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Pediatric Liver Transplantation: A Pictorial Essay of Early and Late Complications¹

¹ From the Department of Radiology, Division of Pediatric Radiology (T.B., M.P., A.A.L., C.P.) and the Department of Pediatric Surgery (M.L.S.), University Hospital La Paz, Paseo de la Castellana 263, 28046 Madrid, Spain. Recipient of a Magna Cum Laude award for an education exhibit at the 2004 RSNA annual meeting. Received April 6, 2005; revision requested June 29 and received August 22; accepted September 6. All authors have no financial relationships to disclose. Address correspondence to C.P. (e-mail: cprieto.hulp{at}salud.madrid.org).

	Abstract

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
Orthotopic liver transplantation is currently the treatment of choice in patients with end-stage liver disease for which no other therapy is available. In children, segmental liver transplantation with living donor, reduced-size cadaveric, and split cadaveric allografts has become an important therapeutic option. However, the resulting expansion of the donor pool has increased the risk for postoperative vascular and biliary complications, which affect children more frequently than adults. Early recognition of these complications requires radiologic evaluation because their clinical manifestations are frequently nonspecific and vary widely. Doppler ultrasonography (US) plays the leading role in the postoperative evaluation of pediatric patients. Current magnetic resonance (MR) imaging techniques, including MR angiography and MR cholangiography, may provide a wealth of pertinent information and should be used when findings at US are inconclusive. Computed tomography is a valuable complement to US in the evaluation of complications involving the hepatic parenchyma as well as extrahepatic sites and is commonly used to guide percutaneous aspiration and fluid collection drainage. Familiarity with and early recognition of the imaging appearances of the various postoperative complications of pediatric liver transplantation are crucial for graft and patient survival.

© RSNA, 2006

	LEARNING OBJECTIVES

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
After reading this article and taking the test, the reader will be able to:

• Describe the different types of liver transplantation procedures used in pediatric patients.
  
• Recognize the imaging manifestations of early and late complications following pediatric liver transplantation.
  
• Discuss the efficacy of conventional and Doppler US, CT, MR imaging, and interventional procedures in the diagnosis and management of these complications.
  

	Introduction

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
Orthotopic liver transplantation is currently the treatment of choice in patients with severe acute or chronic liver failure for which no other therapy is available. In pediatric cases, the number of cadaveric donor livers is not sufficient; therefore, segmental liver transplantation with living donor, reduced-size cadaveric, and split cadaveric allografts has become an important therapeutic option, expanding the availability of size-appropriate organs for pediatric recipients with terminal liver disease (1–3). The successful surgical development of these transplantation modalities has led to a reduction of the pediatric pretransplantation mortality rate to nearly zero (4–6). Advances in organ preservation, improvement in immunosuppressive therapy agents, and adequate choice of the donor organ have marked a turning point such that immediate survival after transplantation is now considered the norm (2). Nevertheless, there are still significant complications, particularly those of vascular origin, that can lead to graft failure and necessitate retransplantation unless prompt treatment is instituted (7–11). Early diagnosis of organ-related complications is essential for achieving the best short- and long-term results. Therefore, it is essential that the radiologist be familiar with the types of transplantation procedures used in children and postoperative imaging appearance of the transplanted liver graft (12,13).

The transplantation procedures performed in children include whole pediatric cadaveric organ grafting, segmental or split adult cadaveric organ grafting, and living related adult organ grafting (segments II and III or segments II–IV) (4,14). The technique of liver splitting consists of dividing a donor liver in such a way that the left lateral liver graft can be transplanted into a small child and the right extended liver graft transplanted into a large child or a small adult (1,4,5). In transplants from living donors, when the vascular pedicle is too short, the use of vascular conduits with an autologous iliac artery from the donor may be required, with a potential increase in the risk of vascular complications.

The main postsurgical complications in patients who have undergone liver transplantation include arterial and venous stenoses and thromboses; biliary strictures, stones, and leakage; liver infarct, abscesses, and bilomas; organ rejection; extrahepatic fluid collections; and posttransplantation lymphoproliferative disorders (PTLDs). In this article, we discuss and illustrate the spectrum of early and late complications of pediatric liver transplantation. In addition, we demonstrate the utility of conventional and Doppler ultrasonography (US), computed tomography (CT), and magnetic resonance (MR) imaging in the diagnosis and management of these complications.

	Clinical Experience

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
In the past 15 years, 389 liver transplantations have been performed in 321 pediatric patients (159 boys, 162 girls; age range, 6 months–17 years) at our institution. Of these 389 procedures, 211 involved whole pediatric cadaveric organ grafts; 126 involved segmental organ grafts (segments II and III)—31 living adult donor grafts, 14 split cadaveric organ grafts, and 81 reduced-size cadaveric organ grafts; 44 involved transplantation of the entire left lobe (segments II–IV), 43 of the transplants coming from a cadaveric donor and one from a living related adult donor; and eight involved transplantation of the right lobe, two of the transplants coming from a living donor.

Vascular and Biliary Anastomoses
Currently, in whole liver transplantation, the donor hepatic artery is usually anastomosed to the recipient hepatic artery in an end-to-end fashion. The portal venous anastomosis is also created in an end-to-end fashion between the main portal vein (MPV) of the donor and that of the recipient. The donor suprahepatic inferior vena cava (IVC) can be attached to the recipient suprahepatic IVC and the donor infrahepatic IVC to the recipient infrahepatic IVC by means of an end-to-end anastomosis. One technical variant is the piggyback technique with conservation of the recipient vena cava, which is anastomosed to the graft hepatic veins. Biliary anastomosis is created in an end-to-end fashion between the common bile duct (CBD) of the donor and that of the recipient, except in patients with biliary atresia, in whom biliary reconstruction is performed by means of hepatic jejunostomy with a Roux-en-Y limb anastomosis.

In reduced-size transplants, when the recipient hepatic artery is too small or too short, arterial reconstruction is performed using a donor conduit from the infrarenal aorta. When possible, portal anastomosis is created in an end-to-end fashion between the donor left portal vein and the recipient MPV. If necessary, venous grafting is performed with use of donor veins. The hepatic venous anastomosis is usually created using the piggyback technique in an end-to-end or end-to-side fashion between the donor left hepatic vein and the recipient hepatic vein orifice, with preservation of the recipient IVC. Biliary reconstruction is performed by means of hepatic jejunostomy with a Roux-en-Y limb anastomosis.

