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Intervention in the Liver Transplant Patient


Since the first clinical attempt by Thomas E. Starzl in 1963, liver transplantation is now accepted as the gold standard treatment of advanced chronic liver disease, of irreversible hepatocellular failure, and for a selected group of patients with hepatocellular carcinoma. There were 7841 liver transplants performed in the United States in 2016 according to the Organ Procurement and Transplantation Network. Actual 1-, 3-, and 5-year survival rates based on Organ Procurement and Transplantation Network 2016 Annual Report data, are 89.5%, 83.9% and 81.5%, respectively. The improving survival rates during the past 10 years are based on progress in medical care and surgical and endovascular techniques.

Technical Features

Orthotopic liver transplantation (OLT) consists of removing the damaged liver and replacing it with a graft in the recipient’s native hepatic bed. Heterotopic liver transplantation is when the graft is placed in an extrahepatic site, usually at the root of the mesentery, but is no longer used because of poor outcomes. Auxiliary liver transplantation is the placement of the donor liver in the presence of the native liver. Such transplants may be either orthotopic after removal of part of the native liver and placement of a portion of the donor liver or heterotopic. Segmental liver transplantation uses a portion of the donor liver. The conventional hepatectomy for OLT requires subdiaphragmatic clamping of the inferior vena cava and resection of the retrohepatic inferior vena cava along with the recipient liver.

Since 1989 another technique known as the piggyback technique has been more and more used. The major hepatic veins of the recipient are clamped and are interconnected, thus forming a cuff that can then be anastomosed to the suprahepatic vena cava of the donor liver, in an end-to-end or end-to-side fashion ( Fig. 38.1 ). This technique preserves the recipient retrohepatic vena cava and avoids vena caval clamping, thus preserving venous return during the operation and avoiding venovenous bypass. The donor-to-recipient portal vein anastomosis is performed in an end-to-end fashion. Arterial anastomosis between the donor and recipient arteries is usually end-to-end. The site usually varies depending on the arterial anatomy of donor and recipient and on the surgeon’s preference. One must recognize that patients with anomalous hepatic arterial anatomy may not have a large enough common hepatic artery to use as inflow. Patients with celiac axis stenosis may also have inadequate inflow. The median arcuate ligament syndrome has been described as affecting arterial inflow in liver transplantation.

FIG. 38.1, (A) and (B) Schematic drawing of the piggyback hepatic vein reconstruction. A common cuff from the confluence of the left and middle hepatic veins of the recipient is created and anastomosed to the donor suprahepatic inferior vena cava.

The biliary connections either involve a primary duct-to-duct technique (choledochocholedochostomy), which is the most commonly used, or require the performance of a choledochojejunostomy (to a Roux-en-Y defunctionalized intestinal loop).

Arterial Complications

Hepatic artery complications after liver transplantation are uncommon but represent an important cause of morbidity, mortality, and retransplantation. In the native liver, the biliary tree is protected from ischemia by a rich arterial network coming from choledochal branches originating from the posterior pancreaticoduodenal arcade, but also from the capsular branches. The liver graft parenchyma receives oxygen from both the portal vein and the hepatic artery, but the biliary tree is fed only by the hepatic artery. Thus arterial stenosis or occlusion may induce severe biliary complications, such as biliary necrosis, biliary leak, or liver abscesses.

In children, hepatic artery complications are more frequent but have fewer complications. In pediatric recipients, revascularization of the transplant through the adhesions to the diaphragm and other adjacent organs may protect the graft from ischemic complications.

Hepatic Artery Stenosis

Hepatic artery stenosis (HAS) occurs in 4% to 11% of transplants (one-third in the first month) with a mean delay between diagnosis and transplantation of 100 to 126 days. The mechanisms and predisposing factors for this complication are allograft rejection, microvascular injury associated with cold preservation of the liver or disruption of the vasa vasorum, failure of the surgical technique, clamp injury, caliber size mismatch, excessive vessel length with kinking and angulations, prior transarterial chemoembolization, and extrinsic compression.

