(Radiographics. 2001;21:53-63.)
© RSNA, 2001
Spectrum of CT Findings in Pediatric Patients after Partial Liver Transplantation1
Fumie Ametani, MD ,
Kyo Itoh, MD ,
Toshiya Shibata, MD ,
Yoji Maetani, MD ,
Koichi Tanaka, MD and
Junji Konishi, MD
1 From the Departments of Nuclear Medicine and Diagnostic Imaging (F.A., Y.M., J.K.) and Transplantation and Immunology (K.T.), Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Radiology, Kyoto University Hospital, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto-shi, Kyoto-fu 606-8507, Japan (K.I., T.S.). Presented as a scientific exhibit at the 1999 RSNA scientific assembly. Received March 2, 2000; revision requested May 22 and received June 20; accepted June 26. Address correspondence to K.I. (e-mail: kyo@kuhp.kyoto-u.ac.jp).
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Abstract
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Liver transplantation is an accepted therapy for patients with severe liver diseases. In pediatric liver transplantation, the application of reduced-size and split-liver transplantation has expanded the donor pool. The development of living related donor partial liver transplantation has further increased the availability of donors. Complications in patients after living related transplantation include hepatic arterial thrombosis, portal venous stenosis and thrombosis, hepatic venous stenosis, biliary stenosis or leak, biloma formation, fatty liver, extrahepatic fluid collection, posttransplantation lymphoproliferative disorder, and organ rejection. Ultrasonography is the primary imaging modality for evaluation of the vascular system of patients after liver transplantation, and computed tomography is useful to help diagnose hepatic parenchymal abnormalities including infarction, congestion, and fatty change; intrahepatic biliary damage; and extrahepatic disorders, including abnormal fluid collections, varicose veins, and lymphadenopathy.
Index Terms: Liver, CT, 76.1211 • Liver, transplantation, 76.45 • Liver, US, 76.1298 • Transplantation, 76.45
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Introduction
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Liver transplantation is performed in an increasing number of patients with severe liver diseases. In pediatric cases, the number of cadaveric donor livers is not sufficient; therefore, living related donor partial liver transplantation or split-liver transplantation has become an important therapeutic option for pediatric patients with terminal liver diseases (1–3). Living related transplantation has some advantages, including the need for only a brief period of cold ischemia, the ability to perform preoperative measurement of the graft size and preoperative evaluation of the vascular anatomy of the donor liver, and the genetic proximity of donors and children. Living related transplantation has a disadvantage in that the donor source is limited to immediate relatives, mainly parents. Thus, the use of "marginal" donor sources is unavoidable, which may allow problems with ABO blood group system incompatibility, size mismatches, and steatotic grafts.
The main complications in patients after living related transplantation include vascular stenosis and thrombosis, biliary stenosis or bilomas, fatty liver, extrahepatic fluid collection, posttransplantation lymphoproliferative disorder, and rejection. Ultrasonography (US) is a less invasive imaging modality than computed tomography (CT) and should be the first choice to evaluate vascular and biliary abnormalities in patients after transplantation. CT is also useful to help evaluate graft growth or possible complications after partial liver transplantation, and there are several reports of CT findings after whole liver transplantation (4–6).
In this article, we illustrate the surgical anatomy during implantation and provide a spectrum of CT findings of various complications in pediatric patients after living related transplantation. Vascular complications include hepatic infarction due to hepatic arterial thrombosis, portal venous stenosis or thrombosis, and hepatic congestion due to hepatic venous anastomotic stenosis. Biliary complications include intrahepatic bile duct dilatation, intrahepatic bile duct stones or debris, and intrahepatic bilomas. Other abnormalities after transplantation include fatty liver, periportal collar, focal fluid collection, posttransplantation lymphoproliferative disorder, and rejection. Some complications specific to pediatric patients, including intrahepatic bile duct damage related to ABO blood group system incompatibility and fatty liver, are also presented.
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Surgical Anatomy
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For most pediatric recipients in our institution, the donor liver graft was the left lobe or lateral segment (Fig 1). The partial liver graft was orthotopically implanted in the recipient after total hepatectomy, with care taken to keep the inferior vena cava intact to maintain constant caval blood flow.
