DOI: 10.1148/rg.235035031
(Radiographics. 2003;23:1093-1114.)
© RSNA, 2003
US of Liver Transplants: Normal and Abnormal1
Jane D. Crossin, MD,
Derek Muradali, MD and
Stephanie R. Wilson, MD
1 From the Department of Diagnostic Imaging, Toronto General Hospital, University of Toronto, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4. Recipient of a Magna Cum Laude award for an education exhibit at the 2000 RSNA scientific assembly. Received February 10, 2003; revision requested March 17 and received May 28; accepted May 30. Address correspondence to S.R.W. (e-mail: stephanie.wilson@uhn.on.ca).
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Abstract
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Whole-liver transplantation is an accepted and successful method of treating end-stage liver disease. As a result of the shortage of cadaveric livers, split-liver transplantation and living donor liver transplantation are becoming more commonplace. Ultrasonography (US) is the initial imaging modality of choice for detection and follow-up of early and delayed complications from all types of liver transplantation. Vascular complications include thrombosis and stenosis of the hepatic artery, portal vein, or inferior vena cava, as well as hepatic artery pseudoaneurysms and celiac artery stenosis. Biliary complications include leaks, strictures, stones or sludge, dysfunction of the sphincter of Oddi, and recurrent disease. Neoplastic disease in the transplanted liver may represent recurrent neoplasia or posttransplantation lymphoproliferative disorder. Parenchymal disease may take the form of a focal mass or a diffuse parenchymal abnormality. Perihepatic fluid collections and ascites are common after liver transplantation. Knowledge of the surgical technique of liver transplantation and awareness of the normal US appearance of the transplanted liver permit early detection of complications and prevent misdiagnosis.
© RSNA, 2003
Index Terms: Aneurysm, hepatic, 952.73 • Bile ducts, stenosis or obstruction, 76.1267, 76.458 • Hepatic arteries, stenosis or obstruction, 952.458 Hepatic arteries, thrombosis, 952.458 • Liver, transplantation, 76.458
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LEARNING OBJECTIVES FOR TEST 3
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After reading this article and taking the test, the reader will be able to:
- Discuss the indications for, contraindications to, and various surgical techniques of liver transplantation.
- Identify the normal appearances of the transplanted liver at gray-scale and Doppler US.
- Describe the range of complications seen after liver transplantation and their US appearances.
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Introduction
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Human whole-liver transplantation as a therapeutic option for end-stage liver disease was pioneered in 1963 by Starzl and colleagues (1). Although initial efforts were unsuccessful, today, following years of modification of surgical techniques and the introduction of new immunosuppressive agents, liver transplantation is an accepted and successful therapy for end-stage liver failure. In the United States in 2001, a total of 5,184 liver transplantations were performed. The 1-year patient survival rate for whole-liver transplantation was 87%, and the rate of 1-year graft survival was 80.3% (2).
The United Network for Organ Sharing estimates that at the beginning of 2003, 17,201 patients were waiting for liver transplants in the United States (2). Unfortunately, over the recent years, cadaveric liver donor rates have not increased significantly. As a consequence, innovative surgical techniques have been used to increase the number of patients receiving transplants from the available limited resources. These include the techniques of living donor liver transplantation (from both related and unrelated donors) and split-liver transplantation. Medical research in hepatocyte transplantation, xenotransplantation (engraftment of organs obtained from one species into another species), and liver-directed gene therapy continues, but as yet, these techniques have no clinical indication (3).
The success of living donor transplantation is based on two major concepts: the distinct segmental anatomy of the liver and its remarkable regenerative potential. Right lobes (segments 5–8) are most commonly implanted, with extended right lobes or trisegments (segments 4–8) required for larger recipients to ensure adequate hepatic volume. In the average-sized adult, left lobe grafts (segments 2–4) do not provide sufficient liver volume to sustain life (4,5). Living donor liver transplantation permits immediate transplantation of the donated portion of the liver, minimizing the ischemic injury. Regeneration of the liver occurs rapidly. The transplant may double in size in as little as 3 weeks (6). Recent studies report a favorable outcome of living related donor liver transplantation, with 1-year patient and graft survival rates of 90% and 88%, respectively (7).
