DOI: 10.1148/rg.275065129
Complications of Liver Transplantation: Multimodality Imaging Approach1
Angela Hissae Motoyama Caiado, MD,
Roberto Blasbalg, PhD, MD,
Antonio Sergio Zafred Marcelino, MD,
Marco da Cunha Pinho, MD,
Maria Cristina Chammas, PhD, MD,
Claudia da Costa Leite, PhD, MD,
Giovanni Guido Cerri, PhD, MD,
André Cosme de Oliveira, MD,
Telésforo Bacchella, PhD, MD, and
Marcel Cerqueira César Machado, PhD, MD
1 From the Institute of Radiology (A.H.M.C., R.B., A.S.Z.M., M.d.C.P., M.C.C., C.d.C.L., G.G.C.) and Liver Surgery Department (A.C.d.O., T.B., M.C.C.M.), University of São Paulo, Medical School, Av Dr Eneas de Carvalho Aguiar 255, 05403–900 São Paulo, Brazil. Recipient of a Certificate of Merit award for an education exhibit at the 2005 RSNA Annual Meeting. Received July 11, 2006; revision requested October 5 and received December 8; accepted January 5, 2007. All authors have no financial relationships to disclose.
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Figure 1. Normal postoperative duplex Doppler US image and pulsed Doppler waveform of the hepatic artery in a liver transplant recipient. The waveform indicates a resistive index of 0.6 (normal range, 0.5–0.8) and acceleration time of less than 0.08 second.
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Figure 2. Duplex Doppler US image and waveform obtained in a 45-year-old patient on the 1st postoperative day after an orthotopic liver transplantation. The pulsed Doppler waveform for the hilar hepatic artery indicates a resistive index at the high end of the normal range (0.8), a finding that is usually attributed to ischemia-reperfusion injury. Follow-up studies demonstrated a normal resistive index.
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Figure 3a. Hepatic artery thrombosis in a 50-year-old man after liver transplantation for alcoholic cirrhosis. (a) Duplex Doppler US image obtained on the 4th postoperative day shows no hepatic arterial flow at either color or pulsed Doppler imaging. (b) Maximum intensity projection image from gadolinium-enhanced MR angiography shows an abrupt cutoff of flow in the proper hepatic artery (arrow), just beyond the vessel origin. (c) Conventional angiogram helps confirm hepatic artery thrombosis (arrow).
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Figure 3b. Hepatic artery thrombosis in a 50-year-old man after liver transplantation for alcoholic cirrhosis. (a) Duplex Doppler US image obtained on the 4th postoperative day shows no hepatic arterial flow at either color or pulsed Doppler imaging. (b) Maximum intensity projection image from gadolinium-enhanced MR angiography shows an abrupt cutoff of flow in the proper hepatic artery (arrow), just beyond the vessel origin. (c) Conventional angiogram helps confirm hepatic artery thrombosis (arrow).
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Figure 3c. Hepatic artery thrombosis in a 50-year-old man after liver transplantation for alcoholic cirrhosis. (a) Duplex Doppler US image obtained on the 4th postoperative day shows no hepatic arterial flow at either color or pulsed Doppler imaging. (b) Maximum intensity projection image from gadolinium-enhanced MR angiography shows an abrupt cutoff of flow in the proper hepatic artery (arrow), just beyond the vessel origin. (c) Conventional angiogram helps confirm hepatic artery thrombosis (arrow).
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Figure 4. Contrast material–enhanced bedside US image obtained in a 23-year-old male patient on the 3rd day after orthotopic liver transplantation clearly demonstrates the hilar hepatic artery (arrow), a finding that excludes the possibility of hepatic artery thrombosis. Because of interposed fat and air, the hilar hepatic artery was not seen at a previous routine bedside examination with Doppler US.
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Figure 5. Three-dimensional volume-rendered angiographic image from multidetector CT in a 23-year-old woman with declining function of a liver transplant shows an abrupt cutoff of flow in the common hepatic artery (arrow).
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Figure 6a. Hepatic artery stenosis at routine Doppler US performed on the 10th postoperative day in a liver transplant recipient with progressively increasing levels of hepatic transaminases. (a) Pulsed Doppler image and waveform of the hepatic artery distal to the anastomosis show a tardus parvus pattern, with a resistive index of 0.43 and acceleration time of more than 0.08 second. (b, c) Multidetector CT angiograms help confirm the presence of hepatic artery stenosis (arrow in b) with reduced intrahepatic perfusion and collateral vessels (arrowheads in c).
