Topic Highlight
Copyright ©The Author(s) 2016.
World J Hepatol. Jan 8, 2016; 8(1): 36-57
Published online Jan 8, 2016. doi: 10.4254/wjh.v8.i1.36
Table 1 Vascular complications following orthotopic liver transplantation
TypeDelay (incidence)Clinical presentationDiagnosisTreatment
Arterial complications
HAT incidence: 3.5%Early HAT (2.9%)Abnormal transaminaseDUSEmergent revascularization
Feverce-MDCTby endovascular intervention
Biliary complicationsAngiographyor surgical revascularization
Graft failureor rLT
Late HAT (2.2%)Asymptomatic
Abnormal transaminase
Bile leak
Hepatic abscess
HAS incidence: 2%-13%Early HASGraft failureDUSEndovascular intervention
Biliary complicationsce-MDCTor surgical revascularization
Late HASAsymptomaticDUSEndovascular intervention
Feverce-MDCTor surgical revascularization
Abnormal liver functionAngiography
HAP incidence: 2.5%AsymptomaticDUSEndovascular intervention
Abdominal paince-MDCTor surgical resection and revascularization
HAR incidence: 0.64%Gastrointestinal bleedingNone in emergencyEmergent surgical hemostasis
Massive bleeding through abdominal drainsand surgical repair
Hemorrhagic shock
Portal vein complications
PVT incidence: < 3%EarlyAbnormal transaminaseDUSrLT
Graf dysfunctionce-MDCTor surgical repair
Multi-organe failure(portal phase)or endovascular interventions
Variceal bleedingPortography
LateAsciteDUSCurative anticoagulant therapy
Portal vein hypertensionce-MDCT
Splenomegaly(portal phase)
Variceal bleedingPortography
PVS incidence: 2%-3%EarlyAsymptomaticDUSEndovascular interventions
Portal vein hypertensionce-MDCT
Abnormal transaminase(portal phase)
LateAsymptomaticDUSAnticoagulant therapy
Abnormal liver test function(portal phase)Endovascular interventions
Caval anastomosis complications
Caval resection and end-to-endEarlyAcute Budd-Chiari syndromeDUSEndovascular intervention
cavo-caval anastomosisGraf failurece-MDCTor surgical repair
Intestinal congestionCavographyor rLT
Renal dysfunction
Lower limb edema
LateModerate Budd-Chiari syndromeDUSEndovascular intervention
Piggy-backEarlyAcute Budd ChiariDUSSurgical repair
Graf failurece-MDCTor rLT
Intestinal congestionCavography
Renal dysfunction
Lower extremity edema
LateModerate Budd-ChiariDUSEndovascular intervention
Lower extremity edemaCavography
Renal dysfunction
Abdormal liver test function
Table 2 Hepatic artery thrombosis highlights
Summary of the clinical characteristics about HAT
HA supplies exclusively the bile duct, so HAT is associated with a high frequency of biliary complications
HAT represents more than 50% of all arterial complications following OL
The incidence of HAT following OLT is 3.5% with early and late HAT incidences of 2.9% and 2.2%, respectively
HAT carries an incidence of graft failure and mortality of more than 50% without prompt treatment
The median time to detection of early and late HAT was 6.9 d (range: 1-17.5 POD) and 6 mo (range: 1.8-79 mo), respectively
No differences in HAT incidences were observed between DDLT and LDLT
Clinical presentation spectrum: Mild elevation of serum transaminase and bilirubin levels (75%), biliary complications (15%), fever and sepsis (6%), graft dysfunction or failure (4%)
Risk factors of early HAT are mainly represented by technical problems, LDLT, cigarette smoking and hypercoagulability state, while late HAT is usually related to ischemic or immunologic injury: CMV positive donor, female donor and male recipient and hepatitis C seropositive recipient
Early diagnosis is achieved by assessing the serum transaminase level and performing Doppler ultrasound monitoring in the postoperative period and confirmed by contrast-enhanced abdominal CT scan and/or visceral angiography
Currently, the literature on the curative management of early HAT suggests the following procedures: First endovascular radiological intervention (IAT, PTA and stent placement), secondly open surgical revascularization, and finally retransplantation, which is associated with the best survival rate compared with revision or thrombolysis, but is a limited therapeutic option due to organ shortage
Table 3 Hepatic artery stenosis highlights
Summary of the clinical characteristics about HAS
Significant HAS is defined as a narrowing of the transverse diameter > 50% on the angiogram associated with clinical suspicion, with a resistive index < 0.5 and a peak systolic velocity > 400 cm/s detected by DUS
HAS occurs in 2% to 13% of transplants, at the level of the anastomosis (59% of cases), graft HA (41%) or recipient HA (2.6%)
HAS has been speculated to progress to HAT in 65% of cases at 6 mo for untreated HAS
The median time to diagnosis is 100 (range: 1-1220) d following OLT
Most of patients with HAS are asymptomatic and most commonly present only with abnormal liver function tests and in rare cases with graft failure
Routine screening by DUS during the postoperative period is mandatory because of the insidious clinical presentation
The risk factors are not really known, but among these, technical and surgical factors (vascular injury such as clamp injury, intimal dissection, faulty placement of anastomotic sutures, excessive length with kinking and angulation, differences in the vessel caliber that require and oblique anastomosis, vasa vasorum disruption) or acute cellular rejection
DUS is a non-invasive method for the assessment of HA patency, but a contrast-enhanced CT scan and angiography are required to confirm the diagnosis
Radiological endovascular intervention by PTA with or without stent placement is often used to treat post-transplant HAS and are both efficacious, with 7% to 12% of complications including dissection and arterial rupture, restenosis or thrombosis (25%) and 12% failed attempts
Surgical revision and retransplant showed a high rate of success, but the overall mortality rate was as high as 20%. In some case, HAS may be an early sign of chronic rejection