Split-liver transplantation, in which two patients undergo transplantation with one donor liver, was initially not favored as a viable transplantation method due to associated increased mortality rates secondary to bleeding and biliary complications (8). More recently, however, the recommended surgical procedure of in vivo splitting of the liver (ie, liver splitting completed in the heart-beating cadaveric donor) rather than ex vivo splitting has led to procedural survival rates comparable with those of whole-organ transplantation (9).
In this article, we present the indications and contraindications for liver transplantation, the surgical technique, the normal ultrasonographic (US) appearance of liver transplants, and the US appearances of posttransplantation complications.
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Indications and Contraindications for Transplantation
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Health care budget limitations and the shortage of available cadaveric donors have resulted in specific indications and contraindications for liver transplantation.
Liver transplantation is performed for a variety of irreversible acute and chronic liver diseases for which no other satisfactory therapy is available. Patients are selected for transplantation when their life expectancy without transplantation is less than the life expectancy following the procedure. Hepatitis C is the most common disease requiring transplantation, followed by alcoholic liver disease and cryptogenic cirrhosis (10). Other end-stage liver disorders treated with transplantation include chronic cholestatic diseases such as primary biliary cirrhosis and primary sclerosing cholangitis; metabolic diseases including hemochromatosis and Wilson disease; other hepatitides such as autoimmune hepatitis and chronic hepatitis B; and acute liver failure. Patients with end-stage hepatitis B cirrhosis were initially regarded as poor transplantation candidates due to the high recurrence rate of hepatitis B in the implant associated with rapid progression to cirrhosis. The use of hyperimmune globulin and the nucleoside analogue lamivudine has changed these expectations to a more favorable outcome.
The percentage of liver transplantations performed for known malignancy is diminishing (10). Most centers now consider transplantation only in patients with early-stage hepatocellular carcinoma or rarely neuroendocrine metastases. The generally accepted guidelines for transplantation in patients with hepatocellular carcinoma are the Milan criteria of no single lesion greater than 5 cm in diameter or three or fewer lesions each less than or equal to 3 cm in diameter (11).
Accepted contraindications include extrahepatic malignancy, active untreated sepsis, advanced cardiopulmonary disease, active alcoholism or substance abuse, or an anatomic abnormality precluding the surgical procedure (10). Although portal vein thrombosis is not an absolute contraindication to liver transplantation, its presence makes the surgery more complex. These patients have higher morbidity and mortality rates, particularly if the thrombus extends into the splanchnic veins (12). Advanced age is also associated with higher mortality rates (13,14). Primary bile duct tumors and most secondary hepatic tumors treated with transplantation have an unfavorable outcome.
Cholangiocarcinoma has a very high risk of recurrence following surgery and has usually been considered an absolute contraindication to liver transplantation (15). Recent research, however, suggests that in selected early cases, transplantation is of benefit (16,17).
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Surgical Technique
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Knowledge of the variety of surgical techniques performed in whole-liver transplantation allows a thorough US study to be performed. Whole-liver transplantation involves one biliary and four vascular anastomoses:
The biliary anastomosis is an end-to-end anastomosis from the donor common bile duct to the recipient common hepatic duct (choledochocholedochostomy). This is the preferred anastomotic technique as it avoids intestinal surgery, preserves the sphincter of Oddi, and reduces the risk of enteric reflux into the biliary tree. If the recipient common hepatic duct is diseased, absent, too short, or too small, then a choledochojejunostomy is fashioned. However, with this technique there is an increased risk of infection from bacterial overgrowth and anastomotic breakdown and bleeding (18). The temporary placement of T tubes across the anastomosis in the early postoperative period has been abandoned in many centers, as following removal there was an associated increase in morbidity secondary to bile leaking from the previous entry site of the tube (19). A cholecystectomy is performed routinely on all implants.