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Figure 6b. Hepatic artery stenosis at routine Doppler US performed on the 10th postoperative day in a liver transplant recipient with progressively increasing levels of hepatic transaminases. (a) Pulsed Doppler image and waveform of the hepatic artery distal to the anastomosis show a tardus parvus pattern, with a resistive index of 0.43 and acceleration time of more than 0.08 second. (b, c) Multidetector CT angiograms help confirm the presence of hepatic artery stenosis (arrow in b) with reduced intrahepatic perfusion and collateral vessels (arrowheads in c).
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Figure 6c. Hepatic artery stenosis at routine Doppler US performed on the 10th postoperative day in a liver transplant recipient with progressively increasing levels of hepatic transaminases. (a) Pulsed Doppler image and waveform of the hepatic artery distal to the anastomosis show a tardus parvus pattern, with a resistive index of 0.43 and acceleration time of more than 0.08 second. (b, c) Multidetector CT angiograms help confirm the presence of hepatic artery stenosis (arrow in b) with reduced intrahepatic perfusion and collateral vessels (arrowheads in c).
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Figure 7a. Doppler US image and waveform in a liver transplant recipient with mild elevation of liver enzyme levels and angiography-proved hepatic artery thrombosis show impairment of the intrahepatic arterial flow, with a low resistive index (0.49) (a) and elevation of the acceleration time (0.14 second) (b). This flow pattern is attributed to the presence of collateral vessels.
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Figure 7b. Doppler US image and waveform in a liver transplant recipient with mild elevation of liver enzyme levels and angiography-proved hepatic artery thrombosis show impairment of the intrahepatic arterial flow, with a low resistive index (0.49) (a) and elevation of the acceleration time (0.14 second) (b). This flow pattern is attributed to the presence of collateral vessels.
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Figure 8. Contrast-enhanced CT image shows a peripheral wedge-shaped area of hypoattenuation (arrow) in the liver transplant that represents an infarction in a patient with hepatic artery thrombosis that developed in the early postoperative period.
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Figure 10a. Stenosis at the portal anastomosis in a 40-year-old patient with severe ascites on the 8th day after liver transplantation. (a) B-mode US image shows a stricture (arrow) at the portal anastomosis. (b) Color Doppler US image demonstrates patency of the portal vein, with turbulent flow at the stenosis (arrow). (c) Pulsed Doppler US image and waveform of a portal vein segment proximal to the anastomosis show normal flow velocity. (d) Pulsed Doppler US image and waveform obtained at the portal anastomosis show an increase from 40 to 130 cm/sec in mean flow velocity.
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Figure 10b. Stenosis at the portal anastomosis in a 40-year-old patient with severe ascites on the 8th day after liver transplantation. (a) B-mode US image shows a stricture (arrow) at the portal anastomosis. (b) Color Doppler US image demonstrates patency of the portal vein, with turbulent flow at the stenosis (arrow). (c) Pulsed Doppler US image and waveform of a portal vein segment proximal to the anastomosis show normal flow velocity. (d) Pulsed Doppler US image and waveform obtained at the portal anastomosis show an increase from 40 to 130 cm/sec in mean flow velocity.
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Figure 10c. Stenosis at the portal anastomosis in a 40-year-old patient with severe ascites on the 8th day after liver transplantation. (a) B-mode US image shows a stricture (arrow) at the portal anastomosis. (b) Color Doppler US image demonstrates patency of the portal vein, with turbulent flow at the stenosis (arrow). (c) Pulsed Doppler US image and waveform of a portal vein segment proximal to the anastomosis show normal flow velocity. (d) Pulsed Doppler US image and waveform obtained at the portal anastomosis show an increase from 40 to 130 cm/sec in mean flow velocity.
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Figure 10d. Stenosis at the portal anastomosis in a 40-year-old patient with severe ascites on the 8th day after liver transplantation. (a) B-mode US image shows a stricture (arrow) at the portal anastomosis. (b) Color Doppler US image demonstrates patency of the portal vein, with turbulent flow at the stenosis (arrow). (c) Pulsed Doppler US image and waveform of a portal vein segment proximal to the anastomosis show normal flow velocity. (d) Pulsed Doppler US image and waveform obtained at the portal anastomosis show an increase from 40 to 130 cm/sec in mean flow velocity.
