Keywords

Introduction

Initial efforts at human liver transplantation in the early 1960s were marred by extremely poor postoperative survival, with the earliest organ recipients surviving for 0–23 days postoperatively [1]. Following improvements in surgical technique, the focus shifted from postoperative patient survival to survival of the graft, and efforts were concentrated on optimizing antirejection regimens [2]. In the current era, patients undergoing liver transplantation have survival rates of 82%, 70%, and 65% at 1, 5, and 10 years, respectively [3]. Despite significant improvements in survival following liver transplantation, posttransplant complications are not uncommon, and image-guided interventional strategies have emerged as a reasonable alternative to open or laparoscopic reoperation in the management of many of these complications.

Postoperative complications following liver transplantation can be divided into three broad categories: arterial, venous, and nonvascular.

Arterial Complications

Hepatic Artery Thrombosis

Hepatic artery thrombosis (HAT ) is the most common arterial complication following liver transplantation, historically affecting 2–12% of liver transplant recipients [4,5,6,7]. More recent studies suggest a drop in incidence to 3–5% [8]. HAT is a leading cause of graft loss, accounting for up to 53% of cases of liver graft failure and carrying a mortality rate of greater than 80% when untreated [9, 10]. Even with intervention, this complication is fatal in approximately 1/3 of affected recipients [11, 12]. Apart from inherent risks related to surgical technique (e.g., kinking at sites of anastomosis), risk factors for the development of HAT include donor age > 60 years, back-table arterial reconstruction, use of an arterial conduit, cytomegalovirus infection, donor death secondary to cerebrovascular accident, increased cold ischemia time, rejection, ABO blood group incompatibility, and primary sclerosing cholangitis [12,13,14,15]. HAT is subdivided into early and late forms, with early HAT typically defined as occurring within 30 days of transplantation. The distinction is an important one as the clinical presentation, urgency of intervention, and impact on graft outcome are different.

The incidence of early HAT in adults ranges from 2.6 to 9% [16]. Early HAT typically occurs prior to the development of any meaningful collateral arterial vasculature, although collateral vessels have been documented angiographically as early as 2 weeks following transplantation [11]. Collateral vessels are largely derived from the phrenic vessels and typically develop 2–4 months following transplantation [16, 17], which may explain the less severe clinical course of late HAT. Early loss of arterial flow to the graft can result in acute fulminant hepatic failure, as well as necrosis of the arterial-dependent biliary ducts and uncontrollable sepsis in the immunocompromised patient [18].

The incidence of late HAT ranges from 1 to 25% [19]. Late HAT typically presents with biliary tract complications with or without fever [4] with a median time to presentation of 6 months [19].

The standard treatment of HAT is liver retransplantation; however, a shortage of available donor organs as well as the associated high mortality with retransplantation has led to a pursuit of alternate treatment options, including surgical thrombectomy (with or without anastomotic revision) and endovascular intervention in the form of intra-arterial thrombolysis (IAT), percutaneous transluminal angioplasty (PTA), and PTA with stent placement [8]. In a study by Duffy et al. [13] evaluating outcomes of vascular complications in 4200 liver transplant recipients, 65% of patients with HAT underwent surgical exploration and thrombectomy with or without anastomotic revision, 17% required retransplantation, and 3% underwent catheter-directed thrombolysis. Despite attempts at revascularization, up to 75% of liver transplant recipients who develop HAT will ultimately require retransplantation [13].

Murata et al. [18] reviewed outcomes of 120 consecutive adult patients who underwent living donor liver transplant. A total of nine patients (7.5%) developed HAT and underwent endovascular treatment with an overall reported technical success rate of 78% (7/9 patients). Intra-arterial thrombolysis (IAT) alone was successful in one patient, six patients were treated with both IAT and percutaneous transluminal angioplasty (PTA) , and two patients underwent IAT with PTA and stenting. The two patients failing endovascular management were observed and did not require further intervention. Complications included hepatic arterial rupture (n = 1) and arterioportal shunt formation (n = 1).

