Keywords
orthotopic liver transplant - Doppler ultrasound - computed tomography angiography - hepatic artery thrombosis - living donor liver transplant
Liver transplantation (LT) is the curative therapeutic option for patients with end-stage liver disease (ESLD) and hepatocellular carcinoma (HCC).[1]
[2] Within the last two decades, LTs have increased in frequency, becoming the second most common organ transplant in the United States as of 2020.[3] However, it is important to note that in South America, access to LT interventions can be more limited compared with other parts of the world due to a variety of factors such as funding, infrastructure, and the availability of organ donors.
The success rates of LT exceed 80% at 1 year and 70% at 5 years.[4] Due to the inherent complexity of the surgery and the presence of comorbidities, it is paramount to become familiar with prompt diagnosis and therapeutic options for perioperative complications. Surgical and minimally invasive approaches can be conducted by multidisciplinary teams to reduce morbidity and improve graft survival.[5]
Despite the challenges, South American countries such as Brazil, Argentina, and Chile have made significant progress in LT interventions over the years. These countries have established specialized transplant centers and have invested in medical training and research to improve patient outcomes.
The most common complications related to LT can be classified based on the time of presentation (intraprocedural or postprocedural) or the affected system (hepatic artery, portal vein, hepatic vein, or biliary system). In this review, we will address the complications based on the affected system.
Vascular Complications
Vascular complications (VCs) may occur after orthotopic liver transplant (OLT) in the immediate, early, or late posttransplant period. The most frequent VCs include stenosis or rupture of the relevant vasculature (as listed in [Table 1]). The incidence of VCs has decreased due to improvements in surgical technique, imaging, and patient care. However, prompt recognition, investigation, and management are still necessary to further reduce patient mortality and morbidity. The incidence of VCs differs between living-donor recipients and the pediatric population.[6]
[7]
[8] In adult deceased donor LT, the overall incidence of VCs is ∼7%, and almost 13% in living donor liver transplantation (LDLT).[9]
Table 1
Description of the different types of vascular complications, including the vascular territory, type of complication, timeframe, and clinical presentation
|
Vessel
|
Pathology
|
Timeframe
|
Clinical presentation
|
|
Hepatic artery
|
Thrombosis
|
Can be early or late
|
Early
Graft failure, sharp rise in transaminases, hemodynamic instability
Late
Fever, biliary complications, asymptomatic
|
|
Stenosis
|
Late
|
Mild
Elevated transaminases, progressive biliary complications
Severe
HAT, graft failure
|
|
Pseudoaneurysm
|
Within the first 2 mo
|
Hypotension, gastrointestinal bleed, elevated transaminases
|
|
Portal vein
|
Thrombosis
|
Can be early or late
|
Early
Graft failure, hemodynamic instability
Late
Portal hypertension—variceal bleeding
|
|
Stenosis
|
Late
|
Portal hypertension—splenomegaly, oesophageal varices
|
|
IVC/Hepatic veins
|
Thrombosis
|
Can be early or late
|
Suprahepatic
Graft failure, sharp rise in transaminases, hemodynamic instability, ascites
Infrahepatic
Ascites, elevated transaminases, ankle edema, portal hypertension
|
|
Stenosis
|
Typically late
|
Abbreviations: IVC, inferior vena cava; HAT, hepatic artery thrombosis.
In the early postoperative period, Doppler ultrasound (DUS) evaluation of the vasculature is crucial.[10] In case of suspected vascular abnormality on DUS, further confirmation with angiography, computed tomography angiography (CTA), or magnetic resonance angiography (MRA) should be performed to depict the anatomy and possible treatment plan better. In the presence of hemodynamic instability or deterioration of the clinical condition, surgical revision is indicated, which can, in some scenarios, lead to reanastomosis or retransplantation (as shown in [Table 1]).
Hepatic Artery Thrombosis
Hepatic Artery Thrombosis
The most common and feared VC in OLT is hepatic artery thrombosis (HAT), which affects 2 to 12% of transplants and can lead to death due to graft failure.[11]
[12]
[13] Mortality has been reported as high as 60%.[14] Early HAT (<30 days after OLT) is more frequent than late HAT (>30 days after OLT).[14]
[15] Many factors can impact the frequency of HAT, including technical, donor, and recipient characteristics. Early thrombosis of the hepatic artery has a dramatic presentation and can lead to postoperative liver failure. Sometimes more indolent presentations can be found with elevated liver enzymes, bacteremia, or ischemic cholangiopathy.[16] Late thrombosis of the hepatic artery has a milder course due to the presence of collateral vessels that provide recanalized arterial flow to the biliary tract.[11]
[17] Absence of blood flow on DUS or lack of contrast opacification distal to the anastomosis in CT, magnetic resonance imaging (MRI), or digital subtraction angiography (DSA) can confirm the diagnosis.
