Transplant Hepatic Artery Rupture

Abstract

A case of transplant hepatic artery thrombosis treated with thrombolysis and vascular stenting is presented. Stenting was complicated by hepatic artery rupture necessitating emergent stent graft placement. Hepatic artery occlusion in a liver transplant often leads to biliary complications such as ischemic cholangiopathy, biliary necrosis, cholangitis, biloma formation, intrahepatic abscesses, and liver failure. Prompt recognition and appropriate treatment of hepatic artery thrombosis are necessary to avoid graft failure and possible death.

A 41-year-old man with a past medical history of ulcerative colitis and primary sclerosing cholangitis had undergone an orthotopic liver transplant 12 years prior. The initial transplant was complicated by hepatic artery thrombosis (HAT). Patient underwent emergent retransplant with a jump graft to the aorta 18 days after initial transplant. The patient did well for the next 12 years until he presented to an emergency department (ED) with nonspecific symptoms of fatigue and headaches. Lab results showed a small rise in bilirubin to 2.4mg/dL (baseline of 1.2–2.0mg/dL; normal range: 0.1–1.2 mg/dL). A computed tomography (CT) of the abdomen and pelvis was performed, and the finding of HAT was missed ( Fig. 1 ). He then re-presented to the ED 5 days later with persistent headaches and fatigue. At this time, a white count of 40×10 ⁹ (normal range: 4.5–11×10 ⁹ /L) and further increase in his total bilirubin to 3.6mg/dL were found. Transplant artery ultrasound (US) showed a tardus parvus waveform in the hepatic artery and the recent CT was re-reviewed. Intravenous antibiotics were initiated, and interventional radiology (IR) was consulted for emergent catheter-based thrombolysis/thrombectomy.

Fig. 1.

Axial contrast-enhanced CT of the abdomen shows thrombosis (black arrow) and partial mural calcifications (white arrow) of a jump graft. Possibly due to the atypical takeoff of the transplant jump graft (below origin of the superior mesenteric artery), this finding was missed.

After cannulation of the jump graft, a 5-Fr sheath was placed into the jump graft with coaxial MicroMewi (Medtronic, Minneapolis, MN). Tissue plasminogen activator infusion at 1.5 mg/hour with 500 U heparin through the sheath was initiated ( Fig. 2 ). In addition, the patient was receiving intravenous heparin with a partial thromboplastin time of 60 to 80. At 18 hours after thrombolysis initiation, the patient acutely decompensated with worsening sepsis. This paradoxical deterioration was thought to be related to reperfusion of the infected and partially necrotic liver. The patient was subsequently stabilized and brought for a thrombolysis check 30 hours after initiation. Angiography revealed marked improvement in hepatic arterial flow with tandem stenoses ( Fig. 3 ). The decision was made to stent these areas of stenosis. The maximal dimension of the jump graft was 9 mm. A 10 mm × 37 mm Express (Boston Scientific, Marlborough, MA) balloon-expandable stent was placed. Post deployment angiogram showed significant contrast extravasation ( Fig. 4 ). A balloon occlusion catheter was inflated at the site of vessel injury and a 9 mm × 10 cm stent graft (GORE VIABAHN, Flagstaff, AZ) was placed. Post deployment angiography showed occlusion of the hepatic artery and the jump graft ( Fig. 5 ). Therefore, thrombolysis was reinitiated. Patency of the hepatic artery and jump graft was restored 24 hours later.

Fig. 2.

Emergent angiography was done with placement of a 5-Fr FlexorAnsel-1 (Cook Medical, Bloomington, IN) sheath into jump graft origin and TPA was infused through a MicroMewi (Medtronic, Minneapolis, MN) catheter at 1.5 mg/h and heparin was infused through the sidearm of the sheath at 500 U/h. Thrombolysis rather than thrombectomy was chosen given the extensive length of the thrombus extending through the intrahepatic artery branches.

Fig. 3.

After 30 hours of thrombolysis, the patient returned to IR for follow-up angiography. Patency of the hepatic artery was restored ( a ) but on oblique imaging, significant stenosis at the origin and a kink in the proximal jump graft were seen ( b ; white arrows).

Fig. 4.

A 10 mm × 37 mm Express (Boston Scientific, Marlborough, MA) balloon-expandable stent, which was erroneously oversized, was deployed, resulting in significant extravasation at the distal end of the stent (black arrow).

Fig. 5.

Balloon tamponade was performed to immediately control the extravasation. Then, a 9 mm × 10 cm long covered stent (GORE VIABAHN, Flagstaff, AZ) was placed. Repeat angiography showed interval rethrombosis of the hepatic artery. Thrombolysis was reinitiated.

Outpatient surveillance Doppler US 4 weeks after stent placement showed tardus parvus of the intrahepatic arteries consistent with stenosis. Angiography was done, confirming stenosis of the distal proper hepatic artery. This was treated with angioplasty ( Fig. 6 ). The patient did well for the following 3 weeks until he presented with polymicrobial sepsis due to multifocal hepatic infarcts/abscesses/bilomas ( Fig. 7 ). Ultrasound was performed showing a widely patent hepatic artery. Unfortunately, he passed away 3 days later.