A review by Singhal et al. [20] examined 69 cases of endovascular treatment of HAT collected from 16 separate published studies. Thrombolysis was found to be successful in 68% of cases (47/69). Among the patients successfully treated with thrombolysis, 62% (n = 29) required further intervention in the form of PTA alone (n = 4), stent placement alone (n = 20), and PTA with stent placement (n = 5). The most common reported complication was hemorrhage (n = 18; 38%), with three cases proving fatal.

Failed endovascular intervention may also complicate subsequent surgical intervention (either in the form or revascularization/anastomotic revision or retransplant) in the early period due to possible catheter-related intimal injury to the artery [18] or at a later period due to the presence of stents at desired anastomotic sites [21].

Sheiner et al. [22] found that graft salvage outcomes were different among patients with HAT who were asymptomatic at time of presentation versus those who were symptomatic (elevated liver function tests, bile leak, sepsis): asymptomatic patients had a graft salvage rate of 81.8% vs. only 40% among those patients with symptomatic HAT. This difference in outcomes led the authors to conclude that attempts at emergent revascularization be reserved for patients with asymptomatic HAT, while those with symptomatic HAT should undergo retransplantation.

Hepatic Artery Stenosis

Unlike HAT, hepatic artery stenosis (HAS ) has a more insidious presentation with more gradual graft dysfunction (Fig. 8.1) [23, 24]. The incidence of HAS ranges from 5 to 15% [25] and typically presents within 3 months of transplant. Risk factors for HAS are similar to those of HAT, with the added risk factor of intraoperative clamp injury [26]. An untreated stenosis can progress to HAT in more than half of the patients, and many stenoses are therefore diagnosed concurrently with HAT [13, 23, 27]. Historically, these lesions were treated surgically with resection of the stenotic segment and reanastomosis with or without the use of an aortic conduit graft, interposition vein/artery graft, or vein patch angioplasty [23]. Endovascular treatment with PTA with or without stent placement has since replaced surgical intervention as the treatment of choice for HAS, except in cases of early (≤7 days posttransplant) thrombosis or stenosis where surgical revascularization remains the standard of care [25]. PTA is successful in 85–100% of patients with HAS and has a 1-year reported patency rate ranging from 50 to 90% [13, 27,28,29,30,31,32].

Fig. 8.1
figure 1figure 1

Hepatic arterial stenosis: (a) Color doppler images of the transplant arterial vasculature demonstrating findings consistent with high-grade anastomotic stenosis. (b) Reconstructed CTA confirming the sonographic findings. (c) Pretreatment DSA of the high-grade stenosis. (d) Balloon angioplasty of the stenotic segment. (e) Post-angioplasty DSA demonstrating improved stenosis

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In a series of 870 patients who underwent liver transplantation, a total of 30 patients (3.4%) developed critical HAS, defined as >50% luminal narrowing, and were treated with endovascular intervention [25]. Patients were not candidates for endovascular intervention within the first 21 days following transplant due to risk of arterial anastomotic rupture and hemorrhage; these patients were therefore managed with systemic anticoagulation and/or antiplatelet agents until 21 days postoperatively and underwent PTA at that time. PTA was successfully completed in 27/30 patients (90%), with 23 patients undergoing PTA with stent placement and 4 undergoing PTA alone. Failed intervention was secondary to an inaccessible hepatic artery in two patients and arterial dissection in one patient. A total of ten patients developed restenosis (33%)—four were restented, three were transplanted due to ischemic cholangitis, and three did not require further intervention. Eight patients were retransplanted following PTA, largely owing to symptomatic ischemic cholangitis (7/8 patients). At 1, 3, and 5 years, overall patency rates were 68%, 62.8%, and 62.8%, respectively.

A meta-analysis comparing treatment outcomes in patients with HAS undergoing either stent placement or PTA alone found similar procedural success rates (98% vs. 89%) and rates of arterial patency at ≥6 months (68% vs. 76%) [31]. There were no significant differences in complication rate or requirement for re-intervention or retransplantation.

