DOI: 10.1148/rg.275065129
RadioGraphics 2007;27:1401-1417
© RSNA, 2007
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.
Address correspondence to A.H.M.C. (e-mail: angelacaiado{at}gmail.com).
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Abstract
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Liver transplantation is currently an accepted first-line treatment for patients with end-stage acute or chronic liver disease, but postoperative complications may limit the long-term success of transplantation. The most common and most clinically significant complications are arterial and venous thrombosis and stenosis, biliary disorders, fluid collections, neoplasms, and graft rejection. Early diagnosis is crucial to the successful management of all these complications, and imaging plays an important role in the diagnosis of all but graft rejection. A multimodality approach including ultrasonography and cross-sectional imaging studies often is most effective for diagnosis. Each imaging modality has specific strengths and weaknesses, and the diagnostic usefulness of a modality depends mainly on the patient’s characteristics, the clinical purpose of the imaging evaluation, and the expertise of imaging professionals.
© RSNA, 2007
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Identify a wide range of complications of liver transplantation according to their imaging features.
- Describe the advantages and limitations of each imaging modality for diagnosing complications of liver transplantation.
- Determine whether follow-up imaging is needed and which modality is most suitable for achieving the clinical purpose.
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Introduction
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Orthotopic liver transplantation has become the treatment of choice for patients with end-stage acute or chronic hepatic disease (1–5). Over the past several decades, advances in surgical techniques, organ preservation, immunosuppressive therapy, and early detection of postoperative complications have increased survival rates after liver transplantation (4). Early detection of postoperative complications is essential for graft and patient survival. Graft loss is a serious problem because of the complexity of the surgical procedures and the shortage of livers available for transplantation (6,7). Clinical signs of complications often are nonspecific, and diagnoses frequently are based on imaging findings.
Ultrasonography (US) is the preferred postoperative screening method because it is cost-effective, accessible, noninvasive, and easily performed at bedside (4,8–10). However, the method has inherent limitations that are well known, and when US findings are inconclusive, imaging with other modalities is necessary. The use of a contrast agent at US may help improve the sensitivity of the modality for detection of vascular flow and thus may obviate angiography (6,11), but US contrast agents are not readily available for use in standard clinical practice in many countries.
Cross-sectional imaging methods such as computed tomography (CT) and magnetic resonance (MR) imaging have greater overall sensitivity and specificity than US; however, moving patients who are in critical condition to the CT suite or the MR imaging unit precludes continuous monitoring and may put them at risk. Angiography is still the reference standard for diagnosing vascular complications of transplantation (12). Angiography also is an important option for guidance of nonsurgical treatment (13). Indeed, its relevance in the therapeutic setting is increasing even as its diagnostic relevance wanes with the use of other modalities.
The article describes the imaging appearances of the most common and most significant postoperative complications after liver transplantation: vascular disorders, biliary disorders, fluid collections, and neoplasms. Graft rejection, which is perhaps the most important complication, is considered only briefly because imaging plays no role in its diagnosis.
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Vascular Disorders
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Vascular complications, with an overall incidence of 9%, are a primary diagnostic consideration in a liver transplant recipient with hepatic failure; bile leakage; gastrointestinal, abdominal, or biliary bleeding; or sepsis (3,12,14). Prompt diagnosis is critical to allow graft salvage (15).
Hepatic Artery
Hepatic artery complications include thrombosis, stenosis, and pseudoaneurysm. At US, the normal hepatic artery waveform shows a rapid systolic upstroke and a continuous diastolic blood flow. The resistive index of a normal hepatic artery is 0.5–0.8 (Fig 1). The resistive index is calculated with the following equation: RI = (SVp = DVp)/SVp, where RI is the resistive index, SVp is the peak systolic velocity, and DVp is the peak diastolic velocity. The normal acceleration time (from end diastole to the first systolic peak) is less than 0.08 second (8,16,17).
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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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It is important to evaluate the right and left hepatic artery branches, because a normal hepatic artery waveform obtained at the porta hepatis does not exclude a hepatic artery obstruction (15). Whenever possible, the anastomosis also should be examined.