The hepatic artery anastomosis is a fish-mouth anastomosis between the donor common hepatic–splenic artery branch point or the celiac axis with an aortic Carrel patch and the recipient right and left hepatic artery bifurcation or the gastroduodenal–proper hepatic artery bifurcation. If the native liver has a dual blood supply, then the larger of the two vessels is used to supply the arterial inflow to the implant. If the native hepatic artery or celiac axis has a high-grade stenosis, then an aortohepatic interposition graft (usually the donor iliac artery) may be required.
The portal vein anastomosis is an end-to-end anastomosis. If the donor portal vein is thrombosed, it may be necessary to use a venous jump graft from the superior mesenteric vein or splenic vein.
The supra- and infrahepatic caval anastomoses are usually end-to-end anastomoses but on occasion may be end-to-side or side-to-side anastomoses.
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Normal US Appearance of Liver Transplants
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US is the primary imaging modality in the detection and follow-up of early and delayed complications of liver transplantation. Awareness of the normal US appearance of the transplanted liver permits detection of complications and prevents misdiagnoses.
A routine postoperative US study entails gray-scale assessment of the liver parenchyma and biliary tree and Doppler evaluation of the vasculature. The normal liver transplant has a homogeneous or slightly heterogeneous pattern at gray-scale imaging (Fig 1). The intrahepatic biliary tree should be of normal appearance. If a biliary T tube is in situ, the extrahepatic biliary ducts may appear thick walled; otherwise, the ducts should be of normal caliber and appearance. In the early postoperative period, there is usually a small amount of free intraabdominal fluid in the perihepatic space, which commonly resolves in 7–10 days.
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Figure 1a. Normal gray-scale US appearance. (a) Subcostal oblique US image obtained through the hepatic confluence shows the middle and left hepatic veins. The hepatic parenchyma appears homogeneous. (b) Right paramedian sagittal US image obtained through the liver and inferior vena cava (IVC) shows the staples (arrows) of the end-to-end IVC anastomosis, the middle hepatic vein, and normal hepatic parenchyma. (c, d) Intercostal gray-scale US (c) and color Doppler (d) images obtained through the anterior axillary line show the porta hepatis along the long axis. On the gray-scale image (c), the portal vein is easily identified. Often, the hepatic artery (arrows) is identified only with color Doppler imaging.
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Figure 1b. Normal gray-scale US appearance. (a) Subcostal oblique US image obtained through the hepatic confluence shows the middle and left hepatic veins. The hepatic parenchyma appears homogeneous. (b) Right paramedian sagittal US image obtained through the liver and inferior vena cava (IVC) shows the staples (arrows) of the end-to-end IVC anastomosis, the middle hepatic vein, and normal hepatic parenchyma. (c, d) Intercostal gray-scale US (c) and color Doppler (d) images obtained through the anterior axillary line show the porta hepatis along the long axis. On the gray-scale image (c), the portal vein is easily identified. Often, the hepatic artery (arrows) is identified only with color Doppler imaging.
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Figure 1c. Normal gray-scale US appearance. (a) Subcostal oblique US image obtained through the hepatic confluence shows the middle and left hepatic veins. The hepatic parenchyma appears homogeneous. (b) Right paramedian sagittal US image obtained through the liver and inferior vena cava (IVC) shows the staples (arrows) of the end-to-end IVC anastomosis, the middle hepatic vein, and normal hepatic parenchyma. (c, d) Intercostal gray-scale US (c) and color Doppler (d) images obtained through the anterior axillary line show the porta hepatis along the long axis. On the gray-scale image (c), the portal vein is easily identified. Often, the hepatic artery (arrows) is identified only with color Doppler imaging.