Hepatic Artery Pseudoaneurysm

Hepatic artery pseudoaneurysms (HAP ) are rare, occurring in 1–2% of liver transplant recipients (Fig. 8.2) [33]. HAP can be subclassified as extrahepatic and intrahepatic pseudoaneurysms. Historically, extrahepatic pseudoaneurysms were thought to be more spontaneous in nature, while iatrogenic pseudoaneurysms were localized to the intrahepatic hepatic arteries [33, 34].

Fig. 8.2
figure 2

Extrahepatic hepatic artery pseudoaneurysm : (a) Sonographic images demonstrating a “yin-yang” sign consistent with a pseudoaneurysm. (b) Post-contrast MRI shows the presence of an extrahepatic pseudoaneurysm. (c) DSA confirms the presence of the pseudoaneurysm

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Extrahepatic pseudoaneurysms typically arise within 30–60 days posttransplant and are generally infectious (mycotic infection, postoperative infectious arteritis) or technical (dissection) in etiology [33, 35,36,37]. They have been reported to occur more frequently in patients with biliary-enteric anastomoses [33, 34]. Ruptured extrahepatic pseudoaneurysms typically present with hemodynamic instability (50–67%) or gastrointestinal bleeding and hemobilia (22–25%) [33, 38, 39]. Other nonspecific signs may include anemia, elevated liver function tests, and infection/sepsis.

Intrahepatic pseudoaneurysms are often iatrogenic in nature and arise either during or shortly after an interventional procedure (e.g., PTAs, percutaneous transhepatic cholangiography, biopsy) within the intrahepatic hepatic arteries [5, 6, 40]. With the advent of minimally invasive management of both HAT and HAS, an increasing number of extrahepatic pseudoaneurysms may now be classified as iatrogenic in etiology [41].

The standard treatment of HAP is surgical resection with arterial reconstruction, particularly in cases of mycotic infection where interventional efforts may provide a nidus for continued infection [42]. HAPs may be asymptomatic or can rupture into the GI tract, peritoneum, or biliary system. In cases of active hemorrhage, emergent occlusion of the hepatic artery may be necessary. For non-mycotic extrahepatic HAPs, coil embolization and stent-graft placement are potential endovascular treatment options [5, 6, 33, 40]. In cases of extremely tortuous arterial vasculature, direct percutaneous access may be necessary for embolization and thrombin injection [37].

In a retrospective study by Saad et al. [41], a total of 20 pseudoaneurysms were identified out of 1857 liver transplants (1.1%). Of these 20, 9 were spontaneous pseudoaneurysms (extrahepatic), while the remaining 11 were iatrogenic (intrahepatic; 4 secondary to angioplasty and 7 after biliary intervention). Endovascular management was attempted in 12 patients with a technical success rate of 83% (10/12). In one patient, attempted selective embolization of the HAP resulted in thrombosis of the entire hepatic artery. Unfortunately, despite the relatively high technical success rate, the overall 1-, 3-, and 6-month graft survival rates were 70%, 40%, and 35%, respectively.

Pseudoaneurysms typically present within the first 60 days after transplant, prior to the development of significant arterial collateral vessels, when preserved arterial flow to the graft is critical [34, 36, 39, 43,44,45]. Incidentally discovered HAPs must be treated due to the high risk of rupture and resultant life-threatening bleeding [35]. During active hemorrhage, occlusion of the hepatic artery, either with surgical ligation or via endovascular intervention, may be necessary, with resultant graft loss [33, 35]. Independent of intervention, HAP confers a high rate of retransplantation (33–45%) and mortality (33–78%) [33, 35, 38, 39, 45,46,47]. Although surgical resection/revision remains the mainstay for definitive management of HAP, there may be a role for endovascular management in stabilizing or temporizing unstable patients either as a bridge to retransplantation or to allow them to undergo definitive treatment in a more elective setting [41].

