An increased number of transplant centers now actively perform deceased-donor as well as living-related liver transplants. Although postoperative vascular and nonvascular complications after liver transplant have been well documented, early diagnosis and intervention are important to increase graft and recipient survival. With improvements in interventional radiologic techniques and a multidisciplinary approach to liver transplant, management of complications by percutaneous and endovascular techniques is possible with less morbidity and mortality. This article outlines the recent developments in, and applications of, interventional radiologic techniques in liver transplant patients.
Key words : Liver transplantation, Interventional radiology, Hepatic artery, Biliary drainage, Stent
Liver transplant is the best treatment for patients with end-stage liver disease for which no other therapy is available. In 1967, Starzl pioneered the first successful deceased-donor liver transplant. Since then, great progress has been made in liver transplant surgery. Improved results are related to better recipient selection, advances in surgical technique, and early diagnosis and treatment of complications. Nonsurgical interventions have become first-line treatments for vascular and nonvascular complications and so, interventional radiology has become an integral part of the management of transplant recipients (1).
Vascular complications
Vascular complications usually occur during the early postoperative period. Clinical manifestations vary from mildly elevated values of liver functions to fulminant hepatic failure. The first diagnostic technique that could confirm vascular integrity was Doppler ultrasonography. A resistive index of less than 0.5 or systolic acceleration times higher than 0.08 seconds is highly suggestive of a stenosis or thrombosis. Computerized tomography and magnetic resonance imaging also provide noninvasive evaluation of the transplanted liver. Angiography may be necessary for definitive diagnosis and endovascular treatment.
Hepatic artery thromboses
Hepatic artery thromboses are seen in 4% to 42% of transplant patients. In children, these rates are higher owing to the small size of the hepatic arteries (1-4). The hepatic artery provides the only vascular supply to the biliary system (5). Clinical presentation of a hepatic artery thrombosis varies from patient to patient. A hepatic artery thrombosis occurring in the first month after transplant has a mortality rate of up to 55%, whereas it decreases to 15% if occlusion occurs after this period. Predisposing factors to hepatic arterial complications are a difficult anastomosis, small vessel size, presence of multiple arteries, complex anatomy, hypercoagulable state, rejection, prolonged ischemia, and transplant for primary sclerosing cholangitis (6, 7). Clinical presentations range from fulminant hepatic failure, biliary ischemia, and strictures, to necrosis, leaks, biloma formation, and abscesses (8).
Management of hepatic artery thrombosis
Early hepatic artery thromboses (those occurring within the first month of the transplant) can be treated with surgical revascularization or endovascular thrombolysis, percutaneous transluminal angioplasty, and/or stent placement (9).
Endovascular technique
Once a hepatic artery occlusion has been confirmed by angiography, the microcatheter and a 0.016-inch guide wire can be negotiated into the thrombosed hepatic artery via a 5-F diagnostic catheter, and a second angiogram can be obtained at that time through the microcatheter to evaluate the extent of the thrombus in the distal branches. Then, the microcatheter is advanced distally, and a 0.014-inch guide wire is placed distally. A 6-F guiding catheter is advanced to the origin of the celiac trunk. A 4-F catheter is advanced to the hepatic artery for thrombolytic infusion, and the thrombus is macerated with an undersized balloon catheter (Figure 1). Underlying anatomic defects can be treated with balloon angioplasty or with bare or graft-covered stents (10, 11). To clear the residual thrombus, arterial thrombolysis can be continued for a few days if flow is established. We believe that endovascular interventions can be done safely, even on the first postoperative day, if graft-covered stents are available to treat possible ruptures (Figure 2) (12, 13).
Hepatic artery stenoses
Hepatic artery stenoses occur in 5% to 13% of liver transplant recipients (14, 15). Early recognition and treatment may prevent significant ischemic organ damage and progression to hepatic artery thromboses. Mainly, a hepatic artery stenosis occurs at the site of the surgical
anastomosis.
Management of hepatic artery stenoses
Surgical revascularization, and even retransplant, can be done if the endovascular techniques fail. The first choice of treatment is balloon angioplasty. If the residual stenosis is greater than 20%, or if there is intimal dissection, a stent must be placed (Figure 3). In the case of a rupture, graft-covered stents must always be at hand. Postprocedural anticoagulation is important to prevent occlusion of the hepatic artery.
Hepatic artery pseudoaneurysm
A hepatic artery pseudoaneurysm is an uncommon vascular complication with a reported incidence of 1% to 2%. Pseudoaneurysm may rupture causing death. Therefore, it must be treated whenever diagnosed. Coil embolization and graft-covered stent placement are the 2 main endovascular alternatives. Percutaneous thrombin injection may be another alternative if there is a narrow neck (16, 17).