Imaging Modalities
Because the clinical manifestations of posttransplantation complications are frequently nonspecific and vary widely, imaging studies are critical for early diagnosis. US (both gray-scale and Doppler) is the initial imaging modality of choice for detection and follow-up of early and delayed complications of all types of liver transplantation (15–19), since it can be performed at the bedside; does not make use of ionizing radiation; is cost effective; and can demonstrate the hepatic parenchyma, vessels, and bile ducts. US is the primary imaging modality used to assess for postoperative complications at our institution. If a US study demonstrates a complication that does not require intervention, it is usually followed up with serial US studies. In cases in which (a) US results are inconclusive, (b) confirmation is required, or (c) clinical suspicion for a complication persists despite normal US results, helical CT or MR imaging is performed. We currently prefer MR imaging because CT involves the use of ionizing radiation. Conventional angiographic and cholangiographic studies are reserved for nonsurgical treatment of some complications at our institution.

We routinely perform the first US examination in the operating room in all reduced-size transplantations. A baseline study is always performed within the first 12 hours after transplantation and every 24 hours thereafter while the patient is in the intensive care unit. Then, a follow-up control study is performed weekly while the patient is in a regular hospital room or whenever clinical changes make it necessary. Every US examination includes gray-scale imaging of the liver and a survey of the peritoneal cavity. The hepatic artery, portal vein, hepatic veins, and IVC are examined with color and pulsed Doppler US. Doppler US examination of the hepatic artery includes measurements of the resistive index and systolic acceleration time. Velocity measurements are obtained from the MPV proximal to, at, and distal to the anastomosis. Doppler waveforms are obtained from the hepatic veins and the IVC, with special attention given to the vena caval anastomoses.

	Vascular Complications

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
Vascular complications can be either arterial or venous, usually occurring in the early postoperative period. Clinical manifestations vary from mildly elevated values on hepatic function tests to fulminant hepatic failure (7,9,11,17). Because these manifestations are so varied, prompt diagnosis and adequate management are critical for graft salvage. US is the primary screening modality used for the detection of vascular complications. MR angiography is performed to confirm abnormalities demonstrated at US or in patients in whom the US study is suboptimal. Conventional vascular studies are currently reserved for endovascular treatment of these complications.

Hepatic Artery Stenosis
Hepatic artery stenosis is estimated to occur in up to 14% of pediatric transplant recipients (6,15, 16). It was the most common vascular complication in our series (12% of cases) and occurred most frequently at the anastomotic site, although it may also be found more distally. Risk factors include clamp injury, intimal trauma caused by the use of perfusion catheters during surgery, and disrupted vasa vasorum leading to ischemia of the arterial ends. Severe rejection is also an important factor in hepatic artery stenosis (8,15,20); it may lead to biliary ischemia, causing hepatic dysfunction and, eventually, hepatic failure (12,17,19).

Doppler US is the imaging modality of choice for diagnosis and follow-up. The reported sensitivity of Doppler US for the detection of hepatic artery stenosis is 80%–90% (11,18,21). At the site of narrowing, spectral analysis reveals a focal accelerated velocity greater than 2 m/sec (11,15, 22). However, the site of narrowing is difficult to identify, and the diagnosis is usually made on the basis of the Doppler US findings obtained distal to the stenosis. Intrahepatic arterial waveforms distal to the stenosis display a tardus parvus pattern with a decreased resistive index (<50) and a prolonged acceleration time (>80 msec) (Fig 1) (19,22–24). Associated turbulences distal to the stenosis are commonly observed at color Doppler US (11,22).

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 1a.  Hepatic artery stenosis in a 5-year-old patient. (a) Duplex Doppler US image of the main hepatic artery obtained proximal to an anastomosis shows a normal pattern. (b) Duplex Doppler US image obtained at the anastomosis shows an elevated peak velocity (1.64 m/sec) and spectral broadening, findings that are consistent with turbulence. (c) Duplex Doppler US image of the intrahepatic artery shows a tardus parvus waveform with a decreased resistive index (0.40). (d) Duplex color Doppler US image shows a prolonged acceleration time (120 msec), a finding that is consistent with hepatic artery stenosis. (e) MR angiogram demonstrates a stenosis (arrow) at the anastomosis.

View larger version (140K): [in this window] [in a new window] [Download PPT slide]   Figure 1b.  Hepatic artery stenosis in a 5-year-old patient. (a) Duplex Doppler US image of the main hepatic artery obtained proximal to an anastomosis shows a normal pattern. (b) Duplex Doppler US image obtained at the anastomosis shows an elevated peak velocity (1.64 m/sec) and spectral broadening, findings that are consistent with turbulence. (c) Duplex Doppler US image of the intrahepatic artery shows a tardus parvus waveform with a decreased resistive index (0.40). (d) Duplex color Doppler US image shows a prolonged acceleration time (120 msec), a finding that is consistent with hepatic artery stenosis. (e) MR angiogram demonstrates a stenosis (arrow) at the anastomosis.

View larger version (93K): [in this window] [in a new window] [Download PPT slide]   Figure 1c.  Hepatic artery stenosis in a 5-year-old patient. (a) Duplex Doppler US image of the main hepatic artery obtained proximal to an anastomosis shows a normal pattern. (b) Duplex Doppler US image obtained at the anastomosis shows an elevated peak velocity (1.64 m/sec) and spectral broadening, findings that are consistent with turbulence. (c) Duplex Doppler US image of the intrahepatic artery shows a tardus parvus waveform with a decreased resistive index (0.40). (d) Duplex color Doppler US image shows a prolonged acceleration time (120 msec), a finding that is consistent with hepatic artery stenosis. (e) MR angiogram demonstrates a stenosis (arrow) at the anastomosis.

View larger version (69K): [in this window] [in a new window] [Download PPT slide]   Figure 1d.  Hepatic artery stenosis in a 5-year-old patient. (a) Duplex Doppler US image of the main hepatic artery obtained proximal to an anastomosis shows a normal pattern. (b) Duplex Doppler US image obtained at the anastomosis shows an elevated peak velocity (1.64 m/sec) and spectral broadening, findings that are consistent with turbulence. (c) Duplex Doppler US image of the intrahepatic artery shows a tardus parvus waveform with a decreased resistive index (0.40). (d) Duplex color Doppler US image shows a prolonged acceleration time (120 msec), a finding that is consistent with hepatic artery stenosis. (e) MR angiogram demonstrates a stenosis (arrow) at the anastomosis.

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 1e.  Hepatic artery stenosis in a 5-year-old patient. (a) Duplex Doppler US image of the main hepatic artery obtained proximal to an anastomosis shows a normal pattern. (b) Duplex Doppler US image obtained at the anastomosis shows an elevated peak velocity (1.64 m/sec) and spectral broadening, findings that are consistent with turbulence. (c) Duplex Doppler US image of the intrahepatic artery shows a tardus parvus waveform with a decreased resistive index (0.40). (d) Duplex color Doppler US image shows a prolonged acceleration time (120 msec), a finding that is consistent with hepatic artery stenosis. (e) MR angiogram demonstrates a stenosis (arrow) at the anastomosis.