Splenic Artery Steal Syndrome

In patients with longstanding liver disease and portal hypertension, splanchnic blood flow can preferentially shunt to regions of lower resistance, namely, the splenic vascular bed, with subsequent development of splenomegaly and enlargement of the splenic artery. When the degree of blood flow shunted away from the high-resistance liver parenchyma becomes clinically significant, this is termed “splenic artery steal syndrome (SASS) ” and may result in hepatic failure and/or biliary injury. The diversion of blood flow away from the hepatic vascular bed can persist even after liver transplantation and may even be further augmented by graft injury, rejection, or hepatitis [48]. Proposed treatment options include splenectomy, splenic artery ligation/embolization, or the use of an interposition graft between the common hepatic artery and aorta to drive blood flow back toward the liver [49].

In a series of 350 patients who underwent orthotopic liver transplantation, Uflacker et al. [48] reported a total of 11 patients with liver ischemia secondary to SASS (3.2%). All 11 patients were treated with splenic artery coil embolization, and all demonstrated improvement in both LFTs and clinical parameters within 24 h. One patient went on to develop hepatic artery thrombosis 24 h after embolization and required surgical intervention with an interposition graft following unsuccessful hepatic artery recanalization.

A larger retrospective series by Nüssler et al. [50] included 1250 consecutive patients who underwent orthotopic liver transplantation and reported a total of 69 cases (5.9%) of SASS via the splenic or gastroduodenal artery. Twenty-five patients were classified as having SASS prior to undergoing liver transplantation, while the remaining 44 patients were diagnosed after transplant. Of the 69 total patients with SASS, 18 were treated with splenectomy, 29 with coil embolization of the splenic or gastroduodenal arteries, and 9 with splenic artery banding.

The highest complication rates were observed in patients diagnosed with SASS after liver transplantation who were subsequently treated with coil embolization. Half of these patients developed local or systemic septic complications, 8 required secondary splenectomy, 7 required retransplantation, and 5 of the 29 patients who underwent coil embolization died (four from graft failure and one from sepsis and multiorgan failure). This high complication rate was attributed to distal placement of embolization coils in the first 15 patients with resultant splenic infarction and abscess. No complications were reported after more proximal placement of embolization coils.

Of the patients treated with splenectomy (n = 18), two patients died from biliary complications despite retransplantation. No complications were reported in the remaining 16 patients. Patients treated with splenic artery banding demonstrated normalization of graft perfusion without any reported associated complications.

Thirteen patients had mild symptoms of SASS and were untreated; however, three of these patients subsequently required retransplantation for biliary ischemia.

Technical Management of Arterial Complications

Hepatic Angiography

Initial angiograms are usually performed through a standard trans-femoral approach, although a trans-brachial or trans-radial approach can also be used. A 5-Fr catheter such as a C-2 Glidecath (Terumo, Tokyo, Japan) is used to select the celiac axis. Initial digital subtraction angiograms (DSA ) are performed. Further DSA images may be obtained in various obliquities depending on patient anatomy. A cone-beam computed tomography (CBCT) may be of benefit to better identify sites of potential pathology.

Arterial Thrombolysis

If HAT is identified during initial angiography, mechanical and/or pharmacologic thrombolysis can be performed. Depending on the size of the occluded vessel, a 2.4- or 2.8-Fr microcatheter or a 4- or 5-Fr catheter can be advanced over a 0.018″ or 0.035″ guidewire, respectively, into the thrombus. Angiograms performed from this point may allow for evaluation of the extent of the thrombus.

Mechanical thrombolysis can be performed using various techniques including balloon maceration or suction thrombectomy. Pharmacologic thrombolysis is often performed in concert with mechanical thrombolysis. A multi-sidehole infusion catheter is positioned in the thrombus with infusion of a thrombolytic agent such as recombinant tissue plasminogen activator (r-tPA, Alteplase; Genentech, San Francisco, CA) over 12–48 h. Alteplase is infused at a rate of 0.5–1.0 μg/h often in conjunction with a basal rate (250–500 U) of heparin delivered through the sheath. Patients are often admitted to a monitored unit for serial neurologic evaluation. Serial lab values including fibrinogen, PTT and PT/INR, and hemoglobin are also assessed in regular intervals.

