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(Radiology. 2000;214:775-779.)
© RSNA, 2000

Vascular and Interventional Radiology

Hepatic Arterial Complications in Liver Transplant Recipients Treated with Pretransplantation Chemoembolization for Hepatocellular Carcinoma1

Howard M. Richard, III, MD, James E. Silberzweig, MD, Harold A. Mitty, MD, W. Y. Wendy Lou, PhD, Jiyong Ahn, MD and James M. Cooper, MD

1 From the Department of Radiology, Division of Interventional Radiology (H.M.R., H.A.M., J.A.) and the Department of Biostatistics (W.Y.W.L.), Mount Sinai Hospital, New York, NY; the Department of Radiology, Division of Interventional Radiology, St Luke's Roosevelt Hospital Center, New York, NY (J.E.S.); and the Department of Radiology, Division of Interventional Radiology, INOVA Alexandria Hospital, Alexandria, Va (J.M.C.). From the 1997 RSNA scientific assembly. Received February 3, 1999; revision requested April 5; final revision received July 1; accepted July 26. Address reprint requests to H.M.R., Department of Diagnostic Imaging, Division of Interventional Radiology, University of Maryland Medical Center, 22 S Greene St, Baltimore, MD 21201-1595 (e-mail: howardrichard@alum.MIT.EDU).


   Abstract
TOP
 Abstract
Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To compare the prevalence of hepatic arterial complications in patients who underwent hepatic arterial chemoembolization for hepatocellular carcinomas before orthotopic liver transplantation with the prevalence of hepatic arterial complications in the total population of liver transplant recipients.

MATERIALS AND METHODS: Forty-seven patients underwent selective hepatic arterial chemoinfusion with mitomycin C, doxorubicin hydrochloride, and cisplatin combined with embolization. The prevalence rates for hepatic arterial complications, including pseudoaneurysm, stenosis, anastomotic disruption, and thrombosis, were tabulated and compared with results in 1,154 patients who underwent orthotopic liver transplantation but not chemoembolization.

RESULTS: Of the 47 patients who had undergone preoperative hepatic arterial chemotherapy, 13% developed hepatic arterial complications within a mean of 7 days after transplantation; an 8% prevalence of hepatic arterial thrombosis was observed. Of the 1,154 patients who underwent orthotopic liver transplantation but not chemotherapy, 6% developed hepatic arterial complications; a 5% prevalence of hepatic arterial thrombosis was observed. There was no statistically significant difference in the prevalence rates for thrombosis and complications between the patients who underwent chemoembolization before orthotopic liver transplantation and those who did not. The mean interval between chemotherapy and orthotopic liver transplantation was 111 days (range, 3–428 days).

CONCLUSION: Patients who undergo hepatic arterial chemotherapy are not at an increased risk of developing hepatic arterial thrombosis or other hepatic arterial complications after orthotopic liver transplantation.

Index terms: Hepatic arteries, chemotherapeutic embolization, 952.1264, 952.1266 • Hepatic arteries, thrombosis, 952.751 • Liver neoplasms, angiography, 761.124 • Liver neoplasms, US, 761.12984 • Liver, transplantation, 761.45 • Vasculitis, 952.62


   Introduction
TOP
 Abstract
 Introduction
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
In patients with impending hepatic failure and nonresectable hepatocellular carcinomas, orthotopic liver transplantation is considered the treatment of choice (1–4). These patients can wait several months until a suitable donor organ becomes available. In the interval between diagnosis of hepatocellular carcinoma and orthotopic liver transplantation, chemoembolization is effective in gaining local control in a subset of these patients (3–10). Chemoembolization is delivered directly by means of selective catheterization into the hepatic arterial branches feeding the tumors. This reduces the chemotherapy dose to the hepatic parenchyma. Since the chemotherapeutic agents are subject to first-pass metabolism in the liver, patients have fewer systemic side effects and generally tolerate the chemoembolization well (4).