Risk factors for HAT include errors in surgical technique, ABO blood group incompatibility, massive transfusion, acute rejection, prolonged cold ischemia time, and the use of jump grafts.[18] Living donor transplantation, split livers, and pediatric LT have been reported to have an increased risk of arterial thrombosis, although some groups of excellence have achieved remarkable good results.[19]
[20] Other risk factors described are locoregional therapies such as transarterial chemoembolization (TACE) used in patients with HCC and aberrant arterial anatomy. TACE can induce vessel wall damage due to the mechanical effect of instrumentation, chemotherapy, and embolic particles.[20]
[21] Arterial mismatch at the anastomotic level can precipitate turbulence and sluggish flow with subsequent thrombosis.[22] The surgical loupes have been shown to reduce the incidence of HAT,[23] and surgical intervention has been the treatment of choice, especially in early complications, due to the fear of inducing serious complications related to endovascular treatment in the first 2 weeks.[24]
Early HAT has generally been managed by urgent revascularization to avoid graft loss.[25] There are reports of graft survival of 48.8 months with thrombectomy and arterial reanastomosis. When performed within the first week after transplantation, the probability of achieving graft salvage is 81%.[25] Some patients may survive with urgent revascularization, but bile duct damage may progress, and retransplantation may be necessary due to ischemic cholangiopathy. Pérez-Saborido et al reported 240 LTs, 8 with HAT (4 early and 4 late), and 4 hepatic artery stenosis (HAS). In this study, all early and late thromboses (except one late thrombosis that was asymptomatic) were treated surgically, including retransplantation.[26] The success rate with surgical management was 75% in early HAT. Of the four patients with HAS, only one achieved a good response to endovascular therapy, with the other three requiring surgical management. Warnaar et al reported 232 pediatric LTs, with 13.7% developing acute HAT (32 patients), 14 of who underwent direct retransplantation, and 16 underwent urgent surgical revascularization (8 thrombectomies, 6 thrombectomies plus thrombolysis, 1 thrombectomy plus arterial reconstruction, and finally 1 thrombectomy plus thrombolysis and arterial reconstruction). The long-term hepatic artery patency in this study was achieved in six patients (38%) and 1-year graft survival in these six patients was 83%. Ten patients required OLT with a survival rate slightly better than that of patients with urgent surgical revascularization, but without statistical significance.[27]
In a systematic review, early HAT was found on 843 (3.86%) patients (a total of 21.822 OLTs) and reported urgent surgical or endovascular revascularization in 257 cases. The success rate was 56%, in those with earlier revascularization.[28] Late management of HAT is directed by complications related to chronic graft ischemia, but surgical management is not indicated because the failure rate is almost 100%.[25]
Endovascular interventions are planned considering longevity of the anastomosis as well as the anatomic location of the thrombosis. In general, it is recommended to perform interventions 6 weeks after the transplant for safe manipulation of the arterial anastomosis. Treatment alternatives include recanalization with selective intra-arterial thrombolysis, angioplasty, and in certain circumstances stent graft insertion if arterial stenosis is suspected.[9] However, when the thrombosis is located within the intrahepatic HA branches, thrombolysis with the use of rheolytic is an important “rescue alternative” to reestablish the flow. Literature reports remain controversial when comparing the outcomes of surgical versus endovascular revascularization in HAT[29]
[30] ([Fig. 1]).
Fig. 1 (a, b, c) Digital subtraction angiography (DSA) demonstrates the absence of blood flow to the thrombosed hepatic artery distal to surgical anastomosis (red arrow). (b) Recanalization of the hepatic artery using a microwire (red arrow) and microcatheter. (c) Angiogram post direct thrombolysis injected in the hepatic artery with recanalization of the artery including intrahepatic branches (red arrows).