Arterial Angioplasty

A long vascular sheath such as a Flexor Ansel Guiding Sheath (Cook Medical, Bloomington, IN) is introduced over a 0.035″ or 0.038″ wire and seated at the celiac artery origin to provide additional support for tracking of an angioplasty balloon. The sheath is sized to accommodate the angioplasty balloon, usually 6- to 8-Fr in size. Initial angiograms can be used to determine the appropriate size of the balloon for angioplasty. Intravenous heparin (3000–5000 U bolus or 50–80 U/kg) should be delivered prior to crossing the HAS/HAT. HAS can be crossed with a 0.035″ hydrophilic guidewire such as a Glidewire (Terumo, Tokyo, Japan) or a 0.010–0.018″ microwire. An over-the-wire or monorail balloon system can be used for angioplasty once the HAS is crossed. Often, serial upsizing of the balloon is performed to reduce potential risks of arterial perforation. If suboptimal results are seen following balloon angioplasty, a scoring or cutting balloon may be utilized followed by a high-pressure balloon. These balloons should be used with caution as they may confer a higher rupture rate.

Arterial Stenting

For inadequate results following angioplasty, or complications such as vessel rupture, a stent may be placed. Given the relative rigidity of stents, a guide catheter should be utilized for delivery. If possible, the guide catheter should be advanced into the common hepatic artery to provide additional support during stent delivery and placement. Bare metal or covered stents can be utilized for persistent HAS; covered stents should be used for pseudoaneurysm or rupture. Self-expanding stents may be utilized for HAS but many prefer to use balloon-mounted stents for more accurate positioning. If a self-expanding stent is used, the stent should be upsized 10–20% above the size of the treatment vessel. Although practice varies, patients are routinely maintained on antiplatelet agents post-stent placement, especially for a covered stent.

Splenic Artery Embolization

Splenic artery embolization is performed after a standard angiogram to delineate the splenic and hepatic arteries. The splenic artery is subselected with a 3–5 Fr catheter. After sizing the vessel, embolization can be performed in the proximal splenic artery. Fibered coils are most often utilized for this purpose; however, vascular plugs can also be used. Care should be taken to perform embolization in the proximal splenic artery as distal embolization can lead to increased complications such as splenic infarction and infection.

Venous Complications

Portal Vein Thrombosis

The incidence of posttransplant portal vein thrombosis (PVT ) ranges from 3 to 10.6% and occurs more frequently in pediatric population as well as in recipients with pre-existing portal hypertension, hypoplastic portal veins, donor-recipient vessel size mismatch, graft edema, significant portosystemic collaterals, prior treatment for portal hypertension (e.g., TIPS), intimal injury at time of surgery, and technical problems with the anastomosis (e.g., kinking/twisting, stenosis) [13, 51,52,53,54,55]. The presence of pre-transplant PVT has also historically been associated with a higher incidence of posttransplant PVT and patients with intrahepatic extension of PVT were previously ineligible for transplant [56]. The data supporting the exclusion of these patients is inconsistent, however, with one published report citing no significantly increased risk of posttransplant portal vein rethrombosis relative to controls [57] and others reporting a highly variable incidence of posttransplant rethrombosis ranging from as low as 5% to as high as 40% in some series [56, 58, 59]. Sharma et al. [60] demonstrated that patients with pre-existing extensive PVT (n = 78) had a significantly higher rate of non-thrombosis-related graft failure (9.0% vs. 1.3%) and retransplantation (17.9% vs. 7.7%) when compared with controls (n = 78). More recently, the decision to offer liver transplant to this patient population has been left to the discretion of the transplant surgical team [61].

PVT typically presents within the first month following liver transplantation (“early”), but may present later (“late”). PVT manifests clinically with symptoms of portal hypertension (e.g., ascites, splenomegaly, variceal bleeding) and with elevation of liver enzymes [21, 62]. Early PVT has been associated with a 100% rate of graft loss [62]. Endovascular treatment options include catheter-directed thrombolysis (via percutaneous or transcatheter approach) followed by angioplasty with or without stent placement and TIPS creation [8, 62].

