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VASCULAR COMPLICATIONS AFTER LIVER TRANSPLANTATION




JP Lerut, MD, PhD , Université Catholique de Louvain, Brussels, Belgium



1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


1. Partial de-arterialization of the liver allograft

The high incidence of arterial anomalies of the liver found in autopsy and extensive procurement studies may account for the occurrence of partial de-arterialization in LT. Indeed, when harvesting a liver without prior arterial mapping, it can sometimes be impossible to determine if the aberrant hepatic artery is a replacing or an accessory one. This differentiation is important in order to preserve as much of the hepatic arterial supply as possible. The problem of the partially de-arterialized liver graft has only been addressed in the Pittsburgh series. Thrombosis or ligation of smaller hepatic arterial aberrant branches may lead to similar, but localized, complications as those seen in complete hepatic artery thrombosis (HAT). These findings underline the importance of a correct liver graft procurement as a baseline of successful liver transplantation.
Figure
Figure 1

Right sectorial hepatic artery occlusion

Figure
Figure 2

Right sectorial hepatic artery occlusion responsible for localized liver necrosis on CT scan

Figure
Figure 3

Liver necrosis secondary to right sectorial hepatic artery occlusion




1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


2. Hepatic artery stenosis

Figure
Figure 4

Hepatic artery stenosis (HAST)

Routine Doppler ultrasound (DUS) arterial survey has not only allowed to diagnose hepatic artery thrombosis (HAT) earlier and more precisely, but has also permitted to detect hepatic artery stenosis (HAST).
HAST is mostly a consequence of inadequate surgical technique such as anastomotic narrowing or kinking. The diagnosis can be made based on calculation of the resistive index (<0.5 or 0.8) and on systolic acceleration time (above 0.08/min).
Figure
Figure 5

DUS showing signs of hepatic artery stenosis; the resistive index is 0.37.

HAST has been systematically looked for in only a few series. Its incidence varies from 4.1 to 7.8%. HAST can be completely asymptomatic but can also lead to biliary tract complications related to a compromised biliary arterial flow, or to an insidious form of graft dysfunction. Liver biopsies in patient s with severe HAST may reveal ischemic changes such as ballooning of hepatocytes, focal cell loss and spotty necrosis.

HAST requiring revision is infrequent after LT. Similarly to the treatment of other visceral arterial stenoses, percutaneous transluminal angioplasty has been successfully applied to HAST.
Figure
Figure 6

Angiography showing HAST in living related right lobe liver transplant

Figure
Figure 7

HAST treated with percutaneous balloon angiography

Figure
Figure 8

HAST treated with percutaneous balloon angiography

Surgical revision or complete redo of the arterial anastomosis may sometimes be necessary.
Biliary tract complications occur commonly if HAST is severe and must be treated using interventional radiology or surgery. Liver re-LT may sometimes be necessary in the presence of extensive biliary tract damage.




1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


3. Hepatic arterial steal syndrome

Adequate arterial perfusion of the liver may be compromised by a steal phenomenon with blood shunting from the hepatic to the splenic artery or with blood shunting to an arterial-venous fistula.
Figure
Figure 9

Small arterial venous fistula (AVF)
due to percutaneous liver biopsy

Figure
Figure 10

Small arterial venous fistula (AVF) due to percutaneous liver biopsy


Reduced arterial perfusion of the allograft may lead to allograft dysfunction with rise of transaminases. Ligation or occlusion of the splenic artery by interventional radiological means may solve this problem.

Hepatic arterial inflow may also be compromised by a celiac compression syndrome. The clinical significance of this syndrome is however debated as it has only been reported extensively by the UCLA group. This group identified the celiac compression syndrome in 10% of transplants. Diagnosis was confirmed by intraoperative blood flow recording demonstrating a typical pattern of accentuated decrease in celiac blood flow during expiration. Surgical transection of the median arcuate ligament resulted in normalization of the hepatic artery blood flow.
The problem of hepatic arterial steal points to the importance of very well documented pre-transplant DUS examinations. In case of unclear or abnormal findings, celiomesenteric angiography should be performed for precise mapping of the splanchnic arterial circulation of the recipient.