Hepatic Artery Stenosis
Hepatic artery stenosis is a less frequent complication after LT, occurring in 0.9 to 9.3% of cases, and typically presents later, ∼3 months after transplantation.[31] Stenosis can also lead to thrombosis of the hepatic artery. HAS is often subclinical, with elevated liver enzymes being the primary manifestation, but it can also lead to bile duct complications. Early diagnosis of HAS is important to prevent complications.[32]
[33] Stenosis usually involves anastomosis, and end-to-end anastomosis is more frequently associated with HAS.[13]
Several risk factors for HAS have been identified, including clamp injury, intimal dissection, vessel caliber discrepancy, excessive length with kinking, angulations, and extrinsic compression, or acute cellular rejection.[34] Low intraoperative hepatic artery and portal flow is also a risk factor for HAS.[35] Doppler imaging is used for the diagnosis of HAS, which can show turbulence with a peak systolic velocity of more than 200 cm/s, or when this velocity is three times greater at the anastomosis than in the preanastomotic segment. The prestenotic segment shows elevation of resistance index (RI; >0.8) and low flow, while the poststenotic segment presents a low RI (<0.5) and a “tardus-parvus” morphology. Arterial kink due to vessel redundancy or mismatch between donor and recipient size can demonstrate similar findings in the DUS.[22]
[32] CTA is the preferred method to obtain more information after Doppler and to increase diagnostic accuracy, and it can be performed quickly in sicker patients as compared with MRA.[32]
[36]
Surgical management of HAS is more difficult due to adhesions. Intervention depends on the degree of stenosis; patients with ∼50% occlusion may not require intervention. Angioplasty with stent placement can carry high risk for patients,[37] and revision of anastomosis can resolve or improve stenosis with controversial results.[13]
[38] In a study by Abbasoglu et al, out of 857 LTs, 41 patients had HAS, with 17 (41.4%, 17/41) being treated with primary reanastomosis. This subgroup had three deaths. Eleven (26.8%) were treated with aortohepatic iliac artery graft, which also had 3 deaths. Percutaneous balloon angioplasty was performed in six patients (14.6%), with one death in this group. Other procedures performed less frequently were interposition vein graft, vein patch angioplasty, and interposition artery graft. Graft survival was 56% and patient survival was 65% at 4 years.[34] Another study by Saad reported successful treatment in 81% of 42 cases of HAS treated by percutaneous transluminal angioplasty (PTA), with a 7% incidence of immediate complications, including dissection and arterial rupture.[39]
After transplantation, patients should have a baseline DUS to assess HA patency and other factors, such as velocity and RI. If findings are consistent with stenosis higher than 70% (with velocities above 400 cm/s or below 50 cm/s, and RI lower than 0.5), prompt intervention is necessary[40]
[41] ([Fig. 2]). CT angiography is a noninvasive test that improves the diagnosis and helps plan future interventions ([Fig. 3]). Previously, surgical repair was the primary treatment for these patients, but now endovascular treatment is almost exclusively used. Techniques such as plain balloon angioplasty (PBA) or stent deployment in the stenotic area have replaced surgical resection or aortic conduit, which were the primary options in the past for a HAS. Both PBA and stenting have a success rate of up to 90% with a low risk of complications[42] ([Fig. 4a, b]). The decision to use stenting is recommended when PBA does not produce good angiographic results, and this decision should be made by the interventional radiologist during the procedure.[35] Recanalization and wire manipulation across the stenosis can cause artery thrombosis; so, anticoagulation is recommended.
Fig. 2 Patient after liver transplantation with hepatic artery thrombosis. Doppler ultrasound (DUS) images showed low velocity of 20 cm/S and RI of 0.48.
Fig. 3 CTA with MIP 3D reconstruction demonstrates narrowing of the hepatic artery at the anastomosis site (red arrow) next to surgical clips, compatible with hepatic artery thrombosis.
Fig. 4 (a) Digital subtraction angiography image demonstrating focal stenosis within the hepatic artery after liver transplantation (red arrow). (b) Postangioplasty angiographic acquisition with the recovery of the caliber within the stenotic portion of the hepatic artery (red arrow) and good distal flow (different oblique view).