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Figure 1. Diagram of the surgical anatomy during living related transplantation shows end-to-end left hepatic venous (LHV), hepatic arterial (HA), and portal venous (PV) anastomo-ses and hepatic jejunostomy. BD = bile duct, GDA = gastroduodenal artery, IVC = inferior vena cava, SMV = superior mesenteric vein, SPV = splenic vein.
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The left hepatic artery of the donor was anastomosed to the appropriate hepatic artery of the recipient in an end-to-end fashion with use of a surgical microscope. The portal venous anastomosis was performed in an end-to-end fashion between the donor's left portal vein and the recipient's main portal vein. When the available portal vein was too short, venous grafting was performed with use of the donor's ovarian vein or the recipient's inferior mesenteric vein (1). The hepatic venous anastomosis was performed in an end-to-end or end-to-side fashion between the donor's left hepatic vein and the recipient's hepatic vein orifice, while the inferior vena cava was preserved (7).
In whole liver transplantation, biliary anastomosis is made in an end-to-end fashion between the donor's common bile duct and the recipient's common bile duct. In living related transplantation, biliary reconstruction is performed by means of hepatic jejunostomy with a Roux-en-Y limb anastomosis (1–3).
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Vascular Complications
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Vascular complications include thrombosis or stenosis of the hepatic artery, portal vein, or hepatic vein. Hepatic arterial thrombosis can result from anastomotic stenosis and usually occurs early after the surgery. Twisting or compression of the vein by the growing graft causes portal venous and hepatic venous stenoses, which may occur either early or late after the surgery. Vascular complications should be first diagnosed with Doppler US, and CT should then be performed to help detect any secondary changes to the hepatic parenchyma and other findings such as ascites or varices. In portal venous or hepatic venous stenosis, angiography is performed to help confirm the stenosis and to help guide balloon dilation of the stenosis and thrombolysis.
Hepatic Infarction due to Hepatic Arterial Thrombosis
Hepatic arterial thrombosis is the most common vascular complication in patients after liver transplantation, and it can lead to devastating complications, such as biliary stricture, leak, biloma, and hepatic infarction or necrosis. Hepatic arterial thrombosis is a major complication that frequently results in graft failure and is more common in children (9%–42%) than in adults (4%–12%) (8,9). Hepatic arterial thrombosis itself can be diagnosed with Doppler US, and any secondary damage to the liver and bile duct can be diagnosed with CT. Hepatic infarction is generally observed at CT as irregular and wedge-shaped low-attenuation lesions that are mainly in the periphery of the liver. The lesions are either not enhanced or are nonhomogeneously enhanced on contrast material–enhanced CT scans (Fig 2).
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Figure 2a. Hepatic infarction following hepatic arterial thrombosis in a 15-year-old girl after living related transplantation to treat biliary atresia. (a, b) Precontrast (a) and postcontrast (b) CT images obtained 11 days after transplantation show large wedge-shaped low-attenuation areas (arrows) in peripheral parts of the transplanted liver. Extrahepatic hematoma (arrowheads) is also seen. (c) Contrast-enhanced CT scan obtained 4 months after a and b shows that the liver has a different shape and is smaller. These changes are most likely due to focal areas of infarction. Regression of the hematoma is seen.
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Figure 2b. Hepatic infarction following hepatic arterial thrombosis in a 15-year-old girl after living related transplantation to treat biliary atresia. (a, b) Precontrast (a) and postcontrast (b) CT images obtained 11 days after transplantation show large wedge-shaped low-attenuation areas (arrows) in peripheral parts of the transplanted liver. Extrahepatic hematoma (arrowheads) is also seen. (c) Contrast-enhanced CT scan obtained 4 months after a and b shows that the liver has a different shape and is smaller. These changes are most likely due to focal areas of infarction. Regression of the hematoma is seen.
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Figure 2c. Hepatic infarction following hepatic arterial thrombosis in a 15-year-old girl after living related transplantation to treat biliary atresia. (a, b) Precontrast (a) and postcontrast (b) CT images obtained 11 days after transplantation show large wedge-shaped low-attenuation areas (arrows) in peripheral parts of the transplanted liver. Extrahepatic hematoma (arrowheads) is also seen. (c) Contrast-enhanced CT scan obtained 4 months after a and b shows that the liver has a different shape and is smaller. These changes are most likely due to focal areas of infarction. Regression of the hematoma is seen.