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Figure 1d. Normal gray-scale US appearance. (a) Subcostal oblique US image obtained through the hepatic confluence shows the middle and left hepatic veins. The hepatic parenchyma appears homogeneous. (b) Right paramedian sagittal US image obtained through the liver and inferior vena cava (IVC) shows the staples (arrows) of the end-to-end IVC anastomosis, the middle hepatic vein, and normal hepatic parenchyma. (c, d) Intercostal gray-scale US (c) and color Doppler (d) images obtained through the anterior axillary line show the porta hepatis along the long axis. On the gray-scale image (c), the portal vein is easily identified. Often, the hepatic artery (arrows) is identified only with color Doppler imaging.
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Assessment of the transplant vasculature involves both gray-scale and Doppler examination. Strictures or thrombi in the portal vein or IVC are often identified first at gray-scale imaging and then confirmed with Doppler studies. Subtle arterial complications may be demonstrable only at Doppler examination. The normal hepatic artery Doppler waveform shows a rapid systolic upstroke with continuous diastolic flow. The acceleration time, which represents the time from end diastole to the first systolic peak, should be less than 80 msec, and the resistive index, which represents the ratio of (peak systolic velocity - peak diastolic velocity)/peak systolic velocity, should be between 0.5 and 0.7. The normal portal vein Doppler waveform is a continuous flow pattern toward the liver with mild velocity variations induced by respiration. The normal Doppler appearance of the hepatic veins and IVC shows a phasic flow pattern, reflecting the physiologic changes in the blood flow during the cardiac cycle (Fig 2).
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Figure 2a. Normal Doppler US appearance. (a) Subcostal oblique color and spectral Doppler image of the right hepatic vein shows normal venous phasicity due to respiration. (b) Intercostal color and spectral Doppler image of the main portal vein shows a normal continuous waveform with mild velocity variations due to respiration. (c) Intercostal color and spectral Doppler image of a normal hepatic artery at the porta hepatis shows a rapid systolic upstroke with continuous low-velocity diastolic flow.
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Figure 2b. Normal Doppler US appearance. (a) Subcostal oblique color and spectral Doppler image of the right hepatic vein shows normal venous phasicity due to respiration. (b) Intercostal color and spectral Doppler image of the main portal vein shows a normal continuous waveform with mild velocity variations due to respiration. (c) Intercostal color and spectral Doppler image of a normal hepatic artery at the porta hepatis shows a rapid systolic upstroke with continuous low-velocity diastolic flow.
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Figure 2c. Normal Doppler US appearance. (a) Subcostal oblique color and spectral Doppler image of the right hepatic vein shows normal venous phasicity due to respiration. (b) Intercostal color and spectral Doppler image of the main portal vein shows a normal continuous waveform with mild velocity variations due to respiration. (c) Intercostal color and spectral Doppler image of a normal hepatic artery at the porta hepatis shows a rapid systolic upstroke with continuous low-velocity diastolic flow.
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US Appearances of Posttransplantation Complications
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Gray-scale and Doppler US evaluation of the posttransplantation liver is the ideal initial imaging modality to detect postoperative complications as it is accessible, accurate, and acceptable to both the patient and physician. It is cost-effective, avoids the use of ionizing radiation, and can be performed at the patient’s bedside. If performed by skilled operators, the results are highly reproducible. US is the primary imaging modality used to assess for postoperative complications at our institution. If a complication is demonstrated that does not require intervention, it is usually followed up with serial US studies. Computed tomography (CT) or magnetic resonance (MR) imaging is performed if the initial US study is technically unsatisfactory or following US demonstration of an abnormality that requires further evaluation. Demonstration of abnormal hepatic artery waveforms suggestive of a more proximal abnormality is confirmed with CT angiography in all cases.
Complications after liver transplantation may involve the vasculature, biliary ducts, liver parenchyma, and perihepatic space.
Vascular Complications
Vascular complications usually occur in the early postoperative period. US is the primary screening modality used for their detection. Prompt diagnosis is critical to allow graft salvage. Angiography is performed to confirm abnormalities demonstrated at US or in patients in whom the US study is suboptimal.