Limited data is available on long-term patency rates following interventional treatment of PVT; however, data is available on long-term patency rates for angioplasty with or without stent placement for portal vein stenosis and will be discussed in the following section.

For patients who are not candidates for endovascular intervention, surgical thrombectomy, anastomotic revision, or retransplantation may be necessary [5, 6, 40, 63].

Portal Vein Stenosis

Portal vein stenosis (PVS ) affects approximately 5% of liver transplants and almost always occurs at the site of anastomosis [41, 62]. The majority present more than 6 months after liver transplant and manifest clinically with symptoms of portal hypertension (including ascites, splenomegaly) and may progress to PVT without treatment [8, 21, 42]. PVS is more common with split grafts, especially pediatric split grafts where the incidence has been reported to be as high as 27% [62, 64,65,66], and is attributed to the relative size mismatch between the recipient portal vein and the graft portal vein. Prior splenectomy has also been associated with a fivefold higher rate of PVS [65].

PVS is treated with balloon angioplasty with technical success rates ranging from 36 to 71% at 2–3 years [62, 67]. In cases of concomitant portal vein thrombus, thrombolysis may be performed for 12–48 h prior to angioplasty. If angioplasty is unsuccessful (pressure gradient >5 mmHg across the stenosis), or if there is recoil stenosis or residual stenosis greater than 30%, then a stent may be placed [8] with long-term patency rates reported to be nearly 100% at 3–5 years [62, 68] (Fig. 8.3).

Fig. 8.3
figure 3figure 3

Portal vein stenosis : (a) ultrasound demonstrates elevated velocities at the portal vein anastomosis. (b) Digital subtraction venography (DSV) of the left portal vein demonstrates stenosis of the main portal vein at the anastomosis (arrow). (c) Balloon angioplasty of the portal vein stenosis. (d) Post-venoplasty DSV demonstrates marked improvement of the stenosis

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Hepatic Venous Outflow Stenosis and Thrombosis

Venous outflow stenosis or occlusion involves the hepatic veins (HV) or inferior vena cava (IVC) at rates of 4–5% and 1%, respectively [69, 70]. It is more commonly seen in livers that are transplanted in piggyback fashion [71]. Patients with Suprahepatic IVC stenosis may present with ascites, pleural effusion, and/or Budd-Chiari-type symptoms, while stenoses involving the infrahepatic IVC manifest with lower extremity edema. Outflow stenosis or obstruction of the hepatic veins, on the other hand, results in vascular engorgement and passive congestion of the transplant liver. Early complications are usually related to technical issues during transplantation, while late complications are more often attributed to intimal hyperplasia and/or fibrosis at the anastomosis [72] (Fig. 8.4).

Fig. 8.4
figure 4

IVC stenosis : (a) CT venogram demonstrates a high-grade stenosis of the intrahepatic IVC. (b) Conventional venacavagram demonstrates complete occlusion of the IVC and development of extensive collateral veins. (c) Venoplasty of the stenotic segment. (d) Post-venoplasty image demonstrates no residual stenosis or collateral venous flow

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The treatment of venous outflow stenosis or thrombosis is similar to PVT/PVS and includes thrombolysis (12–48 h prior to angioplasty, if applicable) and balloon angioplasty with or without stent placement depending on the degree of residual stenosis following balloon dilation [8]. Technical success is defined as a decrease in the trans-anastomotic gradient to less than 3–5 mmHg [72, 73] for both the IVC and HV. The reported patency rate following HV angioplasty is 60% at 1 year, with an increase to nearly 100% with assisted angioplasty [74]. For IVC stenosis/occlusion, patency rates are only 40% at 1 year with angioplasty alone, with an increase to 91% following stent placement [72, 73, 75]. Due to the inferior patency rates with angioplasty alone, primary stenting is recommended for treatment of both HV and IVC stenosis/occlusion [8].

