Hepatic artery dissection is an infrequent vascular complication that can arise after orthotopic liver transplant. Most patients with this complication are diagnosed during the intraoperative period or the first days after liver transplant, with an association shown with living-donor liver transplant. In this study, we discuss a rare case of an extrahepatic artery dissection that was successfully managed through surgical excision and arterial revascularization that was diagnosed 4 years after orthotopic liver transplant. Furthermore, we hypothesize on the potential causes of its occurrence.
Key words : Complications, Doppler, Intimal dissection
Hepatic artery complications are a major risk factor after liver transplant and can commonly lead to death or the urgent need for retransplant.1,2 Patients with this complication are often diagnosed a few days or weeks after liver transplant3; however, there are rare instances of later occurrences. With earlier presentation of this complication, the consequences are more severe.
Among the possible vascular complications, hepatic artery dissection has been seldom described. This complication rarely occurs even in non-transplant patients.4 Because it is rare, its clinical presentation, evolution, and treatment remain unclear. Furthermore, liver transplant patients can have few symptoms or can have severe graft dysfunction. Hepatic artery dissection can remain as an unknown lesion, and patients with uncomplicated hepatic artery dissection can be managed conser-vatively.
In patients who present with symptoms, treatment can include liver retransplant,5 percutaneous endo-vascular treatment,6 or surgical excision of the diseased artery followed by surgical revascularization.3 Moreover, surgical revascularization demands the use of native hepatic artery, preserved arterial allografts, or arterial/venous autograph.3 In this study, we describe a case of uncommon late hepatic artery dissection that was successfully managed through surgical revascularization using the patient’s hepatic artery. We also we suggest a cause for this occurrence.
A 50-year-old male patient who had both hypothyroidism and primary sclerosing cholangitis underwent a piggyback orthotopic liver transplant followed by an uneventful postoperative course. The patient’s donor was a 38-year-old man who died due to subarachnoid hemorrhage. The hepatic arteries and portal veins of the donor and recipient were anastomosed end-to-end, and bile duct recon-struction was performed through Roux-en-Y biliary-enteric anastomosis. Cold and warm ischemia times were 808 minutes and 37 minutes, respectively. We observed no arterial anatomic variations in the donor or recipient, and no postoperative bile leakage occurred during the transplant procedure. Hepatic artery flow was monitored daily through color Doppler ultrasonography during the first postoperative week and subsequently as needed until the patient was discharged. In addition, immunosuppression was achieved using tacrolimus.
Four years and 1 month after the transplant, an increase in liver enzymes was noted in the patient during a medical visit; the patient presented with no other symptoms. At the next follow-up, the trans-aminase levels had increased. An abdominal contrasted-enhanced computed tomography scan of the patient demonstrated no abscess or hepatic mass and no dilation in the intrahepatic ducts. An infection had been ruled out, and no improvement was observed after immunosuppression opti-mization.
A color Doppler ultrasonography was conducted, which revealed a disorganized intrahepatic arterial flow with a tardus-parvus waveform and low resistive index of 0.42, suggesting arterial stenosis. A liver biopsy revealed ischemic liver disease, suggesting a vascular origin for the increased liver enzymes. Furthermore, an arteriography revealed a segmental arterial lesion that presented as stenosis interspersed with areas of dilation (pouch) that sug-gested dissection. A typical angiographic “telescope-like” image (ie, double lumen opacification) favored this diagnosis (Figure 1A).
We considered our patient to be unsuitable for endovascular treatment owing to the long, redundant, and twisting arterial segment and the small caliber of the parent vessel to harbor a covered stent. Moreover, there was the risk of the guidewire going through the false track of dissection, resulting in acute rupture or increasing the false track in conjunction with consequent thrombosis and loss of complete arterial flow to the liver. Because the liver was viable and no liver abscess or biliary complications were observed, the patient was scheduled for surgical revas-cularization.
During surgery, a tortuous hepatic artery was found with fibrotic and inflammatory tissue around it (Figure 1B). The hepatic artery was gently dissected and released from the fibrosis, a segment of about 3.0 cm with the noninfected hepatic artery was resected, and an end-to-end arterial anastomosis was perfor-med. Pathologic examination confirmed hepatic artery dissection (Figure 1C). An arteriography conducted 3 weeks after surgical revascularization revealed a normal arterial hepatic flow with no thrombosis or stenosis of the hepatic artery. The patient is alive and asymptomatic 4 years after liver revascularization.
Hepatic artery complications after liver transplant can have potential lethal progression. Hepatic artery stenosis, thrombosis, pseudoaneurysm, kinking, and dissection are possible vascular complications.4,7,8 Hepatic artery stenosis is estimated to occur in up to 11% of transplant recipients and occurs most frequently at the anastomotic site. Causes include clamp injury, intimal trauma caused by perfusion catheters at the time of surgery or during back-table time, or disrupted vasa vasorum leading to ischemia of the arterial ends. Clinically, it may lead to biliary ischemia, causing hepatic dysfunction and eventual hepatic failure. Treatment includes balloon angio-plasty or retransplant.9,10
Diagnosis of vascular complications can be achieved through Doppler ultrasonography and computerized tomography angiography or by direct arteriography. In the present case, the diagnosis was initially suggested by a color Doppler ultraso-nography and confirmed by a liver biopsy performed at the same time.