In the early postoperative period (<72 hours after transplantation), increased hepatic artery resistance (resistive index of >0.8) is a frequent finding, but resistance ordinarily returns to a normal level within a few days. Increased hepatic artery resistance is associated with older donor age and a prolonged period of ischemia (Fig 2) (18).
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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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Thrombosis.—
The estimated incidence of hepatic artery thrombosis among liver transplant recipients is 4%–12% in adults and 42% in children (12,19). This is one of the most feared complications, as it may lead to fulminant hepatic necrosis. In addition, in liver grafts, biliary ducts are supplied exclusively by small branches of the hepatic artery; therefore, arterial thrombosis may lead to biliary ischemia and necrosis (4,8,15).
Prompt diagnosis of hepatic artery thrombosis is extremely important because early intervention (with thrombectomy, hepatic artery reconstruction, or both) may allow graft salvage. However, most patients ultimately require retransplantation (14). Even after retransplantation, the mortality rate approaches 30% (3).
Risk factors for hepatic artery thrombosis include a significant difference in hepatic artery caliber between the donor and the recipient, an interpositional conduit for the anastomosis, a previous stenotic lesion of the celiac axis, excessive duration of cold ischemia time, ABO blood type incompatibility, cytomegalovirus infection, and acute rejection (12,14,19,20).
The use of US for routine postoperative monitoring of liver transplant recipients has altered the clinical and imaging manifestations of hepatic artery thrombosis at initial diagnosis: Nowadays, fulminant hepatic necrosis is a rare finding (4). A US-based diagnosis of hepatic artery thrombosis is established in the absence of flow in the proper hepatic and intrahepatic artery at color and pulsed Doppler imaging (Fig 3). The duplex Doppler imaging findings allow correct diagnosis in an estimated 92% of cases (21).
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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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A marked reduction of hepatic artery flow in the presence of hepatic edema, systemic hypotension, or high-grade hepatic artery stenosis may lead to false-positive findings of hepatic artery thrombosis (4,8). False-negative findings, on the other hand, may result from the presence of peri-portal arterial collateral vessels in chronic thrombosis (14). Collateral vessel flow causes a dampened (tardus parvus) hepatic artery waveform similar to that distal to a significant hepatic artery stenosis, with a prolonged acceleration time (>0.08 second) and low flow resistance (resistive index of <0.5) (17).
The use of a first- or second-generation contrast agent may be helpful when Doppler US findings are inconclusive. Contrast-enhanced US may provide clearer depiction of vascular structures. Using a second-generation perfluorocarbon-based contrast agent at US, Hom et al (6) demonstrated sensitivity, specificity, and accuracy of 100% for the detection of vascular complications after liver transplantation. Results from another study indicate that the use of a first-generation air-based microbubble contrast agent could obviate arteriography in 62.9% of cases in which initial Doppler US findings are inconclusive (11). At our hospital, a second-generation perfluorocarbon-based contrast agent has proved particularly valuable for the characterization of the hepatic artery. Its persistence in the bloodstream exceeds that of air-based microbubble contrast agents (Fig 4) (22). In addition, artifacts due to heart-related movement, respiration, or a lack of patient compliance during Doppler US acquisitions may be avoided with contrast-enhanced US (23).
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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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CT with standard and angiographic protocols allows the evaluation of parenchymal and vascular structures (3). The use of multidetector CT scanners has led to decreased scanning time and improved overall image quality with thin-section acquisitions. Contrast-enhanced multidetector CT provides a good noninvasive alternative to conventional angiography (Fig 5) (24).
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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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Gadolinium-enhanced MR imaging with three-dimensional spoiled gradient-echo sequences is another accurate and noninvasive method for evaluating the hepatic vessels (2,5,13,25). Good agreement was observed between findings at angiography and those at gadolinium-enhanced MR imaging for the detection of arterial abnormalities (Fig 3b, 3c) (13,26). Three-dimensional spoiled gradient-echo sequences allow evaluation of the liver parenchyma as well as the hepatic vessels. However, contrast-enhanced MR imaging places greater demands on patients than does US or CT: The examination lasts longer (20 minutes or more), and patients must hold their breath for 20–30 seconds. In hypoxic patients, the image acquisition time can be adapted to a shorter breath hold, but this adjustment may compromise anatomic coverage and spatial resolution (13). The criterion for a diagnosis of hepatic artery thrombosis at both CT and MR angiography is the appearance of an abrupt cutoff of flow in the artery, usually at the site of the anastomosis.