Hepatic Artery Complications.—
Hepatic artery complications include thrombosis, stenosis, and pseudoaneurysms.
Hepatic artery thrombosis occurs in up to 8% of transplants (20) and accounts for 60% of all posttransplantation vascular complications (21–25). Hepatic artery thrombosis is associated with a significant mortality of 20%–60% and is the second leading cause of graft failure in the early postoperative period (26). Early hepatic artery thrombosis occurs within 15 days of transplantation. Associated risk factors include increased cold ischemic time of the donor liver, ABO blood type incompatibility, small donor or recipient vessels, and acute rejection. Delayed hepatic artery thrombosis, which may occur years after transplantation, is associated with chronic rejection and sepsis. The hepatic artery is the sole arterial supply of the transplanted liver. The portal vein supplies most of the blood to the hepatocytes. The bile ducts in a liver transplant, unlike in a native liver, are dependent purely on the arterial blood from the hepatic artery. As a result, the clinical presentation of hepatic artery thrombosis ranges from fulminant hepatic failure and delayed biliary leak to relapsing bacteremia. Treatment consists of urgent revascularization of the graft. This may be attempted with thrombectomy with or without arterial revascularization; however, up to 60% of patients ultimately require retransplantation (21).
US allows correct identification of up to 92% of cases of hepatic artery thrombosis (Fig 3) (27). At Doppler examination, there is usually complete absence of both proper hepatic and intrahepatic arterial flow. Nolten and Sproat (28) described "a syndrome of impending thrombosis" occurring over a 3–10-day span in the acute posttransplantation period. They described the initial Doppler waveform of the hepatic artery to be normal, with follow-up Doppler scans progressively showing no diastolic flow followed by dampening of the systolic peak and finally total loss of the hepatic waveform. After hepatic artery thrombosis, arterial collateral vessels can develop and intrahepatic flow may be identified (29). Nevertheless, the intrahepatic arterial waveform will be abnormal, displaying a tardus-parvus pattern with an acceleration time greater than 80 msec and a resistive index less than 0.5 (30).
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Figure 3a. Hepatic artery thrombosis in a 45-year-old man with worsening results on liver function tests 8 days after orthotopic liver transplantation for alcoholic cirrhosis. (a) Subcostal oblique color Doppler image of the right hepatic lobe shows avascular cystic spaces within the hepatic parenchyma, which represent infarcts. Flow is demonstrated in the adjacent hepatic veins. No hepatic artery flow was seen at the porta hepatis or anywhere in the liver on color or spectral Doppler images. (b) Corresponding contrast material-enhanced CT image shows the infarcts.
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Figure 3b. Hepatic artery thrombosis in a 45-year-old man with worsening results on liver function tests 8 days after orthotopic liver transplantation for alcoholic cirrhosis. (a) Subcostal oblique color Doppler image of the right hepatic lobe shows avascular cystic spaces within the hepatic parenchyma, which represent infarcts. Flow is demonstrated in the adjacent hepatic veins. No hepatic artery flow was seen at the porta hepatis or anywhere in the liver on color or spectral Doppler images. (b) Corresponding contrast material-enhanced CT image shows the infarcts.
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However, use of these indexes as sole diagnostic parameters for hepatic artery thrombosis may result in false-positive cases. In the setting of markedly diminished hepatic artery flow, such as in severe hepatic edema, systemic hypotension, or high-grade hepatic artery stenosis, or in a suboptimal US study, perhaps limited by patient obesity or gross ascites, interpretation of intrahepatic tardus-parvus waveforms should be performed with caution (28). If an intrahepatic tardus-parvus waveform is demonstrated, careful gray-scale and Doppler examination of the main hepatic artery is warranted. Dodd et al (30,31) found a sensitivity of 97% for significant hepatic artery complications (including thrombosis and stenosis) if one or more of the following Doppler criteria were demonstrated: resistive index less than 0.5, acceleration time greater than 0.08 seconds, no flow in the main hepatic artery, or a peak hepatic artery velocity greater than 2 m/sec.