Hepatic Artery Pseudoaneurysm
Hepatic Artery Pseudoaneurysm
Hepatic artery pseudoaneurysm (HAP) is a rare VC that can occur within 30 days after LT surgery or due to damage during percutaneous intervention of the hepatic artery[43] ([Fig. 5]). Although HAP is often asymptomatic and detected on routine imaging, it can cause abdominal pain or gastrointestinal bleeding. If HAP ruptures, it can be life-threatening, with a mortality rate up to 75%.[44] Doppler US is useful for identifying HAP, and immediate intervention is required to prevent rupture.[44]
[45] Risk factors include infection, percutaneous liver biopsy, or biliary interventions with bile leak. Diagnosis can be made with DUS, contrast-enhanced CT, or angiography.[46] Interventional radiological coil embolization is becoming the treatment of choice, with direct US-guided puncture and thrombin injection also a feasible treatment. Surgical revision involves resection of the pseudoaneurysm and protection of arterial inflow to the graft via an aortohepatic conduit. Covered stent graft deployment is another option but requires experience in managing complications such as rupture.[47]
Fig. 5 (a
and b) Patient with acute bleeding symptoms 1 month after liver transplant. (a) Digital subtraction angiography demonstrated evidence of a hepatic artery pseudoaneurysm (red arrow) not identified in the CT scan. (b) During angiography, a small, covered stent was advanced but could not navigate to a proper position due to a high tortuosity of the artery (the catheter could not cross distal for a stable position to deploy the stent, red arrow). The surgical team decided to move the patient to the operating room and resect the pseudoaneurysm in a surgical fashion.
Celiac Stenosis
Patients with celiac stenosis post-LT can develop symptoms due to single supply to the hepatic artery of the graft.[48] If detected intraoperatively, median arcuate ligament (MAL) compression can be fixed through surgical division which can improve blood flow to the hepatic artery. The principal treatment is surgical bypass creation, most of the time using a segment of the iliac artery to create an autohepatic bypass. A less frequent option, although less invasive, consists of stenting the origin of the celiac axis, which can be done using a balloon-expandable bare metal stent to improve the flow toward the graft ([Figs. 6] and [7]).
Fig. 6 (a) Celiac axis stenosis at its origin (red arrow). (b) In the angiographic image, there is retrograde flow to the celiac coming from SMA via the duodenal arch (red arrows).
Fig. 7 Patient status posts liver transplant 3 days before (a) celiac axis stenosis was noted (red arrow). (b) Treatment with balloon-expandable bare metal stent improves inflow to the hepatic artery (red arrow).
Portal Vein Thrombosis
The incidence of portal vein thrombosis (PVT) ranges from 1 to 4%.[9]
[15] Its incidence is increased in patients with previous portocaval shunts.[13] The severity of the presentation depends on the time of the PVT, with earlier occurrences (within 3 months) being more severe than later ones (see [Table 1]). Common causes of PVT include surgical technical issues during LT, such as venous redundancy, kinking, or stenosis of the anastomosis.[9] The usual manifestations of PVT are associated with symptoms of portal hypertension. When PVT is found on DUS, the intervention depends on clinical judgment of the severity. Treatment may include thrombectomy, revision of the portal anastomotic site, or retransplantation.[15]
The endovascular management of PVT posttransplant depends on multiple major characteristics, including the acuity of the thrombosis, the time from the transplant that the thrombosis occurs, and clinical conditions such as coexistent procoagulant syndrome. Factors such as the anatomic extent of the PVT based on the Yerdel criteria,[49] the presence of nonocclusive versus occlusive clot, and the type of anastomosis may help set a strategic therapeutic approach.
In acute PVT, mechanical thrombectomy can be a feasible alternative with careful patient selection and very precautious in recent anastomosis (<6 weeks old). In these last scenarios, surgical thrombectomy can be safer and more indicated. Endovascular pharmacological infusion of thrombolytics within the clot is a good alternative whenever there is no clinical contraindication. The portal vein approach for catheter-based thrombolysis and thrombectomy can be percutaneous transhepatic, transsplenic, or transjugular, and both procedures can be performed in one setting.[50] Reestablishing portal vein flow depends on the appropriate inflow from physiologic mesenteric and splenic flow as well as the outflow in the intrahepatic portal vein circulation and sinusoids. If the intrahepatic branches are compromised, the vein can re-thrombose despite efforts, and in this scenario, insertion of a transjugular portosystemic shunt (TIPS) can be beneficial. The time of thrombolytic infusion depends on the levels of fibrinogen, requiring continuous monitoring and management in the intensive care unit if available. If the fibrinogen drops below 150 mg/dL, the risk of bleeding can increase.[51]
Chronic PVT posttransplant is infrequent, and recanalization depends on the type of anastomosis. The combination of transhepatic and transileocolic approach has been reported in the literature.[52] Usage of systemic anticoagulants will prevent the clot to expand into intrahepatic branches (when located in the main portal vein or proximal to it) and these patients need to be closely followed up and under systemic anticoagulation with periodical imaging monitoring. Incidence is very low and most of the patients are asymptomatic because collateral circulation has already formed.