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Figure 11a. Stenosis at the portal anastomosis in a 54-year-old woman with a liver transplant. (a) Color Doppler US image (shown in black and white) obtained on the 1st postoperative day demonstrates a stricture (arrow) at the site of the portal anastomosis. Pulsed Doppler US waveform (not shown) indicated a focal increase in flow velocity to 200 cm/sec. (b) Coronal maximum intensity projection image from gadolinium-enhanced MR angiography demonstrates the stenosis (arrow) with associated poststenotic dilatation of the intra-hepatic portal vein.
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Figure 11b. Stenosis at the portal anastomosis in a 54-year-old woman with a liver transplant. (a) Color Doppler US image (shown in black and white) obtained on the 1st postoperative day demonstrates a stricture (arrow) at the site of the portal anastomosis. Pulsed Doppler US waveform (not shown) indicated a focal increase in flow velocity to 200 cm/sec. (b) Coronal maximum intensity projection image from gadolinium-enhanced MR angiography demonstrates the stenosis (arrow) with associated poststenotic dilatation of the intra-hepatic portal vein.
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Figure 12. Normal Doppler image and waveform obtained in the hepatic vein of a liver transplant recipient. Note the fluctuations across the baseline, which characterize the normal triphasic pattern.
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Figure 13a. (a) Pulsed Doppler waveform obtained in the hepatic vein of a liver transplant recipient demonstrates the loss of the expected triphasic pattern. (b) Pulsed Doppler waveform obtained at the confluence of the hepatic veins shows a stenosis with a focal increase in peak systolic velocity to 175 cm/sec. (c–e) Axial T2-weighted (c), axial contrast-enhanced T1-weighted (d), and coronal contrast-enhanced maximum intensity projection (e) MR images show the stenosis (arrow) at the hepatic vein confluence.
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Figure 13b. (a) Pulsed Doppler waveform obtained in the hepatic vein of a liver transplant recipient demonstrates the loss of the expected triphasic pattern. (b) Pulsed Doppler waveform obtained at the confluence of the hepatic veins shows a stenosis with a focal increase in peak systolic velocity to 175 cm/sec. (c–e) Axial T2-weighted (c), axial contrast-enhanced T1-weighted (d), and coronal contrast-enhanced maximum intensity projection (e) MR images show the stenosis (arrow) at the hepatic vein confluence.
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Figure 13c. (a) Pulsed Doppler waveform obtained in the hepatic vein of a liver transplant recipient demonstrates the loss of the expected triphasic pattern. (b) Pulsed Doppler waveform obtained at the confluence of the hepatic veins shows a stenosis with a focal increase in peak systolic velocity to 175 cm/sec. (c–e) Axial T2-weighted (c), axial contrast-enhanced T1-weighted (d), and coronal contrast-enhanced maximum intensity projection (e) MR images show the stenosis (arrow) at the hepatic vein confluence.
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Figure 13d. (a) Pulsed Doppler waveform obtained in the hepatic vein of a liver transplant recipient demonstrates the loss of the expected triphasic pattern. (b) Pulsed Doppler waveform obtained at the confluence of the hepatic veins shows a stenosis with a focal increase in peak systolic velocity to 175 cm/sec. (c–e) Axial T2-weighted (c), axial contrast-enhanced T1-weighted (d), and coronal contrast-enhanced maximum intensity projection (e) MR images show the stenosis (arrow) at the hepatic vein confluence.
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Figure 13e. (a) Pulsed Doppler waveform obtained in the hepatic vein of a liver transplant recipient demonstrates the loss of the expected triphasic pattern. (b) Pulsed Doppler waveform obtained at the confluence of the hepatic veins shows a stenosis with a focal increase in peak systolic velocity to 175 cm/sec. (c–e) Axial T2-weighted (c), axial contrast-enhanced T1-weighted (d), and coronal contrast-enhanced maximum intensity projection (e) MR images show the stenosis (arrow) at the hepatic vein confluence.