Stenosis.—
Hepatic artery stenosis has been reported to occur in 5%–11% of liver transplant recipients (3,4,12). This complication usually occurs at the site of anastomosis within 3 months after transplantation (3). If left untreated, it may lead to hepatic artery thrombosis, hepatic ischemia, biliary stricture, sepsis, and graft loss. Early detection of hepatic artery stenosis is crucial to allow treatment either with surgical reconstruction or with balloon angioplasty and avoid the necessity of retransplantation. Causes of hepatic artery stenosis may include clamp injury, intimal trauma from a perfusion catheter, or disruption of the vasa vasorum with resultant ischemia of the arterial ends (8).
Duplex Doppler US is the method of choice for postoperative screening of liver transplant recipients because it is capable of depicting any focal increase (of more than two to three times) in peak systolic velocity at the site of stenosis and any poststenotic turbulent flow (17). Sampled intrahepatic waveforms usually show a tardus parvus pattern, which is characterized by an increased acceleration time of more than 0.08 second and a resistive index of less than 0.5 (16) (Fig 6). Severe aortoiliac atherosclerosis and hepatic artery thrombosis with the formation of intrahepatic collateral vessels are two important pitfalls, because flow through collateral vessels also may demonstrate a dampened arterial waveform (14) (Fig 7).
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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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Low-grade narrowing of the hepatic artery may be present without causing apparent Doppler waveform abnormalities (8). Therefore, when clinical suspicion is high, normal findings at Doppler US should not preclude follow-up with cross-sectional imaging modalities (Fig 6b, 6c) or angiography, which are more accurate in demonstrating hepatic artery narrowing (4).
Ischemia and Infarction.—
Hepatic infarction is a rare occurrence in patients who have not undergone liver transplantation; even in cases of hepatic artery occlusion, liver blood flow is maintained via the portal system and collateral vessels. In liver transplant recipients, by contrast, these collateral vessels are usually ligated. As a rule (in 85% of cases), liver infarction in transplant recipients (Fig 8) is associated with hepatic artery complications; less frequently, it results from portal vein occlusion (3). Ischemic lesions have a tendency to undergo liquefaction, which may be complicated by infection. Focal abscesses may be a source of intermittent or remittent sepsis. Calcifications may be observed in long-standing cases.
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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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Pseudoaneurysm.—
A hepatic artery pseudoaneurysm is an uncommon complication that generally develops at the site of anastomosis or arises as a complication of angioplasty (3). It also may occur in an intrahepatic arterial branch as a consequence of a liver biopsy or after a focal parenchymal infection (8).
A hepatic artery pseudoaneurysm may be asymptomatic; however, a ruptured pseudoaneurysm may be manifested by acute shock (4). In addition, a fistula may form between the aneurysm and the biliary tree or the gastrointestinal tract (14), with resultant hemobilia or upper gastrointestinal bleeding. Treatment options for an extrahepatic pseudoaneurysm include surgical resection, embolization, and exclusion with stent placement. Intrahepatic pseudoaneurysms may be treated with endovascular coil embolization (3).
On duplex Doppler US images, a hepatic artery pseudoaneurysm appears as a cystic structure, usually near the course of the hepatic artery; its interior is color-filled, demonstrating a turbulent arterial flow. Both at contrast-enhanced CT and at MR angiography, this arterial lesion appears enhanced (4,14).
Portal Vein
Portal vein complications are relatively rare and include thrombosis and stenosis. Portal vein thrombosis occurs in about 1%–2% of cases (12,19). It most commonly results from technical problems (vessel misalignment, differences in the caliber of the anastomosed vessels, or stretching of the portal vein at the anastomotic site), previous portal vein surgery or previous thrombosis, increased downstream resistance due to a supra-hepatic stricture of the inferior vena cava (IVC), decreased portal inflow, and hypercoagulable states (3,4).
