Answer
HAT is one of the most common and potentially most disastrous arterial complications (see images below). HAT is estimated to occur in 4-12% of adult OLTX patients and in 9-42% of pediatric transplantation patients. [26] Causes include allograft rejection, hepatic artery kinking due to vascular redundancy, underlying HAS, and technical problems at the anastomosis. Doppler ultrasonography (US) has a sensitivity of approximately 90% in detecting HAT. [28]
Spectral Doppler ultrasonographic waveform of the right hepatic artery in a 60-year-old man, 8 years after orthotopic liver transplantation. The image demonstrates the typical rounded tardus parvus waveform morphology, which is indicative of upstream arterial thrombosis or severe stenosis. Subsequent angiography confirmed occlusion at the hepatic arterial anastomosis.
A-1: Magnetic resonance angiogram in a transplantation patient with hepatic artery thrombosis. Magnetic resonance angiogram of the recipient celiac axis depicts complete occlusion of the hepatic artery.
A-2: Magnetic resonance angiogram demonstrates intrahepatic arterial segments reconstituted from mesenteric collaterals. Collateralization explains how, in some patients, intrahepatic flow can be present in the setting of complete extrahepatic arterial occlusion.
A-3: Digital subtraction angiogram shows complete hepatic artery thrombosis in a liver transplant recipient.
A finding on Doppler ultrasound evaluation that would merit close follow-up is the presence of significantly elevated peak systolic velocities in the main hepatic artery, which may be suggestive of hepatic artery stenosis (HAS), an independent risk factor for HAT. [29] Doppler ultrasonographic findings consistent with HAT include absent flow at the porta hepatis (ie, no flow in the donor proper hepatic artery) with absent intrahepatic arterial flow, and absent flow in the donor hepatic artery with abnormal intrahepatic flow. Persistent intrahepatic flow in the setting of complete proper HAT can result from collateralization via nearby superior mesenteric artery branches. Collateralized intrahepatic flow can be differentiated from normal flow by its tardus parvus Doppler waveform morphology. Tardus parvus can be diagnosed objectively when the intrahepatic arterial resistive index (RI) is less than 0.5 and the systolic acceleration time (SAT) is 0.08 second or longer.
Without aggressive diagnosis and treatment, HAT is associated with a mortality rate of greater than 80%. Unfortunately, percutaneous thrombolytic therapy of HAT is problematic, because it often occurs soon after OLTX. Thrombolysis and angioplasty of underlying HAS have been successful in a few patients; however, HAT usually requires urgent retransplantation for patient survival.
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Drawing of the basic anastomoses of an adult-to-adult living-donor liver transplantation. At the author's institution, the right lobe is usually harvested from adult donors and transplanted in orthotopic position after the recipient's native liver is extirpated. Although large vessels and bile ducts must be ligated, control of hemorrhage and bile leakage from the cut surface is possible by performing tissue coagulation with a harmonic scalpel.
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Drawing of an orthotopic liver transplant and the basic surgical anastomoses.
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Spectral Doppler ultrasonographic waveform of the right hepatic artery in a 60-year-old man, 8 years after orthotopic liver transplantation. The image demonstrates the typical rounded tardus parvus waveform morphology, which is indicative of upstream arterial thrombosis or severe stenosis. Subsequent angiography confirmed occlusion at the hepatic arterial anastomosis.
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A-1: Magnetic resonance angiogram in a transplantation patient with hepatic artery thrombosis. Magnetic resonance angiogram of the recipient celiac axis depicts complete occlusion of the hepatic artery.
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A-2: Magnetic resonance angiogram demonstrates intrahepatic arterial segments reconstituted from mesenteric collaterals. Collateralization explains how, in some patients, intrahepatic flow can be present in the setting of complete extrahepatic arterial occlusion.
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A-3: Digital subtraction angiogram shows complete hepatic artery thrombosis in a liver transplant recipient.
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A-4: Digital subtraction angiogram depicts redundant donor-recipient hepatic artery. A stenotic hairpin turn is noted.
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A-5: Digital subtraction angiogram obtained during balloon angioplasty of a stenotic artery.
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A-6: Digital subtraction angiogram shows a widely patent hepatic artery after angioplasty.
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Multiple ischemic biliary strictures documented during interventional external-internal drainage procedure.
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Early posttransplantation evaluation of the portal vein by using spectral Doppler ultrasonography depicts a normal waveform with peak flow velocity of approximately 31 cm/s.
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Spectral Doppler ultrasonogram of the portal vein was obtained at the onset of graft dysfunction. Compared with the baseline examination, markedly accelerated flow to 150 cm/s was documented. Subsequent catheter venography was performed that documented a high-grade venous stenosis. The stenosis was treated successfully by using balloon angioplasty and stent placement.
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Transjugular portography demonstrates extensive portal vein thrombus in the whole-liver allograft of a 40-year-old woman whose clinical condition rapidly deteriorated on postoperative day 39.
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After aggressive percutaneous thrombolysis, balloon dilatation, mechanical thrombectomy, and systemic anticoagulation, patency of the portal vein has been restored. Follow-up portography shows that the portal vein is open. Competing collaterals communicating with the superior mesenteric vein (arrow) and the inferior mesenteric vein (arrowhead) were noted. Subsequently, the collateral gonadal vein draining the superior mesenteric vein to the inferior vena cava was embolized with coils to improve hepatopetal flow.
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The portal-venous phase computed tomography (CT) scan shows somewhat amorphous and irregular fluid-density material surrounding the portal vein and tracking along the portal triads. This is the typical appearance of a branching biloma that results from the diffuse, extensive extravasation of bile from ischemic ducts. This type of bile duct injury is caused by either severe hepatic artery stenosis or hepatic artery thrombosis.
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Contrast-enhanced computed tomography (CT) scan shows a 4 x 5-cm hepatic artery pseudoaneurysm in the porta hepatis. Its contrast enhancement is equivalent to that of the arterial blood pool. The peripheral hypoattenuation is consistent with mural thrombus.
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Hepatic artery graft stenosis: arrows indicate hepatic artery tapering and disappearance.
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B-3: Hepatic artery graft stenosis: arrows indicate hepatic artery tapering and disappearance. The low attenuation area shows infarction.
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B-1: Extrahepatic artery Doppler ultrasonography shows Doppler spectrum with lower normal limits. Intrahepatic artery spectrum could not be sampled.
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B-2: Extrahepatic artery Doppler ultrasonography shows Doppler spectrum with lower normal limits. Intrahepatic artery spectrum could not be sampled.
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C-1: Gortex hepatic artery graft thrombosis in a 59-year-old man (shown by arrow).
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C-2: Gortex hepatic artery graft thrombosis in a 59-year-old man (shown by arrow).
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C-3: Infarction of the lateral part of a graft (multiple arrows); thrombosis of the arterial graft (single arrow).
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C-4: Splenic vein thrombosis of the same patient is marked by arrows.
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C-5: Multiple infarctions of the left lateral aspect are marked by arrows. Bilateral pleural effusion can be seen.
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C-6: Ultrasound image of the same patient showing a larger infarction/collection? (between the cursors) of the hepatic graft.