1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


4. Hepatic artery pseudo-aneurysm

Pseudo-aneurysm of the hepatic artery is a very rare (0.2 – 0.4%), but very severe complication due to its propensity to rupture and cause fatal gastrointestinal or intraperitoneal bleeding.
The most common cause of aneurysm formation is mycotic infection. The arterial infection may originate from an intraperitoneal contamination when performing e.g. a bilio-enteric anastomosis. Intrahepatic pseudo-aneurysms have been reported after percutaneous maneuvers or liver biopsy.
Pseudo-aneurysms are usually asymptomatic and found only on DUS. Rupture of a pseudo-aneurysm may present as gastrointestinal bleeding, hemobilia due to direct rupture into the bile duct, extrahepatic biliary obstruction and intra-abdominal bleeding.
Figure
Figure 11

Hepatic arterial aneurysm (HAA) at anastomotic site between HA and bifurcation of the gastroduodenal and common hepatic arteries

Figure
Figure 12

CT scan and angiography showing HAA at anastomotic site between free iliac graft and infrarenal abdominal aorta

Figure
Figure 13

CT scan and angiography showing HAA at anastomotic site between free iliac graft and infrarenal abdominal aorta

Treatment of a pseudo-aneurysm is difficult as it many times necessitates interruption of hepatic arterial inflow, or vascular reconstruction in an infected site. In order to be successful, the diseased aneurismal artery should be widely excised and arterial inflow restored using uninfected donor and recipient arteries (iliac and renal arteries, infrarenal abdominal aorta). Intraoperative histological examination of the arterial wall, looking specifically for Candida, is very important before proceeding with arterial reconstruction.
Figure
Figure 14

Histological examination of anastomotic aneurismal zone showing presence of Candida at section margin

In some cases, simple ligation is the only solution; many of these grafts will be lost due to severe graft dysfunction or biliary tract lesions.
Intrahepatic pseudo-aneurysms caused by percutaneous maneuvers can be cured (easily) using selective angiography and embolization of the feeding artery with coils or detachable balloons. A direct transhepatic approach to the intrahepatic aneurysm may be a good alternative, especially when trans-arterial embolization is difficult or risky. This mode of treatment eliminates the risk of hepatic ischemia with secondary biliary stricture inherent to segmental or sectorial interruption of hepatic allograft arterialization.
Figure
Figure 15

Arteriography showing major iatrogenic AVF giving rise to formation of huge intrahepatic hematoma

Figure
Figure 16

CT scan showing major iatrogenic AVF giving rise to formation of huge intrahepatic hematoma

Figure
Figure 17

Arteriography showing major intrahepatic hematoma following liver biopsy

Figure
Figure 18

CT scan showing major intrahepatic hematoma following liver biopsy




1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


5. Splenic artery aneurysm

Up to 19% of patients with cirrhosis and portal hypertension have a splenic artery aneurysm (SAA); autopsy series report an incidence as high as 50%.
SAA usually develop in the distal third of the main splenic artery close to the hilum of the spleen; they may also be multiple and intrasplenic. A major pathogenic factor of SAA in these patients is the high flow rate in the splenic artery finally leading to arterial elongation and tortuosity.
It has been reported that SAA does not shrink after successful portal hypertension surgery and that 3 to 10% of aneurysms greater than 2 cm will rupture.
Epigastric pain or pain in the left upper quadrant of the abdomen may be a sign of imminent or contained rupture. In such cases, treatment can be done by splenic artery embolization or by ligation of the splenic artery distal and proximal to the aneurysm.
In any case, every effort should be made to save the spleen to preserve postoperative immunity in the setting of possible post-transplant infectious disease.
Opting for prophylactic treatment of SAA seems to be contradicted by the extremely low reported incidence of rupture in the transplant literature.




1. Partial de-arterialization

2. Hepatic artery stenosis

3. Hepatic arterial steal syndrome

4. Hepatic artery pseudo-aneurysm

5. Splenic artery aneurysm

6. References


6. References

6.1. Hepatic artery stenosis

Abbasoglu O, Levy MF, Vodapally MS, Goldstein RM, Husberg BS, Gonwa TA, et al. Hepatic artery stenosis after liver transplantation--incidence, presentation, treatment, and long term outcome. Transplantation 1997;63:250-5.

Mondragon RS, Karani JB, Heaton ND, Thomas S, Wong PY, O'Grady JG, et al. The use of percutaneous transluminal angioplasty in hepatic artery stenosis after transplantation. Transplantation 1994;57:228-31.

Rode A, Ducerf C, Adham M, Delaroche E, Berthoux N, Bizollon T, et al. Influence of systematic echodoppler arterial survey on hepatic artery thrombosis after liver transplantation in adults. Transpl Int 1998;11:S292-5.