Portal vein stenosis has a reported incidence of 1% after liver transplantation (12). Focal narrowing of the portal vein, usually at the anastomosis, may occur if there is a significant size discrepancy between the donor and recipient portal veins. This focal narrowing is not indicative of stenosis (4).
The normal portal vein in a liver graft appears on US images with a regular contour, an anechoic lumen, and smooth walls, with the exception of a mild reduction in vessel caliber at the anastomotic site. Color and pulsed Doppler US images demonstrate a hepatopetal (toward the liver) monophasic flow that varies with respiration. Turbulent flow may be a normal finding in the early postoperative period (Fig 9) (8).
Signs of stenosis on B-mode US images include poststenotic dilatation and portal hypertension demonstrated by an increase in the number or caliber of collateral vessels. On color and pulsed Doppler images, focal color aliasing occurs in the presence of an increase of more than three-to fourfold in flow velocity at the site of stenosis relative to flow velocity in the prestenotic segment (Fig 10) (14). Patients with symptomatic portal vein stenosis may undergo balloon angioplasty (4).
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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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When thrombosis has occurred, an echogenic filling defect may be seen in the portal vein. Eventually, an acute thrombus becomes anechoic. Color or power Doppler images and pulsed Doppler waveforms may show a lack of portal venous flow (8). Sometimes portal flow is so minimal that it is not detected at US, and further evaluation is necessary. The treatment in symptomatic cases is thrombolysis or surgery (thrombectomy, venous graft) (4).
CT and MR angiography provide excellent depiction of filling defects and focal narrowing of the portal vein (Fig 11) (3,13). Rarely, transhepatic or transjugular portography may be necessary to achieve a definitive diagnosis (27).
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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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IVC and Hepatic Vein
Complications of the IVC and the hepatic vein have a low combined incidence (<1%) (2,12). IVC complications include thrombosis and stenosis, usually at the site of surgical anastomosis. Technical factors, such as a size discrepancy between donor and recipient vessels or suprahepatic caval kinking from organ rotation, may cause acute IVC stenosis. Delayed caval stenosis may be secondary to fibrosis, a chronic thrombus, or neointimal hyperplasia. Chronic caval stenoses are more common after retransplantation and in children (8).
The "piggyback" anastomosis (with preservation of the recipient vena cava and cavocaval anastomosis) has gained wide acceptance internationally and is the preferred technique for orthotopic liver transplantation at many institutions (28). However, it is especially vulnerable to two types of complications: (a) hemorrhage due to hepatic injury during surgery or due to cavocaval dehiscence (3% of cases) and (b) Budd-Chiari syndrome (0.3%–1.5% of cases) due to inadequate venous drainage (29). An obstruction of hepatic venous outflow may be treated with placement of a balloon-expandable stent (28).
The normal Doppler waveform obtained in the hepatic vein in a liver transplant is triphasic because of the effect of pressure variations determined by the right cardiac chambers during the cardiac cycle (Fig 12) (4).
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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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A reduction in the caliber of the IVC or hepatic vein, with impaired flow and resultant prestenotic dilatation of the hepatic veins, is an indirect diagnostic finding of stenosis at Doppler US (4). A persistent monophasic waveform is a sensitive finding, but it is not specific for a substantial hepatic vein stenosis (Fig 13). On the other hand, a triphasic or biphasic waveform may help exclude a substantial hepatic vein stenosis (10).
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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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Direct signs of stenosis include a focal stricture on B-mode US images and turbulent flow with increased velocity on pulsed Doppler images (Fig 13b). Thrombosis of the hepatic vein or IVC may be depicted as an intraluminal echogenic thrombus with no flow on Doppler images (Fig 14) (8).
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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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Cross-sectional modalities such as CT and MR imaging are commonly used to confirm suspicions aroused by Doppler US findings or to exclude a clinical hypothesis when US results are normal or inconclusive (Fig 13c–13e). In addition to stricture or thrombosis, CT and MR images may show additional diagnostic features, such as a mosaic pattern of perfusion (characteristic of Budd-Chiari syndrome) (Fig 14c, 14d) (3).