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 2a.  Hepatic artery stenosis caused by postsurgical edema at the anastomosis in a 3-year-old patient. (a) Control duplex color US image obtained 24 hours after transplantation shows a tardus parvus waveform. (b) Control duplex color US image obtained 2 days later demonstrates a normal hepatic arterial waveform.

View larger version (98K): [in this window] [in a new window] [Download PPT slide]   Figure 2b.  Hepatic artery stenosis caused by postsurgical edema at the anastomosis in a 3-year-old patient. (a) Control duplex color US image obtained 24 hours after transplantation shows a tardus parvus waveform. (b) Control duplex color US image obtained 2 days later demonstrates a normal hepatic arterial waveform.

Doppler US allows correct identification of hepatic artery thrombosis in up to 90% of cases (8,11,15,30). At Doppler US examination, there is usually complete absence of both proper hepatic and intrahepatic arterial flow (Fig 3) (15,17,18). The initial Doppler waveform of the hepatic artery may be normal, with follow-up Doppler US images showing a progressive decrease in systolic and diastolic flow, followed by absent diastolic flow, dampening of the systolic peak, and, finally, total loss of the hepatic waveform (Fig 4) (31). After thrombosis, arterial collateral vessels can develop, especially in children, and intrahepatic flow may be identified. Nevertheless, the intrahepatic arterial waveform will display a tardus parvus pattern with an acceleration time greater than 80 msec and a resistive index less than 0.5 (Fig 5) (11,18,23). Therefore, a complete absence of flow in the main hepatic artery and a tardus parvus pattern in the intrahepatic branches of the hepatic artery are highly suggestive of hepatic artery thrombosis and should be confirmed with other imaging techniques (32). False-positive diagnosis may occur with a low-flow nonocclusive phenomenon caused by massive hepatic necrosis or systemic hypotension that is not distinguishable from arterial occlusion (33).

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 3a.  Hepatic artery thrombosis in a 22-month-old patient. (a) Transverse color Doppler US image obtained at the porta hepatis shows normal flow in the portal vein and total absence of flow in the hepatic artery. (b) Pulsed color Doppler US image demonstrates total absence of arterial flow at the porta hepatis. P = portal vein. (c) MR angiogram helps confirm complete thrombosis of the hepatic artery (arrow).

View larger version (74K): [in this window] [in a new window] [Download PPT slide]   Figure 3b.  Hepatic artery thrombosis in a 22-month-old patient. (a) Transverse color Doppler US image obtained at the porta hepatis shows normal flow in the portal vein and total absence of flow in the hepatic artery. (b) Pulsed color Doppler US image demonstrates total absence of arterial flow at the porta hepatis. P = portal vein. (c) MR angiogram helps confirm complete thrombosis of the hepatic artery (arrow).

View larger version (95K): [in this window] [in a new window] [Download PPT slide]   Figure 3c.  Hepatic artery thrombosis in a 22-month-old patient. (a) Transverse color Doppler US image obtained at the porta hepatis shows normal flow in the portal vein and total absence of flow in the hepatic artery. (b) Pulsed color Doppler US image demonstrates total absence of arterial flow at the porta hepatis. P = portal vein. (c) MR angiogram helps confirm complete thrombosis of the hepatic artery (arrow).

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 4a.  Hepatic artery thrombosis in a 2-year-old girl. (a) Control duplex US image obtained 48 hours after transplantation shows a normal hepatic arterial waveform. (b) Control duplex US image obtained 24 hours later demonstrates low systolic and diastolic flow. (c) Control duplex US image obtained 6 hours later shows total absence of arterial flow. (d) Arteriogram helps confirm hepatic artery thrombosis (arrow) at the level of the graft between the donor hepatic artery and the recipient aorta. A balloon was inserted into the graft, and fibrinolytic therapy was administered to preserve the liver. No retransplantation was necessary.

View larger version (96K): [in this window] [in a new window] [Download PPT slide]   Figure 4b.  Hepatic artery thrombosis in a 2-year-old girl. (a) Control duplex US image obtained 48 hours after transplantation shows a normal hepatic arterial waveform. (b) Control duplex US image obtained 24 hours later demonstrates low systolic and diastolic flow. (c) Control duplex US image obtained 6 hours later shows total absence of arterial flow. (d) Arteriogram helps confirm hepatic artery thrombosis (arrow) at the level of the graft between the donor hepatic artery and the recipient aorta. A balloon was inserted into the graft, and fibrinolytic therapy was administered to preserve the liver. No retransplantation was necessary.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 4c.  Hepatic artery thrombosis in a 2-year-old girl. (a) Control duplex US image obtained 48 hours after transplantation shows a normal hepatic arterial waveform. (b) Control duplex US image obtained 24 hours later demonstrates low systolic and diastolic flow. (c) Control duplex US image obtained 6 hours later shows total absence of arterial flow. (d) Arteriogram helps confirm hepatic artery thrombosis (arrow) at the level of the graft between the donor hepatic artery and the recipient aorta. A balloon was inserted into the graft, and fibrinolytic therapy was administered to preserve the liver. No retransplantation was necessary.

View larger version (172K): [in this window] [in a new window] [Download PPT slide]   Figure 4d.  Hepatic artery thrombosis in a 2-year-old girl. (a) Control duplex US image obtained 48 hours after transplantation shows a normal hepatic arterial waveform. (b) Control duplex US image obtained 24 hours later demonstrates low systolic and diastolic flow. (c) Control duplex US image obtained 6 hours later shows total absence of arterial flow. (d) Arteriogram helps confirm hepatic artery thrombosis (arrow) at the level of the graft between the donor hepatic artery and the recipient aorta. A balloon was inserted into the graft, and fibrinolytic therapy was administered to preserve the liver. No retransplantation was necessary.

View larger version (95K): [in this window] [in a new window] [Download PPT slide]   Figure 5a.  Hepatic artery thrombosis in a 7-year-old boy. (a) Duplex color Doppler US image shows absence of arterial flow at the porta hepatis. (b) Duplex US image shows intrahepatic arterial vessels with a tardus parvus pattern due to collateral vessels. (c) MR angiogram helps confirm hepatic artery thrombosis (arrow) at the anastomosis.

View larger version (122K): [in this window] [in a new window] [Download PPT slide]   Figure 5b.  Hepatic artery thrombosis in a 7-year-old boy. (a) Duplex color Doppler US image shows absence of arterial flow at the porta hepatis. (b) Duplex US image shows intrahepatic arterial vessels with a tardus parvus pattern due to collateral vessels. (c) MR angiogram helps confirm hepatic artery thrombosis (arrow) at the anastomosis.