Since local arteritis may develop as a result of chemoembolization (11,12), we postulated that the prevalence of hepatic arterial thrombosis, a catastrophic graft-threatening complication of orthotopic liver transplantation, might be increased in this subset of orthotopic liver transplantation patients. The purpose of this retrospective review was to determine if the arterial toxicity of chemoembolization predisposes these patients to a higher prevalence of hepatic arterial thrombosis compared with that in the total population of patients who undergo orthotopic liver transplantation.


   MATERIALS AND METHODS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Between May 1992 and January 1998, 1,201 patients underwent orthotopic liver transplantation at our institution (Mount Sinai Hospital, New York, NY). Forty-seven of these patients (15 women, 32 men; mean age, 57.5 years; median age, 60 years; age range, 15–77 years) underwent hepatic arterial chemoembolization for hepatocellular carcinoma before orthotopic liver transplantation. These patients underwent selective chemoembolization with 20 mg of mitomycin C (Mutamycin; Bristol-Myers Squibb, Princeton, NJ), 20 mg of doxorubicin hydrochloride (Adriamycin; Pharmacia & Upjohn, Kalamazoo, Mich), and 90 mg of cisplatin (Platinol; Bristol-Myers Squibb) combined with embolization per protocol (3).

Embolizations were performed with collagen for embolization (Angiostat; Target Therapeutics, Los Angeles, Calif), gelatin sponge pledgets (Gelfoam; Pharmacia & Upjohn), or polyvinyl alcohol particles (Ivalon, San Diego, Calif) until stasis in the tumor vessels was achieved. The initial patients underwent embolization with collagen for embolization. When it was no longer available, patients underwent embolization with gelatin sponge pledgets. In the later part of the series, patients underwent embolization with polyvinyl alcohol particles, as they can provide more precise control of the particle size: 250–350 µm.

The angiograms (Angiostar; Siemens, New York, NY) were reviewed by two authors (H.M.R., J.E.S.) jointly for evidence of vascular disease, such as hepatic arterial to portal venous shunting and portal venous patency. The degree of selectivity of the catheterization in the hepatic vascular tree was tabulated. The angiograms of patients who had multiple chemoembolization sessions were reviewed by two authors (H.M.R., J.E.S.) jointly for evidence of arterial injury, such as arterial stenosis (areas of focal narrowing in vessels that persisted on multiple angiographic views), aneurysm formation (areas of focal widening of vessels that persisted on multiple angiographic views), or occlusion (abrupt ending of vessels that persisted on multiple angiographic views).

The resected liver histopathology reports were reviewed by one author (H.M.R.) for evidence of the chemoembolization effects, such as tumor necrosis and arterial wall toxicity. The pathologist evaluated the arteries grossly and as visualized in the microscopic specimens per routine. However, the evaluation was not directed in a prospective manner.

After orthotopic liver transplantation, the patients were screened for the development of early hepatic arterial thrombosis with serial Doppler Ultrasonography (US) (Quantum 2000, Siemens-Quantum, Issaquah, Wash; Ultramark 9, Advanced Technology Laboratories, Bothell, Wash) of the hepatic vessels daily for the first 3 postoperative days per clinical routine and after that if indicated by deterioration of the patient's condition. Hepatic arterial thrombosis was suspected in the absence of the normal arterial Doppler waveform in the hepatic artery and was confirmed by means of angiography or surgical exploration.

The dictated reports of the Doppler US evaluations were reviewed by one author (H.M.R.) for this study. The patients' clinical courses were reviewed by one author (H.M.R.) for the development of late hepatic arterial thrombosis. The liver transplant database, a compilation of the clinical courses of orthotopic liver transplantation patients, including patients who did not undergo pretransplantation chemoembolization, was queried to identify the prevalence of late hepatic arterial complications. Patients with normal hepatic Doppler examination results and no clinical or laboratory findings to suggest hepatic arterial thrombosis were presumed not to have hepatic arterial thrombosis or hepatic arterial complications such as pseudoaneurysm, stenosis, or anastomotic disruption. The prevalence rates for hepatic arterial thrombosis and hepatic arterial complications were tabulated.