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Biliary Disorders
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Biliary complications occur in an estimated 25% of liver transplant recipients, usually within the first 3 months after transplantation (7). These complications are the second most common cause of graft dysfunction (rejection is the most common) (1). Biliary complications include stenosis, fistula, obstruction, stone formation, dysfunction of the Oddi sphincter, and recurrent biliary disease (7).
The choledochocholedochostomy is the type of biliary anastomosis that is most frequently employed, usually accompanying a cholecystectomy. With this kind of anastomosis, a T-tube may be left in place for 3 months to provide easy access for cholangiography of the biliary tree (3). A Roux-en-Y choledochojejunostomy may be preferred in some situations, such as in the presence of a discrepancy in donor and recipient duct size or of preexistent disease (biliary atresia, sclerosing cholangitis, or primary biliary cirrhosis) (4).
US and T-tube cholangiography are the imaging methods most often used to evaluate the biliary tree in the first months after liver transplantation. After the removal of biliary catheters, other imaging methods must be used; these may include MR cholangiography, endoscopic retrograde cholangiopancreatography, and percutaneous transhepatic cholangiography (30).
MR cholangiography is the best noninvasive technique for evaluation of the biliary tree (1,27). Multiplanar MR imaging enables accurate analysis of the surgically altered biliary anatomy. Although it does not provide a means of therapeutic intervention, it can be used to plan percutaneous, endoscopic, and surgical treatments (1). Despite good sensitivity for the detection of strictures, MR cholangiography tends to lead to their overestimation (31).
Endoscopic retrograde cholangiopancreatography and percutaneous transhepatic cholangiography provide high-quality images of the biliary tree and allow therapeutic intervention. However, the modalities are invasive and are associated with complications, which occur in 3.4% of percutaneous transhepatic cholangiographic examinations and in 5% of endoscopic retrograde cholangiopancreatographic examinations (1,27).
Obstruction and Stenosis
Obstruction is the most common biliary complication both in adults and in pediatric patients and is frequently caused by stenosis at the anastomotic site (1). Anastomotic strictures usually result from fibrotic proliferation with narrowing of the biliary lumen (Fig 15); less frequently, they are due to ischemia caused by hepatic artery thrombosis or stenosis (1). The possible causes of nonanastomotic strictures include pretransplantation biliary diseases such as primary sclerosing cholangitis, biliary ischemia, and infection.
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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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When biliary obstruction is believed to be present in a liver graft, it is of paramount importance that imaging findings be correlated with clinical and laboratory findings. Mild dilatation of the biliary tree may be observed on images in the absence of an actual mechanical obstruction (1). On the other hand, clinical and laboratory evidence of high-grade obstruction may be observed without visible dilatation of the biliary tree (3). Some patients with clinical and biochemical evidence of biliary obstruction may have dilatation of both the donor and the recipient bile ducts. Diffuse ductal dilatation may result from papillary dyskinesia due to devascularization or denervation of the papilla of Vater during transplantation (1).
Bile Leak
The approximate incidence of bile leaks in liver transplant recipients is 5%. Bile leaks usually occur in the early posttransplantation period, and more than 70% occur within the 1st postoperative month (4). Leaks occur most often at the T-tube site and rarely at the site of an anastomosis (3). Bile may leak freely into the peritoneal cavity or may form a perihepatic collection (Fig 16). Treatment includes stent placement and drainage of collections (8).
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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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Ductal Ischemia
Bile duct ischemia is usually a consequence of stenosis or thrombosis of the hepatic artery; the bile ducts are entirely dependent on the hepatic artery for their blood supply (14,32). The results of ductal ischemia are necrosis and its associated complications: bile leak (fistula), ductal scarring with fibrosis (stenosis), and bile collection (biloma) (Fig 17).
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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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A ductal stenosis may be treated with balloon dilation, which frequently is used in drainage procedures (Fig 17c, 17d). However, in most cases, retransplantation ultimately is necessary (3).