View larger version (160K): [in this window] [in a new window] [Download PPT slide]   Figure 5c.  Hepatic artery thrombosis in a 7-year-old boy. (a) Duplex color Doppler US image shows absence of arterial flow at the porta hepatis. (b) Duplex US image shows intrahepatic arterial vessels with a tardus parvus pattern due to collateral vessels. (c) MR angiogram helps confirm hepatic artery thrombosis (arrow) at the anastomosis.

Spiral CT is also useful in confirming or excluding hepatic artery thrombosis by demonstrating (a) patency of the hepatic artery from its origin to the anastomosis, with distal occlusion; or (b) occlusion of the entire hepatic artery (35,36). At times, patency of small distal intrahepatic arterial vessels may be observed, probably due to the formation of collateral vessels (28,36).

Angiography is useful when fibrinolytic endovascular therapy is indicated (Fig 4).

Portal Vein Thrombosis
Portal vein thrombosis occurred in 3.2% of our patients. It occurs more frequently in reduced-size liver transplantation, commonly involving the main extrahepatic segment.

Risk factors include surgical difficulties; decreased portal venous inflow; the presence of portosystemic shunts before transplantation; prior splenectomy; excessive vessel redundancy; and use of the venous conduits, most commonly cryo-preserved iliac veins (6,9,37). With the elimination of venous conduits for portal venous anastomoses, early graft loss was decreased at our institution. Clinical manifestations include new-onset massive ascites, variceal bleeding, elevated values on hepatic function tests, splenomegaly, hepatic failure, and lower extremity edema (37,38).

In children, an acute thrombus is frequently anechoic and may be imperceptible on gray-scale US images, the portal vein appearing normal. In these cases, color flow and spectral Doppler analysis will show no detectable flow within the portal vein (Fig 6) (9,10). Vessel narrowing or an echogenic luminal thrombus with no Doppler flow may also be seen (Fig 7) (15). Partial portal vein thrombosis may appear as a nonocclusive filling defect at US. Resultant luminal narrowing can be mistaken for portal vein stenosis at gray-scale, spectral, and color Doppler US (10,38). Occasionally, reversed flow in the intrahepatic branches may be observed in patients with portal vein thrombosis and complete absence of flow in the MPV. This finding is due to arterioportal shunts that develop soon after the thrombosis. Care should be taken to avoid making a false-negative diagnosis (9,15,16).

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 6.  Portal vein thrombosis in a 12-year-old boy. Color Doppler US image obtained at the porta hepatis shows absence of flow in the portal vein (P). An acute thrombus is anechoic and can be identified only at color flow imaging as a flow defect. Note the normal hepatic artery (AH).

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 7a.  Portal vein thrombosis in a 13-year-old girl. (a) On a subcostal oblique color Doppler US image obtained at the porta hepatis, echogenic material is seen in the lumen of the portal vein (P), a finding that represents thrombus. Note the absence of flow in the vessel. AH = hepatic artery. (b) Pulsed duplex Doppler US image obtained at the portal vein demonstrates no flow. (c) MR angiogram shows a filling defect in the portal vein (arrow) caused by thrombus at the confluence of the splenic and superior mesenteric veins. The MPV is completely thrombosed (arrowhead).

View larger version (87K): [in this window] [in a new window] [Download PPT slide]   Figure 7b.  Portal vein thrombosis in a 13-year-old girl. (a) On a subcostal oblique color Doppler US image obtained at the porta hepatis, echogenic material is seen in the lumen of the portal vein (P), a finding that represents thrombus. Note the absence of flow in the vessel. AH = hepatic artery. (b) Pulsed duplex Doppler US image obtained at the portal vein demonstrates no flow. (c) MR angiogram shows a filling defect in the portal vein (arrow) caused by thrombus at the confluence of the splenic and superior mesenteric veins. The MPV is completely thrombosed (arrowhead).

View larger version (134K): [in this window] [in a new window] [Download PPT slide]   Figure 7c.  Portal vein thrombosis in a 13-year-old girl. (a) On a subcostal oblique color Doppler US image obtained at the porta hepatis, echogenic material is seen in the lumen of the portal vein (P), a finding that represents thrombus. Note the absence of flow in the vessel. AH = hepatic artery. (b) Pulsed duplex Doppler US image obtained at the portal vein demonstrates no flow. (c) MR angiogram shows a filling defect in the portal vein (arrow) caused by thrombus at the confluence of the splenic and superior mesenteric veins. The MPV is completely thrombosed (arrowhead).

At contrast material–enhanced CT, portal vein thrombosis is seen as a low-attenuation filling defect (12,30,40).

Portal vein stenosis with thrombus formation in the immediate postoperative period is quickly diagnosed with Doppler US and is managed surgically. Treatment of portal vein thrombosis may include mechanical thrombectomy, segmental portal vein resection, percutaneous thrombolysis and stent placement, or balloon angioplasty (41–43). However, when the thrombus extends 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 (12). Thus, early diagnosis of portal vein stenosis before formation of a complete thrombus is important. Occasionally, portal vein thrombosis is detected in patients with normal allograft function but no portal hypertension. In these patients, sufficient hepatopetal collateralization has developed to maintain adequate venous flow (39,41). A cavernomatous transformation is the usual finding at Doppler US in these cases (Fig 8).

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 8a.  (a) Portal cavernoma in an 18-month-old boy. Color Doppler US image obtained at the porta hepatis in a reduced-size transplant shows numerous vascular structures. (b, c) Portal cavernoma in a different patient. (b) Pulsed duplex color Doppler US image demonstrates collateral veins representing cavernous transformation of the portal vein caused by long-standing thrombotic occlusion. (c) MR angiogram shows cavernomatous vessels (arrow) and collateralization of preexisting paragastric varices.

View larger version (84K): [in this window] [in a new window] [Download PPT slide]   Figure 8b.  (a) Portal cavernoma in an 18-month-old boy. Color Doppler US image obtained at the porta hepatis in a reduced-size transplant shows numerous vascular structures. (b, c) Portal cavernoma in a different patient. (b) Pulsed duplex color Doppler US image demonstrates collateral veins representing cavernous transformation of the portal vein caused by long-standing thrombotic occlusion. (c) MR angiogram shows cavernomatous vessels (arrow) and collateralization of preexisting paragastric varices.

View larger version (176K): [in this window] [in a new window] [Download PPT slide]   Figure 8c.  (a) Portal cavernoma in an 18-month-old boy. Color Doppler US image obtained at the porta hepatis in a reduced-size transplant shows numerous vascular structures. (b, c) Portal cavernoma in a different patient. (b) Pulsed duplex color Doppler US image demonstrates collateral veins representing cavernous transformation of the portal vein caused by long-standing thrombotic occlusion. (c) MR angiogram shows cavernomatous vessels (arrow) and collateralization of preexisting paragastric varices.

