospitals. However, patients with diffuse hepatic disease usually have coagulation disorders and ascites that may increase the complications of the percutaneous approach. With transjugular liver biopsy (TLB), liver tissue is obtained directly through the vascular system without puncturing the liver capsule. This approach minimizes the risk for bleeding. Transjugular biopsy was first described in dogs in 1964 by Dotter. Since then, multiple studies have been published confirming the usefulness of this alternative biopsy approach. 27'2s Currently, TLB is the method of choice in at-risk patients, when percutaneous puncture is contraindicated or when other complementary studies are needed. 29'3° The indications for transjugular biopsy are outlined in Table 3.

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LONJEDO AND RIPOLLt:S Table 3. TLB Indications

Severe coagulopathy (platelet count < 60,000/ram 3 or PTT > 3 s over control value) Massive ascites Morbid obesity Need for concurrent vascular procedure (hemodynamic study from portal system or TIPS) Need for renal and hepatic biopsy samples Failure of percutaneous approach

No absolute contraindications to TLB exist; however, relative contraindications include a platelet count less than 30,000/mm 3, jugular obstruction or scarring in the jugular area, and inability of the patient to suspend respiration or lie in the supine position. The procedure involves percutaneous puncturing of the right external jugular vein, catheterization of the right hepatic vein, and the introduction of the biopsy needle through the sheath connecting to an external biopsy gun system. After infusion of local anesthesia, and with ultrasound guidance or with anatomic markers, the jugular vein is punctured high in the neck. A 9 F-transjugular sheath is introduced over a .0035-inch guidewire, and with a multipurpose catheter, the right hepatic vein is cannulated, advancing the sheath to this position. Over a stiff guidewire, we introduce the external component of the biopsy needle (18 G Tru-cut), and we retrieve the guidewire once the needle is in place. After removing the guidewire, we introduce the internal component of the needle, pulling the sheath and shooting centrally with the patient in suspended respiration. After obtaining the sample, hepatic venography is performed to evaluate possible complications (Fig 3). In cases of capsular perforation or subcapsular! intraparenchymal hematoma, nonautolimited embolization may be undertaken. After obtaining the necessary number of specimens, the sheath is removed with the patient in a semiseated position. The patient must then be monitored for at least 6 hours. 28 Complications related to TLB are listed in Table 4. The complications occurring at the jugular vein puncture site are the most common, and usually do not have clinical relevance. 11 The next most frequent complication is abdominal pain (6%). 31 Capsular perforation is the more important complication, but occurs rarely (0.5%-1.3%). 13"32-34 Hepatic venography after biopsy is necessary to

assess for possible capsular perforation and free bleeding into the peritoneum. If the bleeding continues beyond 5 minutes, we can embolize the tract to avoid fatal hemorrhage. 11"3~ Mortality from TLB is less than 0.5%. The published results and complications of TLB are listed in Table 5. 9"18'27'28'30'32-34'36'37 TLB is a safe and effective procedure for obtaining liver samples in patients with any contraindications for the percutaneous biopsy approach or in patients requiring intravenous access for other reasons. HEPATOCELLULAR CARCINOMA

Hepatocellular carcinoma (HCC) is the sixth most common cancer in men and the eleventh most common cancer in women. It is the third most common cause of cancer deaths in men and the seventh most common cause of cancer deaths in women. There is an increase in the detection of the HCC because of screening in cirrhotic patients. It has been shown that there is a change in blood supply when an HCC arises from a precancerous hepatic nodule. Regenerating and early dysplastic nodes have mainly portal vascularization. With the development of HCC, the vascularization becomes arterial, and the lesion becomes hypervascular. For both primary HCC and metastatic liver neoplasms, surgical resection has been the only established treatment offering potential cure. There are no widely accepted therapies that are effective against unresectable primary and secondary liver cancers in the liver. Surgical treatment, consisting of tumor resection or liver transplantation, is feasible in some cases. Other therapeutic options for neoplastic masses are percutaneous ethanol injection, radiofrequency

Table 4. TLB Complications

Related function hematoma Carotid function Transient recurrent nerve palsy Transient Homer Syndrome Pneumothorax Abdominal pain Vasovagal reaction Transient arrhythmia Capsular perforation Hemoperitoneum Hemobilia Death

1% 7% 0.2% 0.2% 0.2% 6% 3% 2% 3.5% 0.5%-1.3% 0,5% 0.1%-0.5%

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Table 5. Results and Complications of TLB Series

Patients

Success

Needle

Complications

Goldman, 197833 Lebrec, 198236 Bull, 198332 Velt, 198428

76 1,033 193 160 461 67 146 200 27 44 61 77

83% 97% 97% 81% 92% 93% 92% 77% 96% 84% 98% 96%

Ross Modified Ingenor (aspiration) Tru-cut Ross Modified Ross Modified Ross Modified/Tru-cut Ross Modified/Tru-cut Ross Modified Ross Modified/Menghini Ross Modified/Colapinto/Tru-cut None specified Tru-cut

6.3% 9.8% 20.2% 1.35% 18.4% 6% 16.4% 9% 23% 7% 13% 13.4%

Gamble, 198527 Steadman, 198818 McAfee, 199137 Corr, 199234 Furura, 199234 Sawyerr, 19939 Donaldson, 19933o Gorriz, 199528

ablation, chemoembolization, and, in some instances, combinations of these procedures. The percutaneous treatment of neoplastic masses is discussed in detail elsewhere in this issue. We will only consider hepatic artery embolization in this article.

Hepatic Arterial EmboIization The rationale for hepatic arterial embolization is based on the dual blood supply of the liver parenchyma (25% from the hepatic artery and 75% from the portal venous system), and on the almost exclusive hepatic artery blood supply of tumors.

Hepatic artery embolization selectively deprives tumors of blood flow, whereas normal liver tissue is supported by portal blood flow. Embolization of the hepatic artery has proven effective for palliation of fiver metastases from carcinoid and islet cell tumors. 38 HCC has a more modest response to embolization (50%-60%), with some increase in short-term survival. 39 Currently, this technique is indicated in cases of HCC when the primary clinical manifestation is peritoneal bleeding (Fig 9). Initial survival in these patients can be extended; whereas, without trealanent, the short-term mortality rate is as high as 5 0 % . 10'40

Fig 9, Emergency angiogram performed in a patient with peritoneal bleeding from HCC. (A) The initial study shows a hypervascular lesion (arrows) with arteriovenous shunting. (B) Final result, after embolization of the tumor.

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LONJEDO AND RIPOLLI~S

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