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Fluid Collections
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Seromas and hematomas are commonly observed near areas of vascular anastomosis (the hepatic hilum, the IVC) and biliary anastomosis, as well as in the perihepatic spaces. Such collections usually are found during the first days after transplantation and disappear within a few weeks (Fig 18). Rarely, they are large enough to compress the portal vein or the IVC. Pleural fluid, especially in the right side, also is a common finding. There is rarely a need for intervention if there is no ventilatory compromise (3). Although US is highly sensitive for the detection of fluid collections, it is not specific. A hematoma or purulent abscess may resemble a particulate ascites on US images. However, in most cases, collections of bile, lymph, blood, and pus all have the same appearance of a simple fluid collection (8). As expected, CT and MR imaging (especially the latter) are more useful for differentiating hematomas from seromas and bilomas because blood has higher attenuation at CT than do other fluids (3) and has a characteristic signal intensity at MR imaging. Nevertheless, it is difficult to distinguish a bile leak from a periportal seroma at MR imaging (33). In some cases, the main role of imaging is to pinpoint the amount and location of such collections and, when possible, to guide interventional diagnostic or therapeutic procedures.
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Neoplasms
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Neoplastic complications after liver transplantation may include recurrent tumors and malignant neoplasms. The most commonly occurring neoplasms in patients who have undergone liver transplantation are skin cancers other than melanoma, Kaposi sarcoma, and non-Hodgkin lymphoma (3,14,34). Risk factors for the development of malignancies in liver transplants include long-term immunosuppression, chronic overconsumption of alcohol before transplantation, previous viral infection (with a hepatitis virus, Epstein-Barr virus, cytomegalovirus, or herpesvirus), and acute rejection episodes (34).
Lymphoma associated with Epstein-Barr viral infection is more common among patients who undergo immunosuppressive therapy with cyclosporine and usually occurs 4–8 months after transplantation (14). Involvement of the liver may be intra- or extrahepatic. Extrahepatic involvement, which is more common, is characterized by a poorly defined hypoechoic soft-tissue mass that encases or constricts hilar structures (35). Lymphomatous involvement of the liver parenchyma may be manifested as multiple hypoechoic lesions at US or multiple hypoattenuating nodules at CT, but it occurs more frequently as a diffuse infiltrative process. Other organs that may be involved include the lymph nodes, spleen, small intestine, stomach, kidneys, mesentery, and adrenal glands. In children, the most frequent sites of involvement are the lymph nodes and the gastrointestinal tract (20).
The most common site of recurrence of hepatocellular carcinoma is the lung, and the second most common site is the liver (36).
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Rejection
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Rejection is the most common cause of graft failure. Clinical and laboratory findings are nonspecific and indistinguishable from those observed in transplant loss from other causes. Imaging likewise plays no role in the diagnosis of rejection, which can be achieved only with histologic analysis of a liver biopsy specimen (14).
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Algorithm for Imaging of Complications
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To help guide the postoperative imaging evaluation of liver transplant recipients, we propose a simple algorithm based on our experience (Fig 19). At our institution, on the 1st, 3rd, and 5th days after orthotopic liver transplantation, routine screening with duplex Doppler US usually is performed, even in asymptomatic patients. If the US findings are normal, the follow-up consists only of the collection of laboratory and clinical data. If the US findings are inconclusive or if the presence of a biliary or vascular complication is suspected, further evaluation is performed by using one or more cross-sectional imaging modalities. The use of contrast-enhanced US when a biliary or vascular complication is suspected may obviate reevaluation with more invasive modalities. Conventional cholangiography and angiography are commonly reserved for use in cases in which CT or MR imaging findings are abnormal or inconclusive and for therapeutic intervention.
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Conclusions
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Imaging plays an important role in the diagnosis of liver transplantation complications. Imaging professionals should be familiar with the most important complications and the applicability of each modality. Because of the wide spectrum of possible complications and the inherent complexity of the anatomy in liver transplant recipients, there is frequently a need to tailor the postoperative imaging evaluation to the individual clinical scenario. A multimodality approach often is recommended to determine the type and location of a complication and the most appropriate method of management.
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Acknowledgments
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Manoel de Souza Rocha, PhD, MD, University of São Paulo, Medical School, read the CT images.