Statistical analysis was performed with commercially available software (SPSS version 8.0 for Windows 95; SPSS, Chicago, Ill). The {chi}2, Fisher exact, and Student t tests were used for statistical analysis. P values less than .05 based on two-tailed tests were considered significant.


   RESULTS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Forty-seven patients underwent 70 chemoembolization procedures. Thirty-one patients had one chemoembolization session, nine patients had two, and seven patients had three. Four of the six patients who had hepatic arterial complications each underwent one session, whereas the other two underwent three. All patients underwent third-order distal catheterization for chemoembolization; coaxial microcatheters were used in 21 (45%) of 47 patients. Eighteen patients underwent bilateral, 21 right-lobe, and eight left-lobe catheterization. One patient had minimal hepatic artery to portal venous shunting.

Whereas particle embolization was not performed in four (8%) of 47 patients whose portal vein was initially obstructed, these patients underwent selective chemoinfusion of all three agents. The portal vein was patent in all patients who underwent chemoembolization. Evidence of arteritis, areas of focal stenosis, and aneurysm formation were demonstrated in two (12%) of the 16 patients who had repeat chemoembolization sessions (Fig 1).



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  		Figure 1. Anteroposterior digital subtraction angiogram of a common hepatic artery in a 46-year-old man who had undergone repeated hepatic arterial chemoembolization demonstrates several areas of stenosis (arrowheads).

 
The initial size of the hepatocellular carcinoma was measured by means of computed tomography or US as 5.4 cm ± 2.5 (SD). Analysis of the resected liver histopathology reports revealed a mean tumor size of 5.6 cm ± 3.1. On average, the tumors did not change in size when compared with the size of the tumors at the time of chemoembolization (P = .814). Tumor necrosis was evident in 39 (83%) of the 47 resected livers. Emboli and foreign body giant cell reaction were identified within the walls of branches of the hepatic arteries (Fig 2). Intimal fibrosis and luminal narrowing were identified in the hepatic arterial branches in the porta hepatis. Microscopic evaluation of the common hepatic artery was not performed.



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  		Figure 2. Photomicrograph demonstrates polyvinyl alcohol particles (arrowheads) surrounded by foreign body giant cell reaction in the lumen of a hepatic arterial branch. (Hematoxylin-eosin stain; original magnification, x215.)

 
Four (8%) of the 47 patients developed early hepatic arterial thrombosis. In three, the diagnosis was suspected at Doppler US and confirmed at angiography (Fig 3). The fourth patient required another surgery on the 1st postoperative day secondary to his rapidly deteriorating postoperative course. Three patients had emergent thrombectomy and revision of the hepatic arterial anastomosis. The fourth patient was treated by means of urgent retransplantation. A fifth patient developed hepatic arterial anastomotic disruption 7 days after transplantation. The sixth patient presented to the emergency department hypotensive and underwent emergent exploration and resection of a ruptured hepatic arterial pseudoaneurysm (Fig 4) 22 days after orthotopic liver transplantation.



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  		Figure 3. Anteroposterior celiac angiogram demonstrates abrupt cutoff (arrowhead) of the proximal common hepatic artery in a 49-year-old man with hepatic arterial thrombosis.

 


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  		Figure 4. Anteroposterior selective common hepatic angiogram obtained in a 40-year-old man demonstrates a pseudoaneurysm (arrowhead) at the anastomosis of the donor and recipient common hepatic arteries.

 
Four (8%) of 47 patients who underwent preoperative chemoembolization developed hepatic arterial thrombosis, compared with 62 (5%) of 1,154 patients who underwent orthotopic liver transplantation but not chemoembolization (Table). Six (13%) of the 47 patients who underwent chemoembolization developed hepatic arterial complications within a mean of 7 days after transplantation, compared with 68 (6%) of 1,154 who did not undergo chemoembolization. In comparing the treated and nontreated groups, {chi}2 analysis results did not demonstrate a significant difference for hepatic arterial thrombosis (P = .322) or hepatic arterial complications (P = .064).