Excluding conduits, most hepatic artery stenoses are anastomotic (46% to 75%), with distal stenoses representing 40% to 46% of cases. In 3% to 8% of patients, stenoses are proximal to the anastomosis in the recipient artery. Multiple stenoses are found in 5% to 25%, and in most cases (77%) anastomotic stenosis is coexistent with a distal stenosis.

Clinical presentation varies from asymptomatic with minimal increase in liver function tests results to acute liver failure or biliary complications. Laboratory findings are nonspecific and insidious. Doppler ultrasonography can enable early diagnosis.

Values considered indicative of HAS are a resistive index less than 0.5, a systolic ascending time greater than 100 ms, or an increased velocity at the stenosis of more than 400 to 450 cm/s. The right and the left hepatic arteries must be evaluated to detect more distal stenoses. Furthermore, a gradual decrease of the resistive index on additional ultrasound examinations could indicate imminent thrombosis.

Indications

A protocol for the management of HAS has been proposed by Saad et al., who recommend a combination of surgery and percutaneous transluminal angioplasty (PTA). Initially, hepatic artery PTA was reserved for a solitary focal stenosis and nonsurgical candidates with other types of lesions (tandem lesions, arterial kinking). However, advances in endovascular methods and equipment have increased the role of these interventional radiology techniques for many other indications. Repetitive endoluminal therapy is also required for post-PTA restenosis. Surgical revision is proposed for technical failure of PTA and hepatic artery thrombosis.

Contraindications

HAS with associated kinks (tandem lesions) can be considered a relative contraindication and should be managed surgically.

Equipment

  • Basic angiography set

  • Long 5Fr introducer sheath

  • Hydrophilic 5Fr cobra (or Simmons) catheter

  • Hydrophilic 0.035-inch guidewire

  • 0.014- or 0.018-inch guidewire

  • Balloon (size range: 4 to 6 mm)

  • Stent (size range: 4 to 6 mm)

Technique

Angiography is performed with standard catheter technique, mostly from a transfemoral approach, with 5Fr catheter. A long sheath up to the origin of the feeding vessel may be useful. The size of the balloon used ranges from 4 to 6 mm and can be chosen according to the automatic measurement using the sheath as a reference. Monorail balloon catheters make the procedure safer. Heparin is administered after crossing the lesion with a 0.014- to 0.018-inch guidewire. Recent studies have shown no benefits of primary stent placement versus PTA in procedural success, complications, return to normal liver function, arterial patency, survival, or requirement for reintervention or retransplantation ( Fig. 38.e1 ).

Fig. 38.e1, Percutaneous transluminal angioplasty of an anastomotic hepatic artery stenosis. (A) Selective hepatic artery angiography confirms the Doppler diagnosis of stenosis at the origin of the donor artery. (B) A balloon catheter is advanced over an 0.018-inch guidewire and inflated. (C) Angiogram after the procedure depicts a satisfactory result. No stent was deployed, and the hepatic artery is patent at 3-year follow-up.

Controversies

Numerous authors have described endoluminal treatment of HAS. Nevertheless, treatment of HAS is controversial because a high number of patients are asymptomatic. In fact, some authors reported that, if left untreated, HAS doubles the rate of biliary complications, thus reducing graft life expectancy. Furthermore, there is a progression from stenosis to thrombosis: The hepatic artery thrombosis rate for untreated significant HAS is 65% at 6 months, and hepatic artery thrombosis is associated with a higher morbidity and mortality than HAS.

Finally, a study by Pulitano et al. suggests that HAS intervention is associated with improved biliary stricture-free survival, but only in patients with a stenosis detected within the first 6 months of transplant. Thus patients developing HAS more than 6 months posttransplantation may be managed conservatively.

Outcomes

PTA and stent placement both have a high technical success rate (80% to 93%) and a procedural complication rate of 7% to 10%, including access site complications, arterial dissection, and, less frequently, arterial rupture.

Complications

The rate of immediate complications (rupture and dissection) ranges between 7% and 9.5%. , The hepatic artery thrombosis rate at 30 days is 5% and 19% at 1 year. Postprocedural anticoagulation and antiplatelet therapy may be beneficial in reducing this complication, but further investigations are required.