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Footnotes
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Abbreviations: IVC = inferior vena cava
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References
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|---|
- Fulcher AS, Turner MA. Orthotopic liver transplantation: evaluation with MR cholangiography. Radiology 1999;211:715–722.[Abstract/Free Full Text]
- Glockner JF, Forauer AR, Solomon H, Varma CR, Perman WH. Three-dimensional gadolinium-enhanced MR angiography of vascular complications after liver transplantation. AJR Am J Roentgenol 2000;174:1447–1453.[Abstract/Free Full Text]
- Quiroga S, Sebastia MC, Margarit C, Castells L, Boye R, Alvarez-Castells A. Complications of orthotopic liver transplantation: spectrum of findings with helical CT. RadioGraphics 2001;21:1085–1102.[Abstract/Free Full Text]
- Garcia-Criado A, Gilabert R, Bargallo X, Bru C. Radiology in liver transplantation. Semin Ultrasound CT MR 2002;23:114–129.[CrossRef][Medline]
- Kim BS, Kim TK, Jung DJ, et al. Vascular complications after living related liver transplantation: evaluation with gadolinium-enhanced three-dimensional MR angiography. AJR Am J Roentgenol 2003;181:467–474.[Abstract/Free Full Text]
- Hom BK, Shrestha R, Palmer SL, et al. Prospective evaluation of vascular complications after liver transplantation: comparison of conventional and microbubble contrast-enhanced US. Radiology 2006;241:267–274.[Abstract/Free Full Text]
- Haberal M. Liver transplantation: experience at our center. Transplant Proc 2006;38:2111–2116.[CrossRef][Medline]
- Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal and abnormal. RadioGraphics 2003;23:1093–1114.[Abstract/Free Full Text]
- Garcia-Criado A, Gilabert R, Nicolau C, et al. Early detection of hepatic artery thrombosis after liver transplantation by Doppler ultrasonography: prognostic implications. J Ultrasound Med 2001; 20:51–58.[Abstract]
- Ko EY, Kim TK, Kim PN, Kim AY, Ha HK, Lee MG. Hepatic vein stenosis after living donor liver transplantation: evaluation with Doppler US. Radiology 2003;229:806–810.[Abstract/Free Full Text]
- Sidhu PS, Shaw AS, Ellis SM, Karani JB, Ryan SM. Microbubble ultrasound contrast in the assessment of hepatic artery patency following liver transplantation: role in reducing frequency of hepatic artery arteriography. Eur Radiol 2004;14:21–30.[CrossRef][Medline]
- Wozney P, Zajko AB, Bron KM, Point S, Starzl TE. Vascular complications after liver transplantation: a 5-year experience. AJR Am J Roentgenol 1986;147:657–663.[Abstract/Free Full Text]
- Stafford-Johnson DB, Hamilton BH, Dong Q, et al. Vascular complications of liver transplantation: evaluation with gadolinium-enhanced MR angiography. Radiology 1998;207:153–160.[Abstract/Free Full Text]
- Nghiem HV. Imaging of hepatic transplantation. Radiol Clin North Am 1998;36:429–443.[CrossRef][Medline]
- Tamsel S, Demirpolat G, Killi R, et al. Vascular complications after liver transplantation: evaluation with Doppler US. Abdom Imaging. doi: 10.1007/S00261-006-9041-Z. Published online September 12, 2006. Accessed November 15, 2006.