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  		Prevalence of Hepatic Arterial Thrombosis and Hepatic Arterial Complications
 
Patients waited a mean of 111 days ± 103 (range, 3–428 days) from the last chemoembolization until orthotopic liver transplantation. Patients with hepatic arterial thrombosis had chemoembolization procedures a mean of 61 days ± 57 (range, 9–113 days) before orthotopic liver transplantation (P = .348). Hepatic arterial chemoembolization was performed a mean of 57 days ± 51 (range, 9–113 days) before orthotopic liver transplantation in the patients with hepatic arterial complications. This was not significantly different from the remaining patients, who waited a mean of 114 days ± 105 (range, 3–428 days) for orthotopic liver transplantation (P = .202).


   DISCUSSION
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
Orthotopic liver transplantation is considered the treatment of choice in patients with nonresectable hepatocellular carcinoma (1–4). In patients with a tumor confined to the liver, long-term survival with orthotopic liver transplantation is better than with resection or conventional intravenous chemotherapy (1,3). Unfortunately, these patients must wait for a suitable donor liver for transplantation. During this interval, hepatic arterial chemoembolization is a useful adjuvant therapy (1,3).

Hepatic arterial chemoembolization is an effective treatment for hepatocellular carcinoma (5–11). Selective catheterization allows infusion of the chemoembolization agents into the affected hepatic segments. Microcatheters, such as Tracker catheters (Boston Scientific, Natick, Mass), may be used when standard catheter and guide-wire combinations are unsuccessful. This spares the uninvolved hepatic parenchyma from the toxicity of the chemoembolization and allows higher local doses.

Doxorubicin hydrochloride, mitomycin C, and cisplatin are used for chemoembolization, as these agents are effective against hepatocellular carcinoma (3–5,11,13,14). In addition, doxorubicin hydrochloride and mitomycin C are metabolized primarily by the liver, and these agents are cleared from the hepatic arterial infusion during the first pass. This allows higher doses to be tolerated without systemic side effects. The embolization causes tumor ischemia, which is associated with an increase in the uptake of doxorubicin hydrochloride, and ultimately results in tumor necrosis (6,13).

In 83% of the patients in our study, the tumors in the resected livers exhibited necrosis. There was no growth in the tumors while the patients awaited suitable donors. Hepatocellular carcinoma may respond to chemoembolization with tumor necrosis without a decrease in the volume of the tumor (7).

Doxorubicin hydrochloride and mitomycin C are antitumoral antibiotics that can cause cardiotoxic effects and lung injury. An isolated dog lung model subject to perfusion with doxorubicin hydrochloride demonstrated vascular endothelial damage (15). Doxorubicin hydrochloride caused dose-related damage to the pulmonary endothelial cells and when used in higher doses resulted in endothelial necrosis (15). Mitomycin C can cause arterial injury such as intimal hyperplasia, fibrin thrombus formation in capillaries, and medial hypertrophy of small arteries. At concentrations similar to intravenously administered doses, mitomycin C is taken up by endothelial cells and is converted to the reactive form. It has been shown to cause a dose-related cytolytic injury to cultured arterial endothelial cells (16). Mitomycin C delivered via a micropore balloon catheter failed to inhibit the formation of intimal hyperplasia and was associated with an increased amount of intimal hyperplasia in injured arterial segments (17). As the vascular endothelium is subject to the cytotoxic effects of these agents, the vessel may have a diminished capacity to recover from minor endothelial injury.

Vasculitis is a known complication of chemoembolization (11). In patients subjected to repeated chemoembolization sessions, access to the tumors may sometimes become technically difficult secondary to chemoembolization-induced distal stenosis. Hepatic arterial chemoembolization has been associated with hepatic arterial pseudoaneurysm formation (12). Arterial stenosis and pseudoaneurysm formation were evident on the angiograms of the patients in our study who had repeated chemoembolization sessions. Intimal hyperplasia has been reported with arterial injury from balloon dilation and stent placement (18,19). This is secondary to disruption of the intima and the subsequent recruitment of platelets, which is followed by the proliferation of fibroblasts (19,20). Catheterization for extended periods and chemoembolization are postulated to inflict as much or more damage on the arterial wall endothelium as angioplasty does (17).