At gray-scale US, portal vein stenosis is diagnosed when a reduction of the vessel lumen of 50% or more is observed (Fig 9) at the site of narrowing relative to the prestenotic area, or when the caliber of the vessel is 2.5 mm or less at the site of narrowing (7,8,11). Color Doppler US shows focal color aliasing at the vascular anastomosis. At pulsed Doppler US, the waveform shows a systolic velocity greater than 20 m/sec or a velocity in the stenotic segment that is three to four times greater than that in the prestenotic segment (Fig 9). A poststenotic jet with a velocity between 1 and 3 m/sec is a characteristic finding (Figs 9, 10) (11,15,16).

View larger version (138K): [in this window] [in a new window] [Download PPT slide]   Figure 9a.  Portal vein stenosis in a 5-year-old boy. (a) Longitudinal US image of the MPV shows stenosis (arrow) at the anastomosis between the donor and recipient portal veins. (b, c) Duplex US images show velocities in the stenotic segment (4.55 m/sec) (b) and poststenotic segment (1.27 m/sec) (c) that are more than seven and two times, respectively, greater than the velocity in the prestenotic segment (not shown), which was 0.6 m/sec. These findings are consistent with significant stenosis. (d) MR angiogram reveals portal vein stenosis (arrow) at the anastomosis.

View larger version (96K): [in this window] [in a new window] [Download PPT slide]   Figure 9b.  Portal vein stenosis in a 5-year-old boy. (a) Longitudinal US image of the MPV shows stenosis (arrow) at the anastomosis between the donor and recipient portal veins. (b, c) Duplex US images show velocities in the stenotic segment (4.55 m/sec) (b) and poststenotic segment (1.27 m/sec) (c) that are more than seven and two times, respectively, greater than the velocity in the prestenotic segment (not shown), which was 0.6 m/sec. These findings are consistent with significant stenosis. (d) MR angiogram reveals portal vein stenosis (arrow) at the anastomosis.

View larger version (143K): [in this window] [in a new window] [Download PPT slide]   Figure 9c.  Portal vein stenosis in a 5-year-old boy. (a) Longitudinal US image of the MPV shows stenosis (arrow) at the anastomosis between the donor and recipient portal veins. (b, c) Duplex US images show velocities in the stenotic segment (4.55 m/sec) (b) and poststenotic segment (1.27 m/sec) (c) that are more than seven and two times, respectively, greater than the velocity in the prestenotic segment (not shown), which was 0.6 m/sec. These findings are consistent with significant stenosis. (d) MR angiogram reveals portal vein stenosis (arrow) at the anastomosis.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 9d.  Portal vein stenosis in a 5-year-old boy. (a) Longitudinal US image of the MPV shows stenosis (arrow) at the anastomosis between the donor and recipient portal veins. (b, c) Duplex US images show velocities in the stenotic segment (4.55 m/sec) (b) and poststenotic segment (1.27 m/sec) (c) that are more than seven and two times, respectively, greater than the velocity in the prestenotic segment (not shown), which was 0.6 m/sec. These findings are consistent with significant stenosis. (d) MR angiogram reveals portal vein stenosis (arrow) at the anastomosis.

View larger version (148K): [in this window] [in a new window] [Download PPT slide]   Figure 10a.  Portal vein stenosis in a 13-month-old girl. (a) Longitudinal US image of the MPV shows stenosis of an entire vascular graft (arrows) that was used to anastomose the vein. (b) Duplex US image of the poststenotic area shows a high flow velocity (1.1 m/sec).

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 10b.  Portal vein stenosis in a 13-month-old girl. (a) Longitudinal US image of the MPV shows stenosis of an entire vascular graft (arrows) that was used to anastomose the vein. (b) Duplex US image of the poststenotic area shows a high flow velocity (1.1 m/sec).

With noninvasive imaging, portal vein stenosis must be diagnosed with caution. Hemodynamically significant portal vein stenosis must be distinguished from portal vein pseudostenosis, which results when the recipient portal vein is somewhat larger than the donor portal vein. The difference in caliber causes increased velocity and turbulence at the anastomosis that are not physiologically significant. If portal vein narrowing is associated with a less than three- to fourfold increase in velocity at spectral Doppler analysis, the narrowing likely represents pseudostenosis. Pseudostenosis is not associated with impaired graft function or clinical signs of portal hypertension (8,15).

Portography helps confirm the presence of the stenosis, and a pressure gradient may be obtained to determine the hemodynamic significance of the stenosis (15).

IVC Thrombosis
IVC thrombosis is a rare occurrence that was seen in less than 1% of our patients. It tends to occur at the superior and inferior caval anastomoses. Risk factors include technical problems during transplantation, use of intravascular catheters, and compression of vessels by a fluid collection. IVC obstruction can cause lower extremity edema (41,44).

Color Doppler US may reveal obvious vessel narrowing or an echogenic intraluminal thrombus with absence of flow (Fig 11). At MR angiography, IVC thrombosis is seen as an intraluminal defect. Coronal imaging is useful for determining the extent of IVC thrombosis (17,34).

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   Figure 11a.  (a) IVC thrombosis in a 6-year-old boy. Longitudinal color Doppler US image obtained through the hepatic vein confluence (arrow) shows absence of flow in the preanastomotic IVC. (b) IVC thrombosis in a different patient. Longitudinal color Doppler US image obtained through the retrohepatic vena cava shows an echogenic thrombus (arrows) filling the lumen of the IVC.

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   Figure 11b.  (a) IVC thrombosis in a 6-year-old boy. Longitudinal color Doppler US image obtained through the hepatic vein confluence (arrow) shows absence of flow in the preanastomotic IVC. (b) IVC thrombosis in a different patient. Longitudinal color Doppler US image obtained through the retrohepatic vena cava shows an echogenic thrombus (arrows) filling the lumen of the IVC.

Gray-scale US demonstrates reduction of the caliber of the IVC at the anastomosis (Fig 12) (7,18). At pulsed Doppler US, there is a three- to fourfold increase in velocity through the stenosis relative to that in the prestenotic segment (Fig 12), associated color Doppler aliasing, and absence of phasicity in the IVC. A significant suprahepatic caval stenosis may result in reversed flow or absence of phasicity in the hepatic veins (11). Nevertheless, monophasic waveforms are not specific for hepatic vein stenosis (17). A monophasic flat waveform with a relatively low average peak velocity in the hepatic vein (mean, 11 cm/sec) is a common finding. Sometimes, graft growth and twisting are causes of IVC pseudostenosis (12), which may increase or disappear depending on the patient’s posture. Hemodynamically significant IVC stenosis can be differentiated from pseudostenosis on the basis of the presence of features of Budd-Chiari syndrome and elevated Doppler velocity measurements.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 12a.  IVC stenosis in a 14-year-old boy. (a) Longitudinal US image shows focal narrowing of the IVC lumen. (b, c) Duplex Doppler US images show that the flow velocity in the poststenotic segment of the IVC (c) is nearly four times greater than that in the prestenotic segment (b).