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Portal Venous Stenosis or Thrombosis
Portal venous complication after liver transplantation is uncommon and was seen in 1%–22% of patients in previous studies (8–10). Portal venous stenosis occurs more frequently in reduced-size liver transplantation than in whole liver transplantation owing to the limited length of the portal vein that can be obtained from the donor. Risk factors include decreased portal venous inflow, the presence of portosystemic shunts before transplantation, prior splenectomy, twisting or kinking of the vascular conduit, and tension in the portal venous interposition graft (10,11).
Portal venous stenosis with thrombus formation in the immediate postoperative period is quickly diagnosed with Doppler US and is managed surgically. In most cases, portal venous stenosis develops slowly after transplantation and is suspected on the basis of the presence of gastrointestinal varices, ascites, and splenomegaly.
At contrast-enhanced CT, portal venous thrombosis is seen as a low-attenuation filling defect in the intrahepatic portal vein. In such cases, the extrahepatic portal venous trunk is stenosed and difficult to recognize (Fig 3). Portal venous stenosis without thrombus formation can be diagnosed with contrast-enhanced CT in asymptomatic cases (Fig 4). Portal venous stenosis can be treated with balloon dilation (11), but when the thrombus extends completely to the periphery of the intrahepatic portal venous branches, it can no longer be treated with balloon dilation or thrombolysis, and the patient must undergo repeat transplantation. Thus, early diagnosis of portal venous stenosis before formation of a complete thrombus is important.
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Figure 3a. Portal venous stenosis and thrombosis in a 4-year-old girl 3 years after living related transplantation to treat biliary atresia. The patient suddenly presented with gastrointestinal tract bleeding from esophageal varices. Portal venous thrombosis in the umbilical portion and decreased portal venous flow were found at Doppler US examination (not shown). (a, b) Contrast-enhanced CT images (a at a higher level than b) of the transplanted liver show a low-attenuation thrombus (arrow) in the umbilical portion of the left portal vein. (c) Percutaneous transhepatic portogram obtained 3 days after a and b depicts anastomotic obstruction (solid arrow) of the portal vein. The intrahepatic portal vein is not opacified. Arrowhead = splenic vein, open arrow = superior mesenteric vein.
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Figure 3b. Portal venous stenosis and thrombosis in a 4-year-old girl 3 years after living related transplantation to treat biliary atresia. The patient suddenly presented with gastrointestinal tract bleeding from esophageal varices. Portal venous thrombosis in the umbilical portion and decreased portal venous flow were found at Doppler US examination (not shown). (a, b) Contrast-enhanced CT images (a at a higher level than b) of the transplanted liver show a low-attenuation thrombus (arrow) in the umbilical portion of the left portal vein. (c) Percutaneous transhepatic portogram obtained 3 days after a and b depicts anastomotic obstruction (solid arrow) of the portal vein. The intrahepatic portal vein is not opacified. Arrowhead = splenic vein, open arrow = superior mesenteric vein.
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Figure 3c. Portal venous stenosis and thrombosis in a 4-year-old girl 3 years after living related transplantation to treat biliary atresia. The patient suddenly presented with gastrointestinal tract bleeding from esophageal varices. Portal venous thrombosis in the umbilical portion and decreased portal venous flow were found at Doppler US examination (not shown). (a, b) Contrast-enhanced CT images (a at a higher level than b) of the transplanted liver show a low-attenuation thrombus (arrow) in the umbilical portion of the left portal vein. (c) Percutaneous transhepatic portogram obtained 3 days after a and b depicts anastomotic obstruction (solid arrow) of the portal vein. The intrahepatic portal vein is not opacified. Arrowhead = splenic vein, open arrow = superior mesenteric vein.
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Figure 4a. Extrahepatic portal venous stenosis in a 4-year-old boy 2 years 9 months after living related transplantation to treat biliary atresia. (a, b) Contrast-enhanced CT images (a at a higher level than b) show compression of the extrahepatic portal vein (arrow) by the fully grown transplanted liver. (c) Percutaneous transhepatic portogram obtained 3 days after a and b shows stenosis (arrow) at the anastomosis. Balloon dilation of the stenosis was performed.