Portal Vein Thrombolysis/Venoplasty

Direct portal vein access is obtained with an 18 or 21 gauge needle under direct sonographic guidance. A trans-splenic route may be used if portal access cannot be obtained due to thrombus. A 0.035″ guidewire is advanced (through a transition set if a 21 gauge needle is used). A 6–8 Fr sheath is advanced over the guidewire. For thrombolysis, a multi-sidehole infusion catheter can be placed to perform a prolonged thrombolysis as previously described. For portal vein stenosis, an angled 5-Fr catheter is advanced through the sheath and, along with a hydrophilic wire, is traversed through the stenotic lesion. The 5 Fr catheter can be exchanged for a pigtail catheter to perform a direct portal venogram and to measure the portal venous pressure gradient. After appropriate sizing of the vessel, a prolonged balloon venoplasty is performed. Intravenous bolus of heparin may be delivered prior to venoplasty. For stenosis that is resistant to balloon venoplasty , an intraluminal stent can be placed as described in the arterial intervention section.

Transjugular Intrahepatic Portal-Systemic Shunt (TIPS) Placement

A TIPS shunt may be created to augment portal venous flow prior to thrombolysis. After obtaining jugular access, a 9 Fr sheath is advanced into the SVC. An angled 5 Fr catheter is used to select the right hepatic vein. Over a stiff wire, a TIPS access needle such as the Colapinto needle (Cook Medical, Bloomington, IN) is advanced. The needle is advanced anteriorly in attempt to select a branch of the portal vein. A partially contrast-filled syringe is attached to the back of the needle, and the needle is retracted while negative syringe pressure is applied. Once blood is aspirated, contrast is injected to confirm positioning of the needle within the portal vein. A wire is advanced through the needle into the portal venous system, and the needle is exchanged for a marking pigtail catheter. Here, direct portal venous pressures are obtained and the portal-systemic pressure gradient is calculated. Simultaneous venograms are performed through the sheath (positioned in the hepatic vein) and the pigtail catheter to measure for the appropriate stent length. The liver tract is balloon dilated—we prefer with an 8 mm diameter balloon—followed by stent deployment. A partially covered stent (Viatorr, Gore Medical, Flagstaff, AZ) is preferred due to superior patency rates over bare metal stents. The transjugular route through the TIPS can then be used to position the multi-sidehole catheter in the portal vein thrombus for thrombolysis.

Nonvascular Complications

Biliary Stricture (Anastomotic and Non-anastomotic)

The overall incidence of biliary stricture following liver transplantation is approximately 13%, as reported by a recent large meta-analysis including 14,000 patients [76]. Symptoms of biliary stricture include jaundice, abdominal pain, cholangitis, and increased liver function tests; some patients, however, may be asymptomatic [8]. Magnetic resonance cholangio-pancreatography (MRCP) can aid in the diagnosis of biliary stricture, as well as delineate the affected areas within the biliary system. Owing to the reliance of the biliary system on hepatic arterial blood supply, patients with known or suspected biliary stricture(s) should be further evaluated for arterial complications with either Doppler ultrasound or CT angiography.

The majority (75%) of biliary strictures occur at the anastomosis and may be attributed to surgical error or technique (e.g., anastomotic breakdown, local tissue ischemia, fibrosis) [77,78,79]. Patients with early postoperative bile leak have also been shown to be at increased risk for developing anastomotic stricture [80]. Non-anastomotic strictures occur in the setting of graft arterial compromise (hepatic artery thrombosis/stenosis) or other ischemic cholangiopathy (e.g., prolonged cold ischemia time) [81] and are often hilar in location, although they may be present intrahepatically in a diffuse manner.