Hepatic artery stenosis is estimated to occur in up to 11% of transplant recipients and occurs most frequently at the anastomotic site (21). Causes include clamp injury, intimal trauma caused by perfusion catheters at the time of surgery, or disrupted vasa vasorum leading to ischemia of the arterial ends. Clinically, it may lead to biliary ischemia, causing hepatic dysfunction and eventual hepatic failure. Treatment includes balloon angioplasty or retransplantation (32).
Spectral analysis at the site of narrowing reveals a focal accelerated velocity greater than 2–3 m/sec with associated turbulence distal to the stenosis (Fig 4) (30). Intrahepatic arterial waveforms may display a tardus-parvus pattern with a prolonged acceleration time and decreased resistive index, identical to the waveform that may be seen in hepatic artery thrombosis with collateralization. If a tardus-parvus intrahepatic waveform pattern is identified, it is more likely to be secondary to hepatic artery stenosis than thrombosis. Mild degrees of hepatic artery narrowing may be present without Doppler abnormalities. Therefore, if the clinical suspicion is high, normal Doppler results should not prevent follow-up with angiography, although in such cases the hepatic artery stenosis, if detected, will tend to be of a mild degree (33).
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Figure 4a. Hepatic artery stenosis. (a) Color and spectral Doppler image of the main hepatic artery obtained at the anastomosis shows a focal stricture with aliasing in the middle portion of the main hepatic artery (arrow). The Doppler spectrum shows an elevated peak velocity (220 cm/sec) and spectral broadening, findings consistent with turbulence. (b) Superselective digital subtraction angiogram of the main hepatic artery shows the stenosis (arrow). (c) Color and spectral Doppler image of the left intrahepatic artery shows a tardus-parvus waveform with a prolonged acceleration time and decreased resistive index.
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Figure 4b. Hepatic artery stenosis. (a) Color and spectral Doppler image of the main hepatic artery obtained at the anastomosis shows a focal stricture with aliasing in the middle portion of the main hepatic artery (arrow). The Doppler spectrum shows an elevated peak velocity (220 cm/sec) and spectral broadening, findings consistent with turbulence. (b) Superselective digital subtraction angiogram of the main hepatic artery shows the stenosis (arrow). (c) Color and spectral Doppler image of the left intrahepatic artery shows a tardus-parvus waveform with a prolonged acceleration time and decreased resistive index.
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Figure 4c. Hepatic artery stenosis. (a) Color and spectral Doppler image of the main hepatic artery obtained at the anastomosis shows a focal stricture with aliasing in the middle portion of the main hepatic artery (arrow). The Doppler spectrum shows an elevated peak velocity (220 cm/sec) and spectral broadening, findings consistent with turbulence. (b) Superselective digital subtraction angiogram of the main hepatic artery shows the stenosis (arrow). (c) Color and spectral Doppler image of the left intrahepatic artery shows a tardus-parvus waveform with a prolonged acceleration time and decreased resistive index.
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Celiac artery stenosis may be due to atheromatous disease or, in the younger patient, impingement by the diaphragmatic crura or median arcuate ligament. The latter cause may be corrected surgically at the time of transplantation by dividing the muscular and fibrous bands of the diaphragm, allowing restoration of normal flow to the liver. If a celiac artery stenosis caused by atheromatous disease is severe, an aortohepatic interposition graft anastomosed to the recipient supraceliac or infrarenal aorta may be required to ensure adequate arterial supply to the implant.
Hepatic artery pseudoaneurysms are most often mycotic and occur at the vascular anastomotic site. Occasionally, they may be intrahepatic or peripheral in location secondary to focal parenchymal infection or following percutaneous interventions. The clinical presentation is often late, with hepatic failure or acute shock if the pseudoaneurysm ruptures. Fistula