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Figure 4b. Extrahepatic portal venous stenosis in a 4-year-old boy 2 years 9 months after living related transplantation to treat biliary atresia. (a, b) Contrast-enhanced CT images (a at a higher level than b) show compression of the extrahepatic portal vein (arrow) by the fully grown transplanted liver. (c) Percutaneous transhepatic portogram obtained 3 days after a and b shows stenosis (arrow) at the anastomosis. Balloon dilation of the stenosis was performed.
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Figure 4c. Extrahepatic portal venous stenosis in a 4-year-old boy 2 years 9 months after living related transplantation to treat biliary atresia. (a, b) Contrast-enhanced CT images (a at a higher level than b) show compression of the extrahepatic portal vein (arrow) by the fully grown transplanted liver. (c) Percutaneous transhepatic portogram obtained 3 days after a and b shows stenosis (arrow) at the anastomosis. Balloon dilation of the stenosis was performed.
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Hepatic Congestion due to Hepatic Venous Anastomotic Stenosis
In living related transplantation, the hepatic vein is reconstructed by means of end-to-end or end-to-side anastomosis without harvesting of the vena cava (7). Hepatic venous anastomotic stenoses may occur more frequently in living related transplantation than in whole liver transplantation (7,12). As a result of delayed hepatic venous stenosis, hepatic congestion, portal venous flow decrease, ascites, and varices could be noted. Doppler US should be used primarily for the diagnosis of hepatic venous stenosis, but in our experience US sometimes failed to depict the stenosis. In some cases, this failure may occur because the stenosis is caused by the graft growing and twisting. The stenosis may disappear, depending on patient posture, as when the patient is supine. Contrast-enhanced CT is useful in demonstrating congestive changes in the liver parenchyma as a manifestation of blocked outflow, but it is of little help in depicting the stenosis itself (Fig 5). Once hepatic venous stenosis is suspected, we perform US-guided percutaneous transhepatic venography to confirm it, followed by balloon dilation of the stenotic site.
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Figure 5a. Hepatic congestion due to hepatic venous anastomotic stenosis in a 16-year-old girl after living related transplantation to treat biliary atresia. Four months after transplantation, the patient had decreased hepatic venous flow at Doppler US examination (not shown). Percutaneous liver biopsy revealed centrilobular hemorrhage, which is suggestive of hepatic venous anastomotic stenosis or occlusion. (a) Contrast-enhanced CT image obtained 5 months after transplantation shows irregular enhancement of the transplanted liver. This finding suggests hepatic congestion. (b) Percutaneous transhepatic venogram obtained 20 days after a helps confirm hepatic venous anastomotic stenosis (arrow). (c) Contrast-enhanced CT image obtained the day after venoplasty shows normal enhancement of the hepatic parenchyma.
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Figure 5b. Hepatic congestion due to hepatic venous anastomotic stenosis in a 16-year-old girl after living related transplantation to treat biliary atresia. Four months after transplantation, the patient had decreased hepatic venous flow at Doppler US examination (not shown). Percutaneous liver biopsy revealed centrilobular hemorrhage, which is suggestive of hepatic venous anastomotic stenosis or occlusion. (a) Contrast-enhanced CT image obtained 5 months after transplantation shows irregular enhancement of the transplanted liver. This finding suggests hepatic congestion. (b) Percutaneous transhepatic venogram obtained 20 days after a helps confirm hepatic venous anastomotic stenosis (arrow). (c) Contrast-enhanced CT image obtained the day after venoplasty shows normal enhancement of the hepatic parenchyma.
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Figure 5c. Hepatic congestion due to hepatic venous anastomotic stenosis in a 16-year-old girl after living related transplantation to treat biliary atresia. Four months after transplantation, the patient had decreased hepatic venous flow at Doppler US examination (not shown). Percutaneous liver biopsy revealed centrilobular hemorrhage, which is suggestive of hepatic venous anastomotic stenosis or occlusion. (a) Contrast-enhanced CT image obtained 5 months after transplantation shows irregular enhancement of the transplanted liver. This finding suggests hepatic congestion. (b) Percutaneous transhepatic venogram obtained 20 days after a helps confirm hepatic venous anastomotic stenosis (arrow). (c) Contrast-enhanced CT image obtained the day after venoplasty shows normal enhancement of the hepatic parenchyma.
