Figure 40.1 Intraoperative angiography with injection of papaverine to reverse arterial spasm. Images on the left are from prior to injection. Note the high resistive index (RI) in the extrahepatic artery with flattened arterial waveform within the liver. The corresponding arteriogram reveals two areas of severe allograft arterial spasm (arrows). Posttreatment images reveal resolution of the process, with normalisation of the ultrasound and angiogram. This technique can also be used for intrahepatic thrombolysis and evaluation of parenchymal vessels for the presence of thrombus.
40.2.3 Management of hepatic artery thrombosis
Early postoperative HAT should prompt immediate operative intervention. Angiographic attempts at recanalisation should be followed by operative exploration to evaluate the adequacy of arterial inflow. If adequate inflow is not provided by the recipient hepatic artery, dissection to the coeliac axis and test occlusion of the splenic artery is indicated. If these manoeuvres do not provide improved inflow, the use of an arterial conduit is indicated. The use of thrombolytics has greatly improved upon the initial success rate of mechanical thrombolysis.
Restoration of arterial flow greatly enhances graft survival, despite the possibility of further late biliary complications. Confirmatory angiography is generally not required in cases of HAT diagnosed by Doppler ultrasonography and should not delay operative intervention. Intraoperative arteriography can greatly enhance the diagnosis of intrahepatic arterial complications and may aid in direct mechanical thrombectomy after initial thrombolysis. Intraoperative angiogram may also reveal distal arterial intimal injuries and profound arterial spasm that can be relieved with intra-arterial papaverine injection.
40.3 PORTAL VENOUS COMPLICATIONS
Portal venous thrombosis (PVT) is an infrequent complication of PLT, occurring in less than 5% of cases, and is more frequent in those requiring venous reconstruction or in cases requiring the use of allogenic conduits due to poor portal venous flow or preexisting PVT in the native liver. Portal venous stenosis (PVS) complicates up to 10% of PLT and can progress to thrombosis.
40.3.1 Diagnosis
Portal venous complications generally reflect the resultant high portal pressures encountered as a result of the prehepatic obstruction to flow. Ascites, splenomegaly with thrombocytopenia and portal hypertensive bleeding are the most common presenting signs and symptoms. PVS and PVT often manifest later in the postoperative course and became symptomatic after a mean of 14 months posttransplant in one large series [10]. Doppler interrogation of the portal vein is a noninvasive and rapid way to investigate patients with symptoms associated with PVT or PVS; however, the sensitivity of contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) is far greater, and these studies should be entertained if initial Doppler studies are negative. Contrast-enhanced studies may also reveal the aetiology of the PVS/PVT (vessel redundancy or the presence of spontaneous shunts that could be stealing flow from the allograft portal system) and help in planning treatment. In addition to initial imaging, liver biopsy should be considered in cases of late PVT to ensure a lack of significant allograft fibrosis.
40.3.2 Management of portal vein stenosis (Figure 40.2)
Percutaneous dilatation of short-segment PVS is successful in a majority of cases and should be the initial therapy in cases occurring more than a few weeks after transplant. Early PVS should be managed with open exploration after the diagnosis is confirmed and the anatomy is delineated with contrast-enhanced studies. Careful ligation of portosytemic collaterals should be performed to increase portal flow to the allograft. Patients who fail repeated dilatations of anastomotic strictures should undergo open revision and venoplasty with potential use of mesenteric-to-portal vein interposition grafts using allogenic vein grafts.
40.3.3 Management of portal vein thrombosis (Figure 40.3)
Early PVT mandates operative exploration. We have not performed routine thrombectomy of the native portal vein in cases of PVT, although this has certainly been described in the adult literature. Instead, our operative approach to PVT is to perform a thrombectomy of the allograft with thrombolysis and subsequent anastomosis to a venous conduit with inflow from the superior mesenteric vein. In selected cases of diminutive native portal veins, dissection and anastomosis to the confluence of the splenic and superior mesenteric veins may also be attempted. Late posttransplant PVT can be managed as other cases of extrahepatic PVT, as long as the allograft function is normal. If anatomically possible and if the liver parenchyma is normal on biopsy, our practice has been to attempt the creation of a meso-Rex shunt to the allograft’s left portal vein. In the absence of clinical complications that cannot be managed medically or endoscopically, we have not routinely performed portosystemic shunting. However, if anatomically feasible, the potential physiologic advantages of restoring portal flow to the allograft make a meso-Rex shunt an attractive early option in the management of PVT. Preoperative imaging should be utilised to confirm the presence of a left portal vein, as well as patent superior mesenteric and left internal jugular veins.
Biliary complications remain a significant source of post-transplant mortality after PLT. Most large series have found the overall incidence of biliary complications to be 10%–30%, and they may be more common after the use of technical variant allografts. Biliary complications have not been shown to alter long-term patient survival after PLT. The management of biliary complications has changed dramatically over the past decade, with increasing recognition of percutaneous and multimodal treatment of complex biliary issues.
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