Postprocedural and Follow-Up Care

A monthly Doppler sonogram is recommended in the immediate 6 months after angioplasty.

Hepatic Artery Thrombosis

Hepatic artery thrombosis (HAT) is a rare but serious complication after liver transplantation, requiring retransplantation in almost 50% of patients. It occurs in 2.5% to 6.8% after OLT, and this incidence increases 5.8-fold when the donor hepatic artery has been reconstructed with an interposition graft to the supraceliac aorta. The risk of HAT is increased in children (11% to 26%) but is claimed to have reduced consequences if it occurs late after transplantation.

Celiac trunk compression by the median arcuate ligament and HAS are also described as predisposing factors. HAT is classified as early or late by its occurrence within or after 30 days after OLT. Early HAT represents 33% to 46% of cases, and may have a mortality rate as high as 55%, whereas it decreases to 15% if thrombosis occurs after this period. Furthermore, a recent retrospective review of 1560 patients from 1991 to 2009 demonstrated a progressive decline in the incidence of HAT over the years of the study, with a current rate of 2% to 3%.

Clinical presentation of HAT ranges from an increase in serum transaminase levels with or without cholestasis to liver abscess and biliary complications, including cholangitis, bile duct stenosis, or necrosis; liver dysfunction and hepatic failure may also be seen. Impairment of graft function is observed in patients with early HAT, whereas biliary tract destruction is seen more often in patients with late HAT. Biliary ischemia may manifest itself as a focal biliary problem limited to an anastomotic stenosis or a bile leak. In rare cases HAT can be clinically asymptomatic.

The key diagnostic technique is the detection of a loss of arterial signal by Doppler ultrasonography (potentially supplemented by microbubble contrast medium). This can be confirmed by contrast-enhanced computed tomography (CT) with lack of enhancement of the hepatic artery.

Indications

Emergency revascularization is of paramount importance to prevent the consequences of ischemia, in particular biliary ischemia. Retransplantation was initially considered to be the treatment of choice, but the postoperative survival rates were poor. Now endovascular treatment of HAT has emerged as an alternative procedure in the early phase after transplantation. A rapid intervention limits the consequences of ischemia and is more likely to be effective because the thrombus is fresh.

Contraindications

There are no contraindications except those related to all angiographic procedures (i.e., severe abnormal clotting, severe iodine allergy, renal failure).

Equipment

  • Similar as for stenosis

  • Urokinase or recombinant tissue plasminogen activator

  • ± Balloon and stent (size range: 4 to 6 mm) in case of underlying abnormality

Technique

After selective angiography and confirmation of the diagnosis, a catheter is advanced into the thrombus. The dose and timing of catheter-direct thrombolysis (CDT) vary. For example, Zhou and associates recommend the administration of a 100,000- to 250,000-IU bolus followed by a second bolus injection (250,000 to 750,000 IU) 30 minutes later if there is no response to the first bolus of thrombolytic agent. After the initial bolus injection(s), a continuous perfusion of urokinase (50,000 to 100,000 UI/h) is administered over 12 to 24 hours. During thrombolysis, additional angiography is performed to monitor the progress of treatment, and thrombolysis is discontinued as soon as the arterial thrombus is dissolved and the peripheral branches of the hepatic artery are perfused. If an underlying HAS is revealed after thrombus dissolution, balloon angioplasty with or without stent placement helps to prevent rethrombosis. Some authors also recommend leaving the catheter in place for 2 to 3 days to reintroduce thrombolysis in case of thrombus recurrence. Antibiotic therapy is usually prescribed, aiming at reducing the risk of liver abscess.

Outcomes

In a study in 2015, successful recanalization of the HAT was achieved in 46% of patients, but 30% of patients developed major bleeding complications. This study also showed that there was no difference in survival, the need for surgical revascularization, retransplantation rate, development of ischemic biliary complication, or procedural complications between patients with successful and unsuccessful recanalization.

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