- Vit A, De Candia A, Como G, Del Frate C, Marzio A, Bazzocchi M. Doppler evaluation of arterial complications of adult orthotopic liver transplantation. J Clin Ultrasound 2003;31:339–345.[CrossRef][Medline]
- Dodd GD 3rd, Memel DS, Zajko AB, Baron RL, Santaguida LA. Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time. Radiology 1994;192:657–661.[Abstract/Free Full Text]
- Garcia-Criado A, Gilabert R, Salmeron JM, et al. Significance of and contributing factors for a high resistive index on Doppler sonography of the hepatic artery immediately after surgery: prognostic implications for liver transplant recipients. AJR Am J Roentgenol 2003;181:831–838.[Abstract/Free Full Text]
- Langnas AN, Marujo W, Stratta RJ, Wood RP, Shaw BW Jr. Vascular complications after orthotopic liver transplantation. Am J Surg 1991;161: 76–82; discussion 82–83.[CrossRef][Medline]
- Berrocal T, Parron M, Alvarez-Luque A, Prieto C, Santamaria ML. Pediatric liver transplantation: a pictorial essay of early and late complications. RadioGraphics 2006;26:1187–1209.[Abstract/Free Full Text]
- Flint EW, Sumkin JH, Zajko AB, Bowen A. Duplex sonography of hepatic artery thrombosis after liver transplantation. AJR Am J Roentgenol 1988; 151:481–483.[Abstract/Free Full Text]
- Berry JD, Sidhu PS. Microbubble contrast-enhanced ultrasound in liver transplantation. Eur Radiol 2004;14(suppl 8):P96–P103.[CrossRef][Medline]
- Rossi S, Rosa L, Ravetta V, et al. Contrast-enhanced versus conventional and color Doppler sonography for the detection of thrombosis of the portal and hepatic venous systems. AJR Am J Roentgenol 2006;186:763–773.[Abstract/Free Full Text]
- Kim SY, Kim KW, Kim MJ, Shin YM, Lee MG, Lee SG. Multidetector row CT of various hepatic artery complications after living donor liver transplantation. Abdom Imaging. doi: 10.1007/ S00261-006-9145–5. Published online September 30, 2006. Accessed November 10, 2006.
- Glockner JF. Three-dimensional gadolinium-enhanced MR angiography: applications for abdominal imaging. RadioGraphics 2001;21:357–370.[Abstract/Free Full Text]
- Ernst O, Asnar V, Sergent G, et al. Comparing contrast-enhanced breath-hold MR angiography and conventional angiography in the evaluation of mesenteric circulation. AJR Am J Roentgenol 2000;174:433–439.[Abstract/Free Full Text]
- Pieters PC, Miller WJ, DeMeo JH. Evaluation of the portal venous system: complementary roles of invasive and noninvasive imaging strategies. RadioGraphics 1997;17:879–895.[Abstract]
- Wang SL, Sze DY, Busque S, et al. Treatment of hepatic venous outflow obstruction after piggyback liver transplantation. Radiology 2005;236: 352–359.[Abstract/Free Full Text]
- Navarro F, Le Moine MC, Fabre JM, et al. Specific vascular complications of orthotopic liver transplantation with preservation of the retrohepatic vena cava: review of 1361 cases. Transplantation 1999;68:646–650.[CrossRef][Medline]
- Beltran MM, Marugan RB, Oton E, Blesa C, Nuno J. Accuracy of magnetic resonance cholangiography in the evaluation of late biliary complications after orthotopic liver transplantation. Transplant Proc 2005;37:3924–3925.[CrossRef][Medline]
- Ward J, Sheridan MB, Guthrie JA, et al. Bile duct strictures after hepatobiliary surgery: assessment with MR cholangiography. Radiology 2004;231: 101–108.[Abstract/Free Full Text]
- Orons PD, Sheng R, Zajko AB. Hepatic artery stenosis in liver transplant recipients: prevalence and cholangiographic appearance of associated biliary complications. AJR Am J Roentgenol 1995; 165:1145–1149.[Abstract/Free Full Text]
- Pandharipande PV, Lee VS, Morgan GR, et al. Vascular and extravascular complications of liver transplantation: comprehensive evaluation with three-dimensional contrast-enhanced volumetric MR imaging and MR cholangiopancreatography. AJR Am J Roentgenol 2001;177:1101–1107.[Abstract/Free Full Text]
- Aseni P, Vertemati M, De Carlis L, et al. De novo cancers and post-transplant lymphoproliferative disorder in adult liver transplantation. Pathol Int 2006;56:712–715.[CrossRef][Medline]
- Strouse PJ, Platt JF, Francis IR, Bree RL. Tumorous intrahepatic lymphoproliferative disorder in transplanted livers. AJR Am J Roentgenol 1996; 167:1159–1162.[Abstract/Free Full Text]
- Ito K, Siegelman ES, Stolpen AH, Mitchell DG. MR imaging of complications after liver transplantation. AJR Am J Roentgenol 2000;175:1145–1149.[Free Full Text]
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Abstract
LEARNING OBJECTIVES