Portal Vein Stenosis
Accounting for less than 5% of VCs after LT, portal vein stenosis (PVS) occurs mostly at the anastomosis site.[52] If it occurs within the first 6 months after LT, it is considered related to the procedure itself. However, if it occurs after this time, it is not considered secondary to surgery.
The presentation of PVS varies depending on the degree of occlusion. When the occlusion is more severe, clinical signs of portal hypertension, such as splenomegaly and esophageal varices, with or without graft failure, are observed.[53]
The first screening tool to diagnose PVS is the DUS, which is sensitive but not specific. The criteria for diagnosing PVS include a DUS stenosis ratio > 50% or a portal velocity ratio > 3, confirmed with contrast-enhanced CT and portography.[9]
Asymptomatic patients with normal hepatic function and PVS may not require therapeutic intervention but should be screened periodically due to the risk of PVT.[9]
As PVS typically occurs at the anastomotic site, surgical intervention can be performed as a revision of the portal vein end-to-end anastomosis. However, percutaneous transhepatic approaches, such as balloon angioplasty and stent deployment, are now available and maintain good results with less periprocedural morbidity[54] ([Fig. 8a, b]). Studies have demonstrated that single balloon angioplasty was able to maintain patency in 77.7% of patients in a mean follow-up of 2 years.[55] Another option to improve the outflow and gain access in patients with continuous bleeding is the transjugular intrahepatic portosystemic shunt (TIPS), but this is a more complex procedure in which indications and techniques go beyond the scope of this article.[56]
Fig. 8 (a
and b) Digital subtraction angiography images of venogram showing portal vein stenosis at the anastomosis after a liver transplant. (a) Angiography during venogram, preintervention demonstrating severe portal vein stenosis (red arrow), and (b) post–stent deployment (red arrow) with evidence of improvement of the blood flow toward the graft.
Late PVS is caused by secondary fibrosis or intimal hyperplasia. Some cases of PVS have been reported with neoadjuvant radiotherapy for cholangiocarcinoma as a risk factor for this complication.[9]
Inferior Vena Cava/Hepatic Vein Thrombosis and Stenosis
Inferior Vena Cava/Hepatic Vein Thrombosis and Stenosis
This is a rare complication that can occur in both the suprahepatic and infrahepatic inferior vena cava (IVC) and presents as Budd–Chiari syndrome. It is associated with a high mortality rate of 50 to 70%, which worsens if it occurs in the immediate postoperative stage or if there is severe or complete occlusion of IVC.[13] Suprahepatic occlusion is more severe than infrahepatic occlusion due to the risk of impacting the heart, including graft dysfunction, which is shared by both types of occlusions. Clinically, occlusion by stenosis presents with mildly increased bilirubin and serum transaminases. If the stenotic occlusion is severe or there is a thrombus, graft failure can occur, typically with renal failure and hemodynamic instability depending on the site of the occlusion.
The causes of both stenosis and thrombosis are typically technical in nature, but a patient's history of Budd–Chiari increases the risk of IVC/hepatic vein thrombosis postoperatively.[57] Basic diagnostic tools for diagnosing caval anastomosis complications include DUS and contrast-enhanced CT. A transjugular venogram with pressure gradient measurements is indicated for evaluating the upper caval anastomosis, providing additional access for simultaneous treatment.[50]
Treatment requires immediate intervention and either revision of the anastomosis or urgent retransplantation. If the patient is too unstable, then re-transplantation is preferred. However, depending on the clinical presentation, some patients may require only monitoring, with treatment being dependent on the patient's presentation as well as the radiological findings.[58]
Besides surgical treatment, percutaneous management with angioplasty and stent placement has become a safe procedure with very high success rates even in the long-term (96–100%).[59]
[60] Coexistence of IVC and hepatic vein stenosis is infrequent and reported.[61] The evaluation requires anatomic detail of the IVC or hepatic veins anastomosis via venogram and intravascular ultrasound (IVUS) if available. Hemodynamic pressure measurement can be helpful, especially when the differential diagnosis of outflow impairment includes other causes such as congestive heart failure. In general, a gradient above 3 mm Hg between the right atrium and IVC or hepatic vein, depending on the level of the anastomosis, can be suspicious for stenosis. If obstructive symptoms persist despite venous angioplasty and stenting, consideration of TIPS or direct intrahepatic portal vein shunt can be helpful tools with technical success like nontransplant patients[62] ([Fig. 9a, b]).