Table 4 Hepatic artery pseudoaneurysm highlights
Summary of the clinical characteristics about HAP
The reported incidence of HAP is ranging from 0.27% to 3% following OLT
In most cases, HAP is localized extra-hepatic and occurred in the early postoperative period around 1 mo post-OLT (69% within 20 d and 81% within 35 POD)
Clinical presentation varies from the asymptomatic state and incidental diagnosis to abdominal pain with fever and gastrointestinal bleeding (25% of cases, massive bleeding through the abdominal drain or acutely with hemorrhagic shock)
Risk factors include peritoneal infection, biliary leak, bilbo-digestive anastomosis and digestive leak
Diagnosis of HAP is confirmed by DUS (with lower performance), contrast-enhanced CT scan, magnetic resonance angiography or angiography
Treatment of HAP includes reoperation (urgent laparotomy for HA ligation: Mortality rate 60%; HAP excision and immediate revascularization with a cryopreserved arterial allograft: Mortality rate 28%) or interventional radiology (HA embolization with a coil or HAP exclusion with a covered stent)
HAP has a worse prognosis with an overall mortality of more than 50% (ranging from 53% to 100%)
Early recognition of HAP in the population at high risk is mandatory and allows for a successful therapeutic outcome in 100% of cases
Table 5 Hepatic artery rupture highlights
Summary of the clinical characteristics about HAR
HAT is defined as a severe hemorrhage from the trunk or from a main branch of the HA, resulting in disruption of graft arterial blood supply
This is a very rare (incidence of 0.64%) but a dramatic complication following OLT with a high mortality rate
In most cases, HAR complicates a pseudoaneurysm of the HA
The median time of HAR is 29 d (range: 2-92 d) following OLT
The clinical presentation is always a sudden hemorrhage: Hemoperitoneum, gastrointestinal bleeding, hematoma and hemobilia
Treatment comprises urgent laparotomy with definitive ligation of the HA, anastomotic revision and aortohepatic grafting or interventional radiology with percutaneous embolization
Table 6 Portal vein thombosis highlights
Summary of the clinical characteristics about PVT
The incidence of PVT is uncommon and ranges from < 3% following OLT
PVT incidence is higher in pediatric transplantation, LDLT and split liver transplantation
Early PVT is more frequent than late PVT with a median time to diagnosis of 5 d following OLT (range: 1 to 15 d)
The clinical presentation of early PVT ranges from portal hypertension manifestations (abdominal pain, ascites, gastrointestinal bleeding, splenomegaly) to severe allograft dysfunction and multiorgan failure
The most common causes leading to PVT are technical errors and anatomic complications such as venous redundancy, kinking and/or stenosis of the anastomosis
Risk factors are the presence of portal thrombosis prior OLT, small diameter of the portal vein, previous splenectomy, large portosystemic collaterals and the use of cryopreserved venous conduits for PV reconstruction
DUS, CEUS, contrast-enhanced CT, MRI and portography are imaging tools used for a positive diagnosis
PVT treatment includes systemic anticoagulation therapy, catheter-based thrombolytic therapy by percutaneous radiological intervention (transhepatic or transjugular access depending of the coagulation state) with or without stent placement to portosystemic shunting (TIPS) to retransplantation in highly unresolvable cases
PVT is associated with poor survival without treatment, but with prompt management, outcomes in terms of morbidity and mortality are satisfying
Table 7 Portal vein stenosis highlights
Summary of the clinical characteristics about PVS
The true incidence of PVS is not really known, but is thought to be < 3%
The major complication of PVS is the evolution to PVT if not treated
The majority of patients with PVS are asymptomatic and the diagnosis of stenosis is an incidental finding detected on routine DUS screening
Risk factors of PVS are almost exclusively represented by technical errors, particularly if a tapered anastomosis is required in the case of a vessel size mismatch between donor and recipient
Pre-OLT radiotherapy is another major predisposing factor of PVS
DUS with the finding of a stenosis ratio > 50% or a portal velocity ratio > 3:1 defines PVS. Contrast-enhanced CT and portography are used to confirm the diagnosis
If PVS is asymptomatic, no therapeutic intervention with close surveillance is possible, but anticoagulation therapy is recommended
In patients with clinical manifestations, percutaneous radiological intervention is the method of choice by transhepatic or transjugular access to perform angioplasty with our without stent placement; this prevents recurrence with a high rate of success and low rate of complications
Table 8 Caval anastomosis complication highlights
Summary of the clinical characteristics about CAC
The incidence of CAC is not known and is thought to be less than 3%
CAC is represented by stenosis, thrombosis and kinking depending on the type of caval anastomosis (cava resection or PB)
Clinical presentation of CAC ranges from lower limb edema, hepatomegaly, ascites, pleural effusions, Budd-Chiari syndrome, liver and renal failure, and hypotension, leading to allograft loss and even death
The main risk factor is a technical error in the creation of the anastomosis, which leads to kinking stenosis and thrombosis
Modified-PB with the three-hepatic vein seems to offer better outcomes because it has been demonstrated to be an efficient and safe method
Diagnosis tools include DUS, contrast-enhanced CT and cavography
Percutaneous radiological intervention is the method of choice via a transjugular approach or transhepatic approach if the anastomosis cannot be catheterized
It includes angioplasty by balloon dilatation and recurrences should be prevented by stent placement