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Biliary Complications
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Despite significant improvements that coincide with technical and immunologic advances in living related transplantation, biliary complications remain a significant cause of morbidity. Biliary complications are commonly seen after liver transplantation and occur in approximately 13%–19% of cases (13,14). Children recovering from living related transplantation may have a higher frequency (38%) of biliary complications than do adults (15). In living related transplantation, biliary reconstruction is accomplished by means of hepatic jejunostomy. Complications include anastomotic leakage and stenosis, intrahepatic bile ductal stones or debris, and biloma. These complications are reported to be related to the surgical method of biliary reconstruction and to prolonged cold ischemia time, immunologic reactions, hepatic arterial thrombosis, ABO blood group system incompatibility between donor and recipient, and cytomegalovirus infection (15–17). Hepatic arterial insufficiency from either stenosis or thrombosis may lead to necrosis of the bile ductal epithelium, which may lead to bilomas, abscesses, and nonanastomotic bile leak (18,19).
Anastomotic stenosis first causes cholangitis and does not always manifest as intrahepatic bile duct dilatation. CT, US, and magnetic resonance cholangiography do not reliably depict anastomotic stenosis, and percutaneous cholangiography is needed to diagnose the stenosis (20).
Intrahepatic Bile Duct Dilatation
Intrahepatic bile duct dilatation is not specific to anastomotic stenosis, because a slight asymptomatic dilatation of the intrahepatic bile duct is often seen in transplanted livers. Intrahepatic bile duct dilatation with symptoms such as fever or jaundice should be considered as cholangitis due to biliary anastomotic stenosis. Anastomotic stenosis can be induced by fibrosis around the anastomosis that results from postoperative bile leakage (Fig 6).
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Figure 6a. Intrahepatic bile duct dilatation in a 14-year-old boy 2 months after living related transplantation to treat biliary atresia. Results of liver function tests were abnormal. (a) Contrast-enhanced CT image shows intrahepatic bile duct dilatation (arrows) and perihepatic fluid collection (arrowhead). (b) Percutaneous transhepatic cholangiogram obtained 2 days after a reveals biliary anastomotic stenosis (arrow) and biloma (arrowhead) as a result of anastomotic bile leak.
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Figure 6b. Intrahepatic bile duct dilatation in a 14-year-old boy 2 months after living related transplantation to treat biliary atresia. Results of liver function tests were abnormal. (a) Contrast-enhanced CT image shows intrahepatic bile duct dilatation (arrows) and perihepatic fluid collection (arrowhead). (b) Percutaneous transhepatic cholangiogram obtained 2 days after a reveals biliary anastomotic stenosis (arrow) and biloma (arrowhead) as a result of anastomotic bile leak.
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Another main cause of anastomotic stenosis is hepatic arterial insufficiency. Because the blood supply of the biliary tree in the transplanted liver graft is entirely dependent on the hepatic artery, hepatic arterial stenosis frequently brings biliary complications. Biliary complications related to hepatic arterial thrombosis include either anastomotic stenosis or intrahepatic bile duct damage, which are depicted as irregular dilatation with fusiform morphology (Fig 7).
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Figure 7. Bile duct damage due to hepatic arterial thrombosis in a 1-year-old female infant after living related transplantation to treat biliary atresia. Contrast-enhanced CT image obtained 35 days after transplantation shows an irregularly shaped low-attenuation band that represents intrahepatic bile duct dilatation. Note the fusiform low-attenuation lesion (arrow).
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In cases of ABO blood group system incompatibility between donor and recipient, the frequency of hepatic arterial thrombosis and biliary complications is reported to be high (17). In living related transplantation, ABO blood group system incompatibility is sometimes unavoidable because the possible donors are restricted.
Intrahepatic Bile Duct Stones or Debris
Several factors can lead to the formation of biliary stones and sludge in the transplanted liver. In a previous report, most necrotic debris was found to be caused by bile duct wall ischemia due to hepatic arterial occlusion (21). Persistent sludge may ultimately become formed stones (21) (Fig 8).