Arterial steal syndromes
Arterial steal syndromes are characterized by arterial hypoperfusion of the graft, caused by a shift in blood flow into other arteries that originate from the same trunk. They occur in 0.6% to 5.9% of all transplants. In our series, the incidence was 8.4% (18-20). Most cases are caused by splenic artery steal syndrome, but gastroduodenal steal syndrome also has been reported. Patients may present with elevated liver enzyme levels, cholestasis, or acute graft failure. Doppler ultrasonography shows slow flow of the hepatic artery but no stenotic pattern. Angiography, which shows the portal-venous phase of the angiogram in the arterial phase (due to slow flow in the hepatic arteries), is required to diagnose arterial steal.
Endovascular treatment of this syndrome includes embolization of the splenic or gastroduodenal artery by coils or an Amplatzer vascular device (Figure 4). Also, a narrowed stent may be placed in the splenic artery (21). Splenic artery embolization should be done to occlude the middle part of the splenic artery to avoid splenic parenchymal infarction (22).
Portal vein complications
Portal vein stenoses may be seen in less than 3% of adult liver transplant recipients and in 7% of patients in the pediatric group (23, 24). Most occur at the site of the surgical anastomosis. Patients may be asymptomatic, or they may present with clinical signs of portal hypertension. Doppler ultrasonography and 3-dimensional helical computerized tomography arteriography with maximum intensity projection with shaded-surface display techniques are effective noninvasive approaches. Angiography is rarely necessary for diagnosis. The portal vein can be accessed via the transhepatic, transjugular, or transsplenic route. The transhepatic route for a balloon angioplasty is a direct and safe approach. Intravascular pressures are taken in the portal vein proximal and distal to the stenosis, before and after the angioplasty (Figure 5). If necessary, a stent may be used. Once treatment is complete, the intraparenchymal tract can be embolized with coils and sometimes with glue.
Inferior vena cava and hepatic venous complications
Stenosis of, or a thrombosis in, the inferior vena cava is seen in less than 1% of liver transplant recipients (25). Stenosis of the inferior vena cava generally occurs at the site of the anastomosis. Endovascular intervention like balloon angioplasty or percutaneous transluminal angioplasty stent placement is the preferred method. Surgical revision might be necessary if these procedures fail.
The frequency of hepatic venous outflow obstruction after orthotopic liver transplant is about 1%, and it is about 2% to 4% after living-donor liver transplant (26). Outflow obstruction causes hepatic congestion, massive ascites, and as a result, hepatic dysfunction. Hepatic venous outflow obstruction immediately after transplant is a surgical emergency, and reoperation is usually necessary. Late-onset hepatic vein stenosis may cause insidious deterioration of liver function. Surgical correction is usually difficult because of fibrotic changes around the anastomosis. On ultrasonography, flattened monophasic flow with decreased velocities of less than 10 cm/second may be observed. Balloon angioplasty is the first choice of treatment (Figure 6) (27).
Biliary complications
Bile duct complications are a significant cause of postsurgical morbidity. Biliary complications vary in their occurrence from 6% to 30%; this range represents differences of complications in orthotopic liver transplant and living-donor liver transplant (28-30). The method of surgical anastomosis, cold and warm ischemic liver injury, and pre-existing biliary disease are all factors that critically influence the frequency, development, and type of complication. The choledochocholedochostomy and the Roux-en-Y choledochojejunostomy are the 2 standard biliary reconstruction procedures. Biliary complications are frequently seen in the first few months after transplant (31). The most common complications are biliary leaks and stenoses. Generally, biliary leaks observed after transplant tend to occur early and stenoses later (32, 33).
Bile duct obstruction
Strictures are the most common cause of biliary obstruction, and their cause is multifactorial. The incidence of biliary strictures after liver transplant is 4% to 15%; it is 8% to 35% after living-donor liver transplant. Biliary strictures can be classified as anastomotic and nonanastomotic (34). Approximately two-thirds of all biliary strictures are anastomotic. The anastomotic strictures are the fibrotic strictures that are often the result of fibrotic healing and this type of stricture may be related to ischemia (35). Percutaneous or endoscopic intervention is the first choice of treatment for anastomotic strictures. The majority of patients who develop anastomotic strictures can be managed by percutaneous dilatation. Both ultrasonography and fluoroscopy-guided percutaneous biliary interventions can be performed easily, and combined use of these techniques significantly decreases the number of complications seen with percutaneous biliary interventions. These strictures usually require 2 to 3 percutaneous intervention sessions. The success rate is in the range of 75% to 85% (36). Several reports about the use of a cutting balloon for biliary strictures have been published and show varying results (Figure 7) (37). Our experiences with a cutting balloon for anastomotic biliary strictures are no different from those of a conventional balloon. Another alternative treatment for biliary strictures that we have used on several patients is percutaneous placement of double 10-F to 14-F plastic biliary stents (Figure 8). Early results of this technique are promising. Recurrent strictures or interventional radiology failures are managed by surgical reconstruction (38-40).