Endoscopic retrograde cholangio-pancreatography (ERCP) is often attempted initially with cholangioplasty and stent placement [8]. Although treatment success rates can be as high as 90%, multiple treatment sessions are generally needed [77, 78, 82]. For patients with endoscopically inaccessible biliary systems, e.g., those with biliary-enteric anastomoses, percutaneous intervention with transhepatic biliary drain placement and cholangioplasty may be performed. Similar to ERCP intervention, sequential dilatation with or without concomitant catheter drainage is necessary for achieving the best clinical outcome. Patency rates have been reported to be close to 90% at 5 years following transplantation [83, 84] in patients amenable to percutaneous intervention. For the small subset of patients who cannot be managed endoscopically or via percutaneous methods, surgical revision of the anastomosis may be necessary.

Regarding patients with non-anastomotic strictures, treatment success is dependent on the number, location, and severity of strictures [81], with extrahepatic strictures being more likely to respond to therapy. Patients who fail treatment or who develop secondary biliary cirrhosis, recurrent cholangitis, or progressive cholestasis may require retransplantation.

Biliary Leak

Bile leaks have been reported in up to 25% of patients undergoing liver transplantation and can be classified as either early (within 4 weeks of transplant) or late (more than 4 weeks after transplant) [80, 85,86,87]. They generally occur at the anastomosis and may be secondary to T-tube removal, ischemia, or downstream obstruction (including sphincter of Oddi dysfunction) [88] or can occur at the cystic duct stump or along the cut edge of the graft in living donor liver transplant [89]. Patients with bile leak typically present with abdominal pain, fever, and signs of peritonitis, although these symptoms may be masked by corticosteroid administration.

Biliary leaks, including non-anastomotic leaks and communicating bilomas, may be successfully treated with diversion, either via ERCP with sphincterotomy and stent placement or with percutaneous transhepatic cholangiography and stent placement in patients not amenable to ERCP due to anatomic considerations. These interventions have been reported to be successful in 85–100% of cases [90].

Non-communicating bilomas may be treated with antibiotics with or without accompanying percutaneous drainage [76, 77]. Finally, biliary leaks occurring secondary to ischemia are more difficult to treat as the underlying cause may not be amenable to endoscopic or percutaneous intervention; in these cases, surgical intervention may be necessary for definitive management [80].

Percutaneous Transhepatic Cholangiogram (PTC) and Cholangioplasty

Pre-procedural antibiotics should be administered to reduce the risk of cholangitis. PTC can be performed through the left or the right lobe of the liver. Direct access to the biliary tree can be obtained with a 21 gauge needle under sonographic guidance. If the bile duct is not visible, the needle can be advanced under fluoroscopic guidance especially if accessing the right liver lobe. For a right liver lobe access, the access site should be below the tenth intercostal space and anterior to the mid-axillary line to reduce the risk of pneumothorax. The needle is then slowly retracted with contrast administration under fluoroscopic guidance to demonstrate filling of the biliary tree. Once the needle tip is confirmed to be within the biliary tree, a 0.018″ wire is advanced into the biliary system. A transition set is then advanced over the wire. We prefer to perform a complete cholangiogram through the outer catheter of the transition set to assess areas of stricture or leak. A combination of an angled catheter and hydrophilic wire can be used to cross areas of stricture or leak. For lesions which are difficult to traverse, an external drain may be placed for decompression with a reattempt at crossing the lesion in 1–2 weeks. Once the stricture is crossed, an internal/external biliary drain is placed (Fig. 8.5).

Fig. 8.5
figure 5

Bile duct stricture : (a) MRCP demonstrating bile duct stricture with more proximal dilatation of the intrahepatic bile duct. (b) This finding was confirmed on PTC. (c) Biliary drain placed for decompression and dilation of stricture with contrast flowing through the bile duct into the duodenum

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For bile leaks, repeat cholangiograms may be performed every 6–12 weeks to assess for sealing of the leak. For biliary stenosis, serial cholangioplasties may be performed every 4–6 weeks. With each cholangioplasty , the drain may be exchanged for a larger diameter catheter. This may be a prolonged process, and patients should expect to have a drain in place for weeks to months. Once there is evidence of resolution of the stricture, the internal/external biliary drain is exchanged for an external biliary drain. The patient is then reevaluated in 1–2 weeks to ensure resolution of the stricture at which point the drain may be removed.