View larger version (98K): [in this window] [in a new window] [Download PPT slide]   Figure 12b.  IVC stenosis in a 14-year-old boy. (a) Longitudinal US image shows focal narrowing of the IVC lumen. (b, c) Duplex Doppler US images show that the flow velocity in the poststenotic segment of the IVC (c) is nearly four times greater than that in the prestenotic segment (b).

View larger version (111K): [in this window] [in a new window] [Download PPT slide]   Figure 12c.  IVC stenosis in a 14-year-old boy. (a) Longitudinal US image shows focal narrowing of the IVC lumen. (b, c) Duplex Doppler US images show that the flow velocity in the poststenotic segment of the IVC (c) is nearly four times greater than that in the prestenotic segment (b).

View larger version (74K): [in this window] [in a new window] [Download PPT slide]   Figure 13a.  Budd-Chiari syndrome in a 9-year-old boy who had undergone whole liver transplantation. (a) Sagittal oblique duplex US image shows a monophasic wave pattern of the hepatic vein. (b) Duplex color Doppler US image shows biphasic hepatofugal flow in the portal vein.

View larger version (68K): [in this window] [in a new window] [Download PPT slide]   Figure 13b.  Budd-Chiari syndrome in a 9-year-old boy who had undergone whole liver transplantation. (a) Sagittal oblique duplex US image shows a monophasic wave pattern of the hepatic vein. (b) Duplex color Doppler US image shows biphasic hepatofugal flow in the portal vein.

View larger version (125K): [in this window] [in a new window] [Download PPT slide]   Figure 14a.  IVC stenosis in a 4-year-old patient with a left caval vein. (a) MR angiogram shows stenosis (arrow) in the superior IVC anastomosis. (b) Angiogram also demonstrates the stenosis (arrow), which was treated with endovascular balloon dilation.

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   Figure 14b.  IVC stenosis in a 4-year-old patient with a left caval vein. (a) MR angiogram shows stenosis (arrow) in the superior IVC anastomosis. (b) Angiogram also demonstrates the stenosis (arrow), which was treated with endovascular balloon dilation.

	Biliary Complications

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

Complications include anastomotic leakage and stenosis with bile duct dilatation; intrahepatic bile duct stones, sludge, or debris; and biloma. These complications are related to the surgical method of biliary reconstruction and to prolonged cold ischemia time, immunologic reactions, hepatic artery thrombosis, ABO blood group system incompatibility between donor and recipient, and cytomegalovirus infection (12). Nonanastomotic strictures are probably caused by hepatic arterial insufficiency from either stenosis or thrombosis. These ischemic arterial events may result in bile duct strictures or leaks, increasing the risk of cholangitis, sepsis, and abscess (7,8). The blood supply to the recipient CBD is rich because of collateral flow, whereas the vascularity of the donor duct and the proximal intrahepatic ducts is derived solely from the reconstructed hepatic artery. Biliary disease should be suspected in a post-transplantation patient who presents with elevated values on hepatic function tests, jaundice, fever, or abdominal pain (13,48).

Biliary Obstruction
Strictures can occur at both anastomotic and nonanastomotic sites. Most anastomotic strictures are secondary to scar tissue causing retraction and narrowing of the CBD at the suture site (6,41), although ischemia may also be a factor. Anastomotic strictures often require surgical or radiologic intervention. Nonanastomotic strictures are probably caused by bile duct ischemia due to arterial insufficiency. This ischemic phenomenon is responsible for infarction of the biliary epithelium, producing multiple focal areas of intrahepatic biliary duct strictures separated by dilatations (17). These strictures may occur anywhere in the biliary tree (48,49).

US typically shows dilated intrahepatic ducts with dilatation of the proximal CBD to the level of the anastomosis (Fig 15). In patients with an end-to-end anastomosis, the CBD distal to the anastomosis is of normal or near-normal size (3). However, US is not considered reliable for the early detection of these complications because biliary strictures or generalized ductal changes cannot be excluded on the basis of normal US findings (50,51). MR cholangiography can be used to delineate the anatomy and morphologic features of bile ducts and to screen for biliary strictures (Fig 15c) (49,52–54) and has made it possible to reduce the frequency with which diagnostic percutaneous transhepatic cholangiography is performed. Nevertheless, if a biliary stricture is suspected and US or MR imaging shows no dilatation, percutaneous transhepatic cholangiography should be performed, since many liver transplants do not develop bile duct dilatation even in high-grade stenosis. Percutaneous transhepatic cholangiography can also be performed for initial treatment, including balloon dilation, drainage, and stent placement; however, surgical reconstruction or retransplantation may be required (55–58).

View larger version (184K): [in this window] [in a new window] [Download PPT slide]   Figure 15a.  (a, b) Biliary dilatation in a 4-year-old girl with severe hepatic artery stenosis who had undergone reduced-size liver transplantation. (a) Transverse US image shows segmental dilatation of the biliary tree. (b) Duplex Doppler US image of the hepatic artery shows a tardus parvus waveform with low systolic and diastolic velocities, a low resistive index, and a prolonged acceleration time, findings that are consistent with stenosis. (c) Biliary dilatation in a different patient who had undergone whole liver transplantation. MR cholangiogram shows postsurgical biliary stenosis (arrow) with dilatation from the anastomosis with an intestinal loop. A stent was placed at the stenosis.

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 15b.  (a, b) Biliary dilatation in a 4-year-old girl with severe hepatic artery stenosis who had undergone reduced-size liver transplantation. (a) Transverse US image shows segmental dilatation of the biliary tree. (b) Duplex Doppler US image of the hepatic artery shows a tardus parvus waveform with low systolic and diastolic velocities, a low resistive index, and a prolonged acceleration time, findings that are consistent with stenosis. (c) Biliary dilatation in a different patient who had undergone whole liver transplantation. MR cholangiogram shows postsurgical biliary stenosis (arrow) with dilatation from the anastomosis with an intestinal loop. A stent was placed at the stenosis.

View larger version (157K): [in this window] [in a new window] [Download PPT slide]   Figure 15c.  (a, b) Biliary dilatation in a 4-year-old girl with severe hepatic artery stenosis who had undergone reduced-size liver transplantation. (a) Transverse US image shows segmental dilatation of the biliary tree. (b) Duplex Doppler US image of the hepatic artery shows a tardus parvus waveform with low systolic and diastolic velocities, a low resistive index, and a prolonged acceleration time, findings that are consistent with stenosis. (c) Biliary dilatation in a different patient who had undergone whole liver transplantation. MR cholangiogram shows postsurgical biliary stenosis (arrow) with dilatation from the anastomosis with an intestinal loop. A stent was placed at the stenosis.