Fig. 9 (a and b) Digital subtraction angiography images in a patient with severe ascites post-transplant. (a) Angiography demonstrated stenosis within the inferior vena cava at the level of anastomosis (red arrow). (b) A bare metal stent was deployed with the recovery of the caliber (red arrow) and good flow to the RA restored.
Hepatic Artery Hypoperfusion Syndrome (Splenic Artery Steal Syndrome)
Hepatic Artery Hypoperfusion Syndrome (Splenic Artery Steal Syndrome)
Hepatic arterial hypoperfusion of the liver graft can be related to preferential flow into the splenic and gastroduodenal arteries. This situation can be associated with portal hyperperfusion and, if left untreated, can result in devastating effects on the liver graft, potentially leading to loss and ischemic cholangiopathy. Portal hyperperfusion, especially in patients with prior portal hypertension, can cause arterial vasoconstriction, which decreases the hepatic artery flow. The incidence of this condition after LT is almost 4%, and most of the patients (80%) are identified within 2 months of the transplantation.[50] The diagnosis of this entity can be challenging, and if suspected, the patient requires angiographic evaluation. Once hyperperfusion from the portal vein is documented, proximal splenic artery embolization is a safe treatment alternative to divert the flow into the hepatic artery. Once the arterial flow in the spleen is reduced, the splenic and portal vein flow will decrease. In many cases, the splenic flow will recanalize through arterial collaterals such as the left gastric and intercostals, with less risk of splenic ischemia.[50]
Biliary Complications Posttransplant
Biliary Complications Posttransplant
These are the most common complications after OLT, with an incidence of 10 to 25%. They usually occur in the first 3 months but can occur several years after LT. A systematic review performed by Akamatsu et al, which included 61 articles, showed an incidence of 12.8% in 11,397 OLT in adults, 12% in cadaveric donors, and 19% in living donors (p = 0.0001).[63] The clinical presentation varies from asymptomatic to cholangitis. There are four main biliary complications, including anastomotic and non-anastomotic bile duct strictures, bile duct leakage, and ischemic cholangitis. Other less frequent complications include dysfunction of the sphincter of Oddi, hemobilia, and mucocele in the cystic duct remnant. Non-anastomotic bile duct stenosis is less frequent but much more complex due to the high rate of retransplantation (60–70%).
A review by Nemes et al in 14,400 patients found that patients with MELD >25, primary sclerosing cholangitis (PSC), and malignant neoplasms are at increased risk of biliary complications.[64] Anastomotic bile duct strictures, which are isolated stenoses located less than 1 cm from the surgical anastomosis, constitute 80% of bile duct complications, and the general incidence in LT is 4 to 9%. These can be early (<3 months) or late (after 3 months). Strictures are usually present during the first year. Technical problems are the most important risk factor, including the small caliber of the ducts, the tension in the anastomosis, the infection, and the inadequate suture material.[65] Cholangiocytes are more sensitive to ischemia than hepatocytes or Kuppfer cells; so, any damage to the blood supply during artery reconstruction or graft procurement can cause serious damage to the bile ducts. In addition, cold ischemia time for more than 9 hours increases the incidence of cholangiopathy, and during reperfusion, oxidative stress can activate Kuppfer cells and progress to more damage in the bile ducts.[66]
[67] Multiple other risk factors have been described, such as immunological factors, cytomegalovirus infection (by interaction with human leukocyte antigens [HLA]), and donor-specific alloantibodies. Donor characteristics, including graft steatosis and marginal grafts, can impact biliary outcomes. Etiology in early presentation (<1 year) is hepatic artery ischemia in 40 to 50% or preservation injury. Late presentation (>1 year) is due to an immunologic origin, for example, recurrence of primary sclerosant cholangitis, CMV infection or rejection.[68] For diagnosis, the sensitivity of ultrasound is 40 to 70%.[69] Note that the graft bile duct is not prone to dilatation with obstruction like the recipient bile duct.[68] MRI is the preferred method for diagnosis, and in duct-to-duct anastomosis, endoscopic retrograde cholangiopancreatography (ERCP) is the preferred method of treatment with a recurrence rate of 20 to 30%. Surgical technique: the use of T-Tube in the reconstruction of the bile duct after OLT is considered deleterious, and the decrease in its use in recent years is part of the lower rate of biliary complications after OLT.[70]
[71] Surgery is indicated when ERCP or percutaneous treatment fails, and Roux-en-Y anastomosis is the preferred method of treating this complication.[68]
The treatment of this complication is more complex, due to the multifocality and compromise of the small intrahepatic bile ducts. When endoscopic and percutaneous treatment fails to control this condition, retransplantation is often necessary.