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Figure 14a. Budd-Chiari syndrome in a 36-year-old woman after liver transplantation for fulminant hepatic failure. (a, b) Doppler US images obtained on the 2nd postoperative day show no flow in the right hepatic vein (arrow in a) and a compensatory inversion of flow in the right portal branch (arrow in b). A normal direction of flow is depicted in the left portal branch (arrowhead in b). (c) Coronal reformatted image from contrast-enhanced multidetector CT demonstrates no opacification of the right hepatic vein (arrow). (d) Axial contrast-enhanced multidetector CT image shows a mosaic pattern of perfusion in the posterior segments of the right hepatic lobe (arrow), a finding indicative of right hepatic vein thrombosis.
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Figure 14b. Budd-Chiari syndrome in a 36-year-old woman after liver transplantation for fulminant hepatic failure. (a, b) Doppler US images obtained on the 2nd postoperative day show no flow in the right hepatic vein (arrow in a) and a compensatory inversion of flow in the right portal branch (arrow in b). A normal direction of flow is depicted in the left portal branch (arrowhead in b). (c) Coronal reformatted image from contrast-enhanced multidetector CT demonstrates no opacification of the right hepatic vein (arrow). (d) Axial contrast-enhanced multidetector CT image shows a mosaic pattern of perfusion in the posterior segments of the right hepatic lobe (arrow), a finding indicative of right hepatic vein thrombosis.
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Figure 14c. Budd-Chiari syndrome in a 36-year-old woman after liver transplantation for fulminant hepatic failure. (a, b) Doppler US images obtained on the 2nd postoperative day show no flow in the right hepatic vein (arrow in a) and a compensatory inversion of flow in the right portal branch (arrow in b). A normal direction of flow is depicted in the left portal branch (arrowhead in b). (c) Coronal reformatted image from contrast-enhanced multidetector CT demonstrates no opacification of the right hepatic vein (arrow). (d) Axial contrast-enhanced multidetector CT image shows a mosaic pattern of perfusion in the posterior segments of the right hepatic lobe (arrow), a finding indicative of right hepatic vein thrombosis.
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Figure 14d. Budd-Chiari syndrome in a 36-year-old woman after liver transplantation for fulminant hepatic failure. (a, b) Doppler US images obtained on the 2nd postoperative day show no flow in the right hepatic vein (arrow in a) and a compensatory inversion of flow in the right portal branch (arrow in b). A normal direction of flow is depicted in the left portal branch (arrowhead in b). (c) Coronal reformatted image from contrast-enhanced multidetector CT demonstrates no opacification of the right hepatic vein (arrow). (d) Axial contrast-enhanced multidetector CT image shows a mosaic pattern of perfusion in the posterior segments of the right hepatic lobe (arrow), a finding indicative of right hepatic vein thrombosis.
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Figure 15. Bile duct obstruction in a 31-year-old patient with progressive jaundice 2 months after liver transplantation. MR cholangiogram clearly demonstrates a focal stenosis at the choledochocholedochostomy (arrow).
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Figure 16. Sagittal B-mode US image of the right hypochondrium demonstrates a perihepatic fluid collection (arrow) secondary to a biliary fistula in a liver transplant recipient. (Image courtesy of Gisele Warm-brand, PhD, MD, University of São Paulo, Medical School.)
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Figure 17a. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangiogram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Figure 17b. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangiogram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Figure 17c. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangiogram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Figure 17d. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangiogram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Figure 17e. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangio-gram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Figure 17f. Bile duct stenosis and dilatation in a 50-year-old liver transplant recipient with jaundice and a previous diagnosis of hepatic artery thrombosis. (a) Axial B-mode US image demonstrates dilatation of the intrahepatic biliary tree (arrows). (b) MR cholangiogram shows a stenotic bile duct segment (arrow) with associated upstream dilatation of the biliary tree. (c, d) Endoscopic retrograde cholangiograms show the stenosis (arrow in c) and the bile duct after successful hydrostatic dilation with a 6-mm inflatable balloon (arrow in d). A new stenosis developed within a short time after treatment. (e) Contrast-enhanced T1-weighted spoiled gradient-echo MR image shows multiple infected bilomas (arrow). (f) Follow-up MR cholangiogram obtained 1 year later shows residual dilatation of the biliary tree and bilomas (arrow).
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Copyright © 2007 by the Radiological Society of North America.