Doxorubicin hydrochloride, mitomycin C, or both may be directly cytotoxic. Alternatively, they may decrease the ability of the hepatic arterial endothelium to recover from the trauma of the catheterization. The injury from the chemotherapeutic agents and the trauma of catheterization may be additive. Patients with hepatic arterial complications had a shorter interval between chemoembolization and orthotopic liver transplantation. The response to the chemoembolization may be temporal, and in these cases the recovery of the vascular endothelium may not have been adequate. Studies by Borner et al (14) and Daniels et al (21) suggest that the hepatic vasculature requires 3 months to recover from chemoembolization. Within this interval, the vessel walls may be more thrombogenic.

Alternatively, the subendothelial layers of the vessel wall may be somewhat weakened by the proliferation of fibroblasts and the production of the extracellular matrix, which leads to intimal hyperplasia. These changes probably are limited to the distal hepatic arterial branches. The proximal hepatic artery is probably not affected to a considerable degree, as there is no statistically significant increase in the prevalence of hepatic arterial complications in these patients after orthotopic liver transplantation.

A limitation of this retrospective study is that it was not possible to review the microscopic histopathologic findings in the common hepatic artery immediately after the chemoembolization. To our knowledge, the extent and time course of the arterial response to the trauma of chemoembolization is currently unknown. In the early postprocedural period, evaluation of the arteries could reveal evidence of the chemoembolization effect such as the presence of embolic material. Damage to the endothelium would look similar in the weeks to months after the chemoembolization, as the body's response to injury is essentially the same whatever the mechanism. If the endothelium is damaged by cytotoxicity, direct trauma from catheterization, thrombosis of the vessels secondary to the embolization, or a combination of these, then the recruitment of platelets and fibroblasts and the production of extracellular matrix leading to intimal hyperplasia will result (19). In the patients in our study, evidence of arterial damage was found in the hepatic branch vessels.

Hepatic arterial thrombosis is a catastrophic graft-threatening complication of orthotopic liver transplantation, with a reported prevalence of 2%–25% (22,23). Early hepatic arterial thrombosis may manifest as fulminant hepatic necrosis in the early posttransplantation period. Rapid clinical deterioration often manifests as rising hepatic enzyme levels. Alternatively, late hepatic arterial thrombosis may manifest as a bile leak secondary to ischemia of the biliary tree and result in biloma formation (22,23). Other manifestations include relapsing bacteremia, fever of unknown origin, and sepsis.

Doppler US is the best noninvasive screening examination for hepatic arterial thrombosis (24). Doppler US is most helpful in excluding the diagnosis of hepatic arterial thrombosis and has a greater than 90% negative predictive value (25). In the setting of rapid clinical deterioration and equivocal US findings, patients often undergo arteriography for a definitive diagnosis.

Hepatic arterial chemoembolization is effective in slowing the progression of hepatocellular carcinoma in patients awaiting orthotopic liver transplantation. The toxicity of chemoembolization may cause an arterial injury or decrease the arteries' ability to tolerate the trauma of catheterization of the hepatic arterial tree. This may explain the vasculitis associated with hepatic arterial chemotherapy. The vasculitis associated with hepatic arterial chemotherapy and the resultant changes probably are limited to the distal arterial branches, as there is no statistically significant increase in the prevalence of hepatic arterial complications after orthotopic liver transplantation.


   Footnotes
 
Author contributions: Guarantors of integrity of entire study, H.M.R., H.A.M.; study concepts and design, H.M.R., J.E.S., H.A.M.; definition of intellectual content, H.M.R., J.E.S., H.A.M.; literature research, H.M.R.; clinical studies, H.M.R., J.E.S.; data acquisition, H.M.R.; data analysis, H.M.R., W.Y.W.L., H.A.M.; statistical analysis, H.M.R., W.Y.W.L.; manuscript preparation, H.M.R.; manuscript editing, H.M.R., W.Y.W.L., H.A.M.; manuscript review, all authors.


   References
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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