Fig. 6.

The patient was discharged, and parvus tardus waveforms were again seen on follow-up surveillance Duplex ultrasound. The patient returned to IR for repeat angiography, which showed patent jump graft and intrahepatic arteries but stenosis of the distal proper hepatic artery (black arrow) ( a ). Angioplasty was performed gently with a 3 mm × 2 cm Armada balloon (Medtronic Abbott Park, IL) ( b ) with moderate luminal gain (white arrow) ( c ).

Fig. 7.

Despite patency of hepatic artery confirmed on subsequent follow-up ultrasounds and CT, the patient's clinical condition deteriorated and 7 weeks after initial procedures, the patient re-presented to the emergency department with sepsis and was found to have multifocal hepatic infarctions, bilomas, and abscesses (white arrowheads). Despite medical therapy, the patient passed away 3 days after presentation.

Discussion

The hepatic artery is of prime importance in transplanted livers. HAT is a significant complication and may result in ischemic cholangiopathy, bile leak, graft loss, and/or patient death. Early HAT, variably defined as thrombosis within 21 or 30 days after transplant, is often fatal if left untreated. ¹ Late HAT, which can be due to a variety of causes including rejection and cytomegalovirus infection, is serious, but less likely to be fatal. ²

Unlike hepatocytes, whose blood supply is from both the portal vein and hepatic artery, the biliary endothelium is solely dependent on arterial supply. In native livers, transcapsular arteries (e.g., intercostal arteries or inferior phrenic arteries) allow collateral perfusion of the biliary endothelium in the event of hepatic artery occlusion. In a transplant liver, these extrahepatic collateral supplies are less consistently present and, when present, they are less robust. Additionally, in native livers, retrograde perfusion (portal vein to arteriole) via the peribiliary plexus provides blood supply to the biliary endothelium in the setting of HAT. In a transplant liver, the peribiliary plexus is damaged. ^{3 4 5 6} There are multiple potential clinical manifestations of ischemic cholangiopathy ( Table 2 ). Survival rates in patients with HAT are significantly lower than those without. ^{7 8 9}

Table 2. Varied clinical manifestations of hepatic artery thrombosis ^{4 8 9} .

Manifestations of ischemic cholangiopathy
Abnormal liver function tests/hyperbilirubinemia
Bile leak
Bile cast formation
Bile duct necrosis
Biliary strictures, often multifocal
Bilomas

In our patient, HAT was missed on the initial CT scan; examination of the hepatic vascular supply is essential when interpreting imaging of a patient who has previously undergone liver transplantation. By the time the artery occlusion was recognized, significant damage to the graft had occurred, as evidenced by the developing bilomas seen on imaging and marked hepatic laboratory abnormalities.

In this patient, two focal areas of stenosis were seen in the jump graft. The decision was made to stent these stenoses to maximize future patency. Two errors led to oversizing and subsequent jump graft rupture. The first was that the stent was sized at an area of post-stenotic dilation. Then, graft degeneration and ballooning, possibly related to a kink in the vein graft, had occurred over time. ¹⁰ Therefore, the size of the initial stent placed, while slightly oversized to the measurement of the widest part of the jump graft, was significantly oversized compared with the original jump graft width. While balloon-expandable stents allow for precise deployment, tradeoff is acute wall stress during deployment. ¹¹

Stent grafts are a well-known bail out in the setting of iatrogenic vessel rupture. ¹² Immediate availability of the appropriately sized stent graft should be part of planning for any procedure in which vessel rupture is possible. In this case, an approximate 10-minute delay to obtain the appropriately sized stent with ongoing balloon tamponade of the hepatic artery likely led to rethrombosis, further delaying durable patency of the hepatic artery by another 24 hours.

Conclusion

Patency of the hepatic artery is of paramount importance in the transplant liver, and HAT often results in biliary complications ( Table 1 ) and is associated with a higher mortality rate. Prompt recognition and treatment of HAT is essential to avoid biliary endothelial necrosis and its possible sequelae. In this case, after successful thrombolysis, two inciting areas of stenosis were revealed. The chosen stent was erroneously significantly oversized leading to extravasation and graft disruption. While the site of injury was effectively treated with stent graft placement, the irreparable damage to the transplant liver and bile ducts due to the initial delay in recognition of hepatic artery thrombosis as well as the subsequent rethrombosis resulted in biliary necrosis, bilomas, sepsis and ultimately the patient's death.

Table 1. Potential etiologies of hepatic artery thrombosis.

Etiology of HAT

Vessel injury/kink

ABO incompatibility

Prior transarterial chemoembolization

Hypercoagulability

CMV infection

Chronic rejection

Notes: Early and late etiologies may overlap, but early etiologies are most likely surgical issues/vessel injury during transplant acute rejection. Late hepatic artery thrombosis (HAT) etiologies are more commonly cytomegalovirus (CMV) infection and chronic rejection.