Nonanastomotic strictures (hilar or intrahepatic) carry a less favorable prognosis. These strictures occur predominantly at the hepatic bifurcation but are often multiple (41). They often do not respond to nonsurgical techniques and require surgery.
Bile leaks and bilomas
Common causes of a bile leak include anastomotic leaks and leaks from the T-tube exit site. Bile leaks may be seen in 9% to 25% of liver transplant recipients (28). Treatment of bile leaks varies among centers. Ultrasonography and fluoroscopic-guided percutaneous transhepatic cholangiography and percutaneous biliary drainage provide effective treatments even with an undilated biliary system (42, 43). A severely disrupted anastomosis may require surgical revision. Computerized tomography and ultrasonography can easily identify biliary collections, and these can be percutaneously drained if needed (Figure 9).
In conclusion, liver transplant requires a team approach, and the interventional radiologist plays a key role in the treatment of complications from liver transplant.
References:
mec P, Ondrásek J, Studeník P, Hökl J, Cerný J. Biliary complications in liver transplantation. Ann Transplant. 2001;6(2):24-28.
Volume : 6
Issue : 2
Pages : 105 - 112
From the Departments of 1Radiology and 2General Surgery and Tranplantation, Baskent University Faculty of Medicine, Ankara, Turkey
Address reprint requests to: Fatih Boyvat, Baskent University Medical Faculty, Department of Radiology, Fevzi Cakmak Cad. 10. Sok. No. 45, 06490, Bahcelievler Ankara, Turkey
Phone: +90 312 212 6868
Fax: +90 312 223 7333
E-mail: boyvatf@yahoo.com
Figure 1. Ahepatic artery thrombosis in a 1-year-old boy 5 days after a left lobe living-related donor transplant. (a) Selective celiac arteriogram demonstrating hepatic artery occlusion. (b) Subsequent selective hepatic arteriogram through a microcatheter showing a thrombus at the origin of the hepatic artery. (c) Thrombolytic infusion and balloon angioplasty are undertaken with use of a 2.5-mm balloon over a 0.014-inch guide wire. (d) An excellent angiographic result is seen with no residual stenosis.
Figure 2. Ahepatic artery thrombosis in an 8-year-old boy 1 day after surgery. (a) Celiac arteriogramshowing no flowin the hepatic artery. (b) Contrast extravasation is observed while trying to establish flow. (c) Flow is established after placement of graft-covered stents.
Figure 3. (a) Severe hepatic artery stenosis is seen on a celiac arteriogram. (b) Stent is placed after unsatisfactory balloon angioplasty.
Figure 4. A42-year-old patient 33 days after a right lobe transplant. (a) Celiac arteriogram showing diversion of blood to the spleen and slow flow to the hepatic artery. (b) Even in the late phase of the arteriogram, there is still contrast in the hepatic artery. (c) Celiac arteriogram after coil occlusion of the splenic artery showing early and predominant filling of the hepatic artery.
Figure 5. A3-year-old patient 14 months after surgery in whom a left lobe has been transplanted. (a) Saggital and (b) axial computerized tomography images showing portal vein stenosis at the anastomotic site. (c) Atranshepatic portography was done, and severe portal vein stenosis was confirmed with a significant gradient of 14 mm Hg. (d) Aballoon angioplasty was done, and the stenosis was dilated producing a good result: the gradient was reduced to 2mmHg.
Figure 6.Hepatic vein stenosis in a 47-year-old patientwith transplanted right lobe. (a) Saggital computerized tomography image showing hepatic vein stenosis. (b) Transjugular hepatic venography demonstrating severe stenosis and prominent gradient. (c) Subsequent hepatic venography after balloon dilation showing an excellent result with a pressure gradient of 3mmHg.
Figure 7. Bile duct obstruction in a 3-year-old girl. (a)Apercutaneous transhepatic cholangiography showing complete obstruction of the common bile duct. (b) Several balloon angioplasty procedures were done with conventional and cutting balloons. (c) The obstruction was completely abolished.
Figure 8. Severe recurrent anastomotic stenosis of the common bile duct in a 10-year-old boy. (a) Percutaneous drainage was done. (b) Two 8-F plastic biliary stents were placed through 1 percutaneous entrance.
Figure 9. Aleft lobe transplanted in a 2-year-old child because of biliary atresia. (a) Cholangiography showing a biliary leak. (b) Percutaneous biliary drainage was done and follow-up a cholangiography several days later showed no leaks.