Differences between the arterial dissection and the pseudoaneurysm are conceptual, and an apparent misunderstanding exists among authors about this issue. Arterial dissection corresponds to dissecting hematoma into the media layer that can compress the vessel lumen and cause stenosis (subendothelial type) or form dilatation (aneurysm-like; subadventitial type) or both. Adventitia remains preserved. Hepatic artery dissection is even rarer than hepatic artery stenosis, and its occurrence is often related to the percutaneous arterial procedure,11 the intraoperative technique,12 or has no identified cause. Furthermore, there is no consensus about the risk factors related to hepatic artery dissection. In the pseudoaneurysm, the adventitia is injured and the hemorrhage can be contained by abluminal hematoma (called “pulsatile hematoma”) or it will expand to the abdominal cavity.
Because of the few experiences in the literature and because the risk of rupture is unknown, the consensual treatment for spontaneous celiac and hepatic artery dissection has not yet been established. Surveillance,4,13 surgery,14 and endovascular treatment6 are the options according to the clinical presentation. Patients who have been diagnosed during routine image examination and have few symptoms can be treated conservatively, which has shown the best results for these patients.15 Hwang and colleagues reviewed tomographic findings of 43 patients after living-donor liver transplant and found that diagnosis of hepatic artery dissection is often underestimated and that most cases will exhibit spontaneous recovery due to an ongoing healing process that includes absorption of mural hematoma and restoration of the downstream flow, with no major consequences.4 Symptomatic dissection presenting with continuous pain, an increase of a false lumen, and aneurysmal dilatation and rupture require urgent treatment because these presentations have high chances of mortality.
Endovascular management of a dissection artery has been developed as a suitable therapeutic approach5,16 and has possible benefits compared with a surgical approach. Endovascular management can be performed with local anesthesia or sedation, avoiding general anesthesia and orotracheal tube. The collateral vessels can be straightforwardly assessed, and fewer postoperative complications and shorter hospital internment are expected, although this approach is not free from risk of severe complications.5 Clinical experiences with endo-vascular technique have been accumulating since 2000.13,16 Appropriate patient selection is critical for the technical success and safety of endovascular interventions; in addition, a favorable anatomy with a short diseased segment and straight course without extreme tortuosity are also needed for success.
Our patient was considered unsuitable for endovascular treatment owing to the long, redun-dant, and twisting arterial segment to harbor a covered or flow diversion stent. Difficulties such as the extension of intima dissection could make it impossible to employ the hepatic artery for revas-cularization or even prevent liver rescue. Arterial autographs have been successfully used in this regard. Fortunately, we found a focal dissection occurring in a redundant arterial segment that could be excised, and the liver could be revascularized by end-to-end arterial anastomosis.
Our patient had no postoperative infections, and we had no technical difficulties in performing arterial anastomosis. In addition, the patient did not have any previous percutaneous vascular procedure. Moreover, hepatic artery dissection had been diagnosed exceptionally late. Herein, we believe that segmental arterial injury resulted from a metal vascular clamp applied on the hepatic artery for proximal hemostasis control during arterial anas-tomosis. This injury consequently triggered a subsequent injury to the vessel layers, such as a wall hematoma, that subsequently remodeled over time and formed subadventitial areas (pouch) and subendothelial areas (stenosis) of dilatation. Therefore, we have used delicate plastic vascular clamps to protect the vascular intima layer from inadvertent injury. Furthermore, we demonstrated the hepatic artery dissection through a histopathologic image, which has been rarely shown in the published literature and leaves no doubt about the diagnosis.
A late increase of serum liver enzymes after liver transplant in a patient with suspected arterial stenosis, which can be revealed through a Doppler scan in the absence of chronic rejection, should alert the clinic regarding the possibility of a late hepatic artery complication. Intraoperative injury to the hepatic artery by a vascular clamp should be considered as a possible cause for no explicated hepatic artery dissection. Surgical excision and immediate revascularization offer a good treatment option if the less invasive endovascular approach is not feasible.
DOI : 10.6002/ect.2019.0016
From the Division of General Surgery and Liver Transplantation, Hospital Oswaldo
Cruz, Pernambuco University, Recife, Pernambuco, Brazil
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Luiz Eduardo Correia Miranda, Division of General Surgery and Liver Transplantation, Hospital Oswaldo Cruz, Rua Arnóbio Marques, 310, Bairro de Santo Amaro, Recife, PE, Brasil
Phone: +55 81 3183 3522
Figure 1. Dissection of the Hepatic Artery