Bile duct leak can occur at anastomosis, cystic remnant, and the transection area in split and living donors. The incidence rate is between 1 and 25%.[63] The systematic review conducted by Akamatsu et al with 55 papers included showed an incidence of 8.2% in 11,397 OLT in adults, 7.8% in cadaveric donors, and 9.5% in living donors. The onset of bile leak was between 1 day and 6 months after surgery.[72] Very early leaks (< 3 months) are due to technical problems or ischemia in the donor conduit. In LDLT, the section surface may also be the source of the bile leak. Late bile leak was associated with T-tube use but is now less common.[73]
[74] Surgery is indicated when percutaneous drainage fails, and re-anastomosis is necessary when the dehiscence is wide. The predominant symptoms are fever, bilio-peritonitis, abdominal pain, and in extreme cases, shock. Bilomas can also be present. CT and hepatobiliary iminodiacetic acid (HIDA) scintigraphy are perhaps the most important diagnostic tools. ERCP with stent insertion is an important initial tool in diverting the bile and bypassing the leak. However, in some types of bilioenteric reconstructions (e.g., hepatic jejunostomy), this approach can be challenging. Percutaneous drainage can also be challenging in nondilated biliary ducts. In that scenario, the patient will require general anesthesia. If a wire cannot cross the structure with the leakage area, an external drain will be recommended as the first step. In cases where multiple separate ducts are anastomosed, the cholangiogram will need to evaluate each different anastomosis, and eventually, multiple drainage catheters will be required. In cases of intrahepatic biloma, percutaneous drainage will allow injection contrast and identify a possible bile duct communication. In this case, the duct can be accessed to insert an internal external biliary drain.
Biliary stenosis occurs in 5 to 15% of transplant recipients after deceased donor and up to 30% in living donor recipients[75] ([Fig. 10a, b]). The anastomotic type manifests early and is related to donor–recipient mismatch or factors that affect surgical technique like fibrosis. A non-anastomotic stricture is associated with recurrent PSC, graft rejection, or prolonged ischemia during surgery. Percutaneous management includes internal external biliary drain insertion and bilioplasty or dilation protocol. Dhondt et al reported a 3-day balloon dilation protocol initially inflating the balloon during 20 minutes with a relatively good patency rate of 56% at 1 year.[76] Surgical anastomosis is the option if the dilation is refractory and persists during a dilation protocol. Ischemic cholangiopathy is a very difficult condition related to HAS or stenosis and in certain cases requires retransplantation. Palliative treatment includes percutaneous drainage with modest results due to the extension and multifocality of this disease.
Fig. 10 (a
and b) Fluoroscopy images of percutaneous cholangiogram in a posttransplant patient present with two separate bilioenteric anastomoses. (a) Right anterior and posterior ducts and severe stenosis at the anastomosis (red arrow). (b) After inserting two separate internal–external biliary drains (thick arrows), a biloma was developed in the right anterior system (red thin arrow).
Conclusions
Liver transplantation is a frequent procedure worldwide, which is not exempt from complications, some of which represent a diagnostic and therapeutic challenge. We present the most frequent complications from a combined surgical and imaging perspective, to provide a useful tool for multidisciplinary teams in these scenarios. The prompt suspicion, identification, and treatment minimally invasive, percutaneous, endovascular, or surgical, of these complications, is essential for the good outcome of patients.
Summary
It is important to promptly recognize post-LT complications to define the best available treatment and to improve the prognosis of these highly complex patients. With the review performed, we give greater clarity regarding the different complications, their classification, and their management by interventional radiology and surgery.