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   Figure 16a.  Bile leaks. (a) US image obtained in an 8-year-old boy shows a large infrahepatic fluid collection (cursors), a finding that represents an extensive biloma. (b) US image obtained in a different patient shows a septated fluid collection (cursors) at the right iliac fossa.

View larger version (124K): [in this window] [in a new window] [Download PPT slide]   Figure 16b.  Bile leaks. (a) US image obtained in an 8-year-old boy shows a large infrahepatic fluid collection (cursors), a finding that represents an extensive biloma. (b) US image obtained in a different patient shows a septated fluid collection (cursors) at the right iliac fossa.

Bile Duct Stones
Although stones and sludge occur only infrequently after transplantation, they are associated with high morbidity. Several factors can lead to the formation of biliary stones and sludge. Cyclosporine can alter the bile composition, inducing crystal formation, which results in biliary sludge and stone formation (53). Other causes include retained stones within the graft or stones secondary to bile stasis from biliary strictures. Biliary stones are well depicted with US and MR imaging (51,54,55). Interventional procedures may be useful for obviating surgery in these patients (Fig 17) (56).

View larger version (148K): [in this window] [in a new window] [Download PPT slide]   Figure 17a.  (a) Biliary stones in a 15-year-old boy who had undergone liver transplantation 8 years earlier. Longitudinal US image obtained at the porta hepatis shows a distended CBD and two rounded echogenic calculi (arrows and cursors). (b) Biliary stones in a different patient. Cholangiogram shows multiple filling defects (arrows) within the biliary tree, findings that represent biliary stones.

View larger version (165K): [in this window] [in a new window] [Download PPT slide]   Figure 17b.  (a) Biliary stones in a 15-year-old boy who had undergone liver transplantation 8 years earlier. Longitudinal US image obtained at the porta hepatis shows a distended CBD and two rounded echogenic calculi (arrows and cursors). (b) Biliary stones in a different patient. Cholangiogram shows multiple filling defects (arrows) within the biliary tree, findings that represent biliary stones.

View larger version (105K): [in this window] [in a new window] [Download PPT slide]   Figure 18.  Mucocele in an asymptomatic 11-year-old patient who had undergone whole liver transplantation. Transverse color Doppler US image obtained at the porta hepatis shows a large, rounded fluid collection (arrow), a finding that corresponds to dilatation of the bile duct remnant.

	Abnormalities of the Liver Parenchyma

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

As previously noted, extrahepatic arterial supply (eg, via parabiliary arteries), which is present in native livers, is disrupted after transplantation. Therefore, when the transplanted hepatic artery blood supply is insufficient, bile duct necrosis develops, possibly leading to hepatic parenchymal infarction, bilomas, or abscesses.

At US, infarcts may manifest as round or geographic lesions, which are often solid and contain central hypoechoic areas that represent liquefaction and necrosis (Fig 19) (11). Hepatic infarction generally manifests at CT as irregular and wedge-shaped low-attenuation lesions located primarily in the periphery of the liver. The lesions are either unenhanced or heterogeneously enhanced on contrast-enhanced CT scans. Infarction may also manifest as irregularly shaped lesions that follow the course of the bile duct. The larger areas of infarction may liquefy, become infected, and (occasionally) calcify (28,36).

View larger version (128K): [in this window] [in a new window] [Download PPT slide]   Figure 19a.  (a) Hepatic infarct in a 22-month-old patient who had undergone liver transplantation 2 weeks earlier. Transverse US image of the liver shows focal areas of heterogeneous parenchyma (arrows and cursors). These lesions contain central hypoechoic areas that represent necrosis. (b) Hepatic bilomas following hepatic artery thrombosis in a 12-year-old boy who had undergone living related donor liver transplantation for biliary atresia 24 days earlier. US image shows irregular anechoic areas (arrows and cursors) in the transplanted liver.

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 19b.  (a) Hepatic infarct in a 22-month-old patient who had undergone liver transplantation 2 weeks earlier. Transverse US image of the liver shows focal areas of heterogeneous parenchyma (arrows and cursors). These lesions contain central hypoechoic areas that represent necrosis. (b) Hepatic bilomas following hepatic artery thrombosis in a 12-year-old boy who had undergone living related donor liver transplantation for biliary atresia 24 days earlier. US image shows irregular anechoic areas (arrows and cursors) in the transplanted liver.

Bilomas can also manifest as periportal cuffing, thereby mimicking periportal edema. Although these peculiar-appearing bilomas are often amorphous, they usually reflect severe and extensive bile duct necrosis and suggest a poor outcome for the graft. The patency of the hepatic artery should always be assessed with Doppler US, since complications resulting from vascular compromise require correction of the underlying problem (15,16,18).

	Organ Rejection

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Organ rejection develops in about 50% of patients, but improved immunosuppressive medications permit successful management of this problem in most cases (61).

The diagnosis of acute rejection, one of the most serious complications following liver transplantation, is established with graft biopsy and histologic study (9). The US appearances of acute rejection are nonspecific, and often the only identifiable abnormality is heterogeneity of the liver parenchyma, which may, however, have other causes (11,61–63). The role of imaging consists of excluding these other possible causes, which can manifest with clinical signs and symptoms similar to those of acute rejection (62).

	Localized Fluid Collections

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 
Fluid collections and hematomas are common in the areas of vascular and biliary anastomosis, as well as in the lesser sac, surrounding the ligamentum teres hepatis, and in peri- and subhepatic spaces (7). They rarely complicate the postoperative course and usually resolve spontaneously without complication. Localized fluid collections are commonly seen adjacent to the parenchymal resection site of the graft after reduced-size liver transplantation and include hematomas, bilomas, and abscesses (Figs 20, 21). These collections probably form because small vessels or radicles have coagulated incompletely. Differentiation between infected and uninfected fluid is difficult with imaging techniques. Localized low-attenuation fluid collections at the edge of the liver are extrahepatic bilomas in most cases. They usually regress in size without medical treatment but sometimes require percutaneous drainage (58,60). Attention should be paid to any increase in size or change in echogenicity of these collections, findings that may indicate bleeding or infection in the parenchymal resection site of the graft (Fig 21). Superinfection (when it occurs) can be treated with percutaneous drainage (58,60).