6.2. Hepatic arterial steal syndrome

Dunbar JD, Molnar W, Beman FF, Marable SA. Compression of the celiac trunk and abdominal angina. Am J Roentgenol Radium Ther Nucl Med 1965;95:731-44.

Jurim O, Shaked A, Kiai K, Millis JM, Colquhoun SD, Busuttil RW. Celiac compression syndrome and liver transplantation. Ann Surg 1993;218:10-2.

Manner M, Otto G, Senninger N, Kraus T, Goerich J, Herfarth C. Arterial steal: an unusual cause for hepatic hypoperfusion after liver transplantation. Transpl Int 1991;4:122-4.

6.3. Hepatic artery aneurysm

Bonham CA, Kapur S, Geller D, Fung JJ, Pinna A. Excision and immediate revascularization for hepatic artery pseudoaneurysm following liver transplantation. Transplant Proc 1999;31:443.

Fichelle JM, Colacchio G, Castaing D, Bismuth H. Infected false hepatic artery aneurysm after orthotopic liver transplantation treated by resection and reno-hepatic vein graft. Ann Vasc Surg 1997;11:300-3.

Goldman DE, Colquhoun SD, Ghobrial RM, Arnaout WS, Farmer DG, Markmann JF, et al. Mycotic aneurysm of arterial conduit presenting as massive upper gastrointestinal hemorrhage after liver transplantation. Liver Transpl Surg 1998;4:435-6.

Houssin D, Ortega D, Richardson A, Ozier Y, Stephan H, Soffer M, et al. Mycotic aneurysm of the hepatic artery complicating human liver transplantation. Transplantation 1988;46:469-72.

Lowell JA, Coopersmith CM, Shenoy S, Howard TK. Unusual presentations of nonmycotic hepatic artery pseudoaneurysms after liver transplantation. Liver Transpl Surg 1999;5:200-3.

Madariaga J, Tzakis A, Zajko AB, Tzoracoleftherakis E, Tepetes K, Gordon R, et al. Hepatic artery pseudoaneurysm ligation after orthotopic liver transplantation--a report of 7 cases. Transplantation 1992;54:824-8.

Marujo WC, Langnas AN, Wood RP, Stratta RJ, Li S, Shaw BW, Jr. Vascular complications following orthotopic liver transplantation: outcome and the role of urgent revascularization. Transplant Proc 1991;23:1484-6.

Merhav H, Zajko AB, Dodd GD, Pinna A. Percutaneous transhepatic embolization of an intrahepatic pseudoaneurysm following liver biopsy in a liver transplant patient. Transpl Int 1993;6:239-41.

Mor E, Emre S, Schwartz ME, Sheiner PA, Miller CM. Aneurysm of the celiac artery in a liver allograft. Transplantation 1993;56:1548-9.

Narumi S, Osorio RW, Freise CE, Stock PG, Roberts JP, Ascher NL. Hepatic artery pseudoaneurysm with hemobilia following angioplasty after liver transplantation. Clin Transplant 1998;12:508-10.

Sheiner PA, Nurzia MJ, Cooper J, Miller CM. In situ prosthetic graft repair of a mycotic aneurysm of the aorta after orthotopic liver transplantation. Transplantation 2000;69:999-1001.

Sheng R, Orons PD, Ramos HC, Zajko AB. Dissecting pseudoaneurysm of the hepatic artery: a delayed complication of angioplasty in a liver transplant. Cardiovasc Intervent Radiol 1995;18:112-4.

Stange B, Settmacher U, Glanemann M, Nuessler NC, Bechstein WO, Neuhaus P. Aneurysms of the hepatic artery after liver transplantation. Transplant Proc 2000;32:533-4.

Yoshida EM, Erb SR, Morris DC, Wall WJ, Scudamore CH. Hepatic artery interruption followed by portal vein thrombosis in an adult liver transplant. Transpl Int 1994;7:434-7.

6.4. Splenic artery aneurysm

Ayalon A, Wiesner RH, Perkins JD, Tominaga S, Hayes DH, Krom RA. Splenic artery aneurysms in liver transplant patients. Transplantation 1988;45:386-9.

Bronsther O, Merhav H, Van Thiel D, Starzl TE. Splenic artery aneurysms occurring in liver transplant recipients. Transplantation 1991;52:723-4.

Trastek VF, Pairolero PC, Bernatz PE. Splenic artery aneurysms. World J Surg 1985;9:378-83.