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Figure 8a. Intrahepatic bile duct damage due to hepatic arterial thrombosis and biliary stones in a 16-year-old girl after living related transplantation to treat biliary atresia. This is a case of ABO blood group system incompatibility. (a) Contrast-enhanced CT image obtained 2 months after transplantation shows intrahepatic bile duct dilatation due to anastomotic stricture. (b) Contrast-enhanced CT image obtained 4 months after transplantation shows small high-attenuation lesions (arrows) in the dilated intrahepatic bile duct. (c) Nonenhanced CT image obtained 8 months after transplantation demonstrates multiple high-attenuation lesions (arrows) in the dilated intrahepatic bile duct.
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Figure 8b. Intrahepatic bile duct damage due to hepatic arterial thrombosis and biliary stones in a 16-year-old girl after living related transplantation to treat biliary atresia. This is a case of ABO blood group system incompatibility. (a) Contrast-enhanced CT image obtained 2 months after transplantation shows intrahepatic bile duct dilatation due to anastomotic stricture. (b) Contrast-enhanced CT image obtained 4 months after transplantation shows small high-attenuation lesions (arrows) in the dilated intrahepatic bile duct. (c) Nonenhanced CT image obtained 8 months after transplantation demonstrates multiple high-attenuation lesions (arrows) in the dilated intrahepatic bile duct.
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Figure 8c. Intrahepatic bile duct damage due to hepatic arterial thrombosis and biliary stones in a 16-year-old girl after living related transplantation to treat biliary atresia. This is a case of ABO blood group system incompatibility. (a) Contrast-enhanced CT image obtained 2 months after transplantation shows intrahepatic bile duct dilatation due to anastomotic stricture. (b) Contrast-enhanced CT image obtained 4 months after transplantation shows small high-attenuation lesions (arrows) in the dilated intrahepatic bile duct. (c) Nonenhanced CT image obtained 8 months after transplantation demonstrates multiple high-attenuation lesions (arrows) in the dilated intrahepatic bile duct.
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Intrahepatic Bilomas
Intrahepatic peripheral cystic lesions that communicate with the bile duct may be caused by bile duct wall ischemia in patients with hepatic arterial thrombosis after liver transplantation (Fig 9). These bilomas could be infected and result in abscesses.
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Figure 9. Intrahepatic biloma in a 16-year-old girl 2 months after living related transplantation to treat biliary atresia. Contrast-enhanced CT image shows multiple round low-attenuation areas (arrows) and intrahepatic bile duct dilatation (arrowheads).
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Other Abnormalities
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Fatty Liver
Low-attenuation changes in transplanted liver grafts imply various pathologic changes: cholestasis, fatty changes, acute cellular rejection, acute hepatitis, liver cell swelling, necrosis, centrilobular congestion, or necrosis. Recognition of the significance of low attenuation is important for the treatment of patients after liver transplantation. Fatty change occurs universally in response to hepatocytic toxic reactions, injury, or overnutrition. In patients after liver transplantation, fatty changes may be induced by either hyperalimentation or serious liver damage, and it is not possible to distinguish them on the basis of CT findings alone (Fig 10).
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Figure 10. Decreased liver parenchymal density in a 16-year-old girl 45 days after living related transplantation to treat biliary atresia. Contrast-enhanced CT image reveals homogeneous low-attenuation parenchyma of the transplanted liver, which is obviously less dense than the spleen. Microvesicular steatosis in the hepatic lobule was confirmed with 18-gauge needle biopsy.
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Periportal Collar
The presence of a central or peripheral periportal collar at CT is not sufficiently sensitive, specific, or accurate to help reliably diagnose or exclude acute allograft rejection. Periportal collars are seen with greater frequency in patients a short time after transplantation and in those with ascites. This finding supports the role of generalized postoperative lymphedema in production of the sign, which is most likely caused by surgical interruption of the periportal lymphatic vessels (22) (Fig 11).
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Figure 11a. Periportal collar in an 8-year-old girl 17 days after living related transplantation to treat biliary atresia. (a) Contrast-enhanced CT image demonstrates a central periportal low-attenuation area (arrows) and a small perihepatic fluid collection (arrowhead). (b) Contrast-enhanced CT image of a more cephalic section shows peripheral periportal collar signs (arrows). Biopsy performed the day after acquisition of these studies revealed acute purulent cholangitis and cholestasis.