View larger version (113K): [in this window] [in a new window] [Download PPT slide]   Figure 20a.  Hematoma in the parenchymal resection site of the graft in a 2-year-old girl. (a) Transverse US image obtained 2 days after partial liver transplantation demonstrates a fluid collection (H). (b) Contrast-enhanced CT scan demonstrates a low-attenuation fluid collection (arrows). (c) US image obtained 10 days later shows regression of the hematoma (arrows). C = spine, R = kidney.

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   Figure 20b.  Hematoma in the parenchymal resection site of the graft in a 2-year-old girl. (a) Transverse US image obtained 2 days after partial liver transplantation demonstrates a fluid collection (H). (b) Contrast-enhanced CT scan demonstrates a low-attenuation fluid collection (arrows). (c) US image obtained 10 days later shows regression of the hematoma (arrows). C = spine, R = kidney.

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 20c.  Hematoma in the parenchymal resection site of the graft in a 2-year-old girl. (a) Transverse US image obtained 2 days after partial liver transplantation demonstrates a fluid collection (H). (b) Contrast-enhanced CT scan demonstrates a low-attenuation fluid collection (arrows). (c) US image obtained 10 days later shows regression of the hematoma (arrows). C = spine, R = kidney.

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   Figure 21a.  Abscess in the parenchymal resection site of the graft in a 4-year-old girl. (a) US image obtained 1 week after reduced-size liver transplantation shows a homogeneous fluid collection (cursors) that represents a hematoma. One month later, the patient developed a fever. (b) US image shows a heterogeneous, encapsulated fluid collection (arrowheads) containing gas (arrows). (c) CT scan obtained during percutaneous drainage helps confirm that the collection is an abscess. Arrow indicates the needle used for drainage.

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 21b.  Abscess in the parenchymal resection site of the graft in a 4-year-old girl. (a) US image obtained 1 week after reduced-size liver transplantation shows a homogeneous fluid collection (cursors) that represents a hematoma. One month later, the patient developed a fever. (b) US image shows a heterogeneous, encapsulated fluid collection (arrowheads) containing gas (arrows). (c) CT scan obtained during percutaneous drainage helps confirm that the collection is an abscess. Arrow indicates the needle used for drainage.

View larger version (168K): [in this window] [in a new window] [Download PPT slide]   Figure 21c.  Abscess in the parenchymal resection site of the graft in a 4-year-old girl. (a) US image obtained 1 week after reduced-size liver transplantation shows a homogeneous fluid collection (cursors) that represents a hematoma. One month later, the patient developed a fever. (b) US image shows a heterogeneous, encapsulated fluid collection (arrowheads) containing gas (arrows). (c) CT scan obtained during percutaneous drainage helps confirm that the collection is an abscess. Arrow indicates the needle used for drainage.

	Posttransplantation Lymphoproliferative Disorder

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The most common sites of involvement are lymph nodes and the gastrointestinal tract. Common features of PTLD include lymph node enlargement, a focal bowel mass with wall thickening, and necrosis or focal hepatic lesions that are hypoechoic at US and hypoattenuating at CT (Fig 22) (49,65–67). A mass in the porta hepatis is another common manifestation (66,68). The most common appearance in the chest is multiple pulmonary nodules with or without mediastinal adenopathy, but patchy air-space consolidation and pleural or pericardial effusions or thickening have also been reported (69–71). CT or MR imaging may demonstrate brain involvement. PTLD preferentially affects the periventricular white matter at one or more sites (15,64).

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 22a.  PTLD in a 12-year-old patient with Burkitt lymphoma who had undergone liver transplantation 4 years earlier. (a) US image shows solid hepatic nodules and enlarged retroperitoneal lymph nodes (arrows). A = aorta, VC = inferior vena cava. (b) US image shows concentric thickening of a bowel loop. Arrow indicates the bowel lumen. V = bladder. (c) Contrast-enhanced lung CT scan shows a solid nodule (arrow) in the left lung.

View larger version (119K): [in this window] [in a new window] [Download PPT slide]   Figure 22b.  PTLD in a 12-year-old patient with Burkitt lymphoma who had undergone liver transplantation 4 years earlier. (a) US image shows solid hepatic nodules and enlarged retroperitoneal lymph nodes (arrows). A = aorta, VC = inferior vena cava. (b) US image shows concentric thickening of a bowel loop. Arrow indicates the bowel lumen. V = bladder. (c) Contrast-enhanced lung CT scan shows a solid nodule (arrow) in the left lung.

View larger version (129K): [in this window] [in a new window] [Download PPT slide]   Figure 22c.  PTLD in a 12-year-old patient with Burkitt lymphoma who had undergone liver transplantation 4 years earlier. (a) US image shows solid hepatic nodules and enlarged retroperitoneal lymph nodes (arrows). A = aorta, VC = inferior vena cava. (b) US image shows concentric thickening of a bowel loop. Arrow indicates the bowel lumen. V = bladder. (c) Contrast-enhanced lung CT scan shows a solid nodule (arrow) in the left lung.

View larger version (131K): [in this window] [in a new window] [Download PPT slide]   Figure 23a.  (a) Non-Hodgkin lymphoma in a 9-year-old girl. Contrast-enhanced CT scan shows an intraperitoneal solid mass containing prominent enhanced vessels (arrow). Note also the enhancement of the small bowel wall (arrowheads). (b) Non-Hodgkin lymphoma in a different patient who had undergone liver transplantation 7 years earlier. Contrast-enhanced CT scan shows a solid mass in the right hepatic lobe.

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 23b.  (a) Non-Hodgkin lymphoma in a 9-year-old girl. Contrast-enhanced CT scan shows an intraperitoneal solid mass containing prominent enhanced vessels (arrow). Note also the enhancement of the small bowel wall (arrowheads). (b) Non-Hodgkin lymphoma in a different patient who had undergone liver transplantation 7 years earlier. Contrast-enhanced CT scan shows a solid mass in the right hepatic lobe.

	Summary

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

Current MR imaging techniques, including MR angiography and MR cholangiography, may provide a comprehensive evaluation of the transplanted liver; reveal abnormalities of vascular structures, bile ducts, and liver parenchyma; and depict extrahepatic tissues. If available, MR imaging should be used when US is inconclusive. CT is a valuable complement to US in the evaluation of complications involving the hepatic parenchyma as well as extrahepatic sites, especially the thorax. CT is commonly used to guide percutaneous aspiration and fluid collection drainage. A number of complications can be corrected by using interventional radiologic techniques.

	Footnotes

 

Abbreviations: CBD = common bile duct, IVC = inferior vena cava, MPV = main portal vein, PTLD = posttransplantation lymphoproliferative disorder

	References

Top Abstract LEARNING OBJECTIVES Introduction Clinical Experience Vascular Complications Biliary Complications Abnormalities of the Liver... Organ Rejection Localized Fluid Collections Posttransplantation... Summary References

 

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