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Figure 11b. Periportal collar in an 8-year-old girl 17 days after living related transplantation to treat biliary atresia. (a) Contrast-enhanced CT image demonstrates a central periportal low-attenuation area (arrows) and a small perihepatic fluid collection (arrowhead). (b) Contrast-enhanced CT image of a more cephalic section shows peripheral periportal collar signs (arrows). Biopsy performed the day after acquisition of these studies revealed acute purulent cholangitis and cholestasis.
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Focal Fluid Collection
Localized fluid collections are commonly seen after liver transplantation. They include hematomas, bilomas, and localized ascites. Distinction of infected and uninfected fluid is difficult with CT. In most cases, high-attenuation fluid collections are hemorrhagic (Figs 12, 13). Localized low-attenuation fluid collections at the liver edge are extrahepatic bilomas in most cases. They usually regress in size without medical treatment, but sometimes require percutaneous drainage.
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Figure 12. Intraperitoneal hematoma in an 11-year-old girl 30 days after living related transplantation to treat biliary atresia. Contrast-enhanced CT image reveals a large intraperitoneal hematoma (arrows).
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Figure 13a. Paraduodenal hematoma in a 9-year-old girl 28 days after living related transplantation to treat biliary atresia. Precontrast (a) and postcontrast (b) CT images show a high-attenuation focal fluid collection (arrow) at the paraduodenal space.
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Figure 13b. Paraduodenal hematoma in a 9-year-old girl 28 days after living related transplantation to treat biliary atresia. Precontrast (a) and postcontrast (b) CT images show a high-attenuation focal fluid collection (arrow) at the paraduodenal space.
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Posttransplantation Lymphoproliferative Disorder
Organ transplant recipients undergoing immunosuppressive therapy are at increased risk of developing malignancy. The Epstein-Barr virus has been associated with posttransplantation lymphoproliferative disorder and lymphoma in such patients. Abdominal examination of patients with posttransplantation lymphoproliferative disorder shows various findings, such as lymph node swelling (abdominal and retroperitoneal), splenic involvement, and extranodal involvement mainly in the liver and small intestine (Fig 14). In a recent report, extranodal involvement was seen more commonly than were splenic and nodal involvement in patients with abdominal posttransplantation lymphoproliferative disorder (23).
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Figure 14a. Posttransplantation lymphoproliferative disorder in a 9-year-old boy 2 years after living related transplantation to treat cryptogenic liver cirrhosis. The patient presented with sudden gastrointestinal tract bleeding. (a) Contrast-enhanced CT image shows a low-attenuation lymph node mass (arrows) that invades the duodenum. The node was proved to be Epstein-Barr virus lymphoma. (b) Contrast-enhanced CT image was obtained 10 months after a. After chemotherapy, abdominal lymphadenopathy is no longer seen.
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Figure 14b. Posttransplantation lymphoproliferative disorder in a 9-year-old boy 2 years after living related transplantation to treat cryptogenic liver cirrhosis. The patient presented with sudden gastrointestinal tract bleeding. (a) Contrast-enhanced CT image shows a low-attenuation lymph node mass (arrows) that invades the duodenum. The node was proved to be Epstein-Barr virus lymphoma. (b) Contrast-enhanced CT image was obtained 10 months after a. After chemotherapy, abdominal lymphadenopathy is no longer seen.
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Rejection
The presence or absence of rejection cannot be determined with CT alone (22). In our limited experience with acute cellular rejection, the liver parenchyma showed low-attenuation changes at CT in some cases, but there was no specific finding at CT in others. When rejection is suspected, we perform both CT and US to rule out any causes other than rejection.
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Conclusions
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US is the primary imaging modality in the evaluation of patients after liver transplantation, because it can be performed easily at the bedside and is sensitive to blood flow. CT is another important imaging modality for the evaluation of not only liver grafts but also extrahepatic abnormalities. Both CT and US are noninvasive imaging modalities, and their findings are complementary in the treatment of patients after liver transplantation.
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Acknowledgments
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The authors thank Takanori Sakurai, MD, for suggesting the pathologic findings.
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Footnotes
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See also the article by Bassignani et al (pp 39–52)
in this issue.
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References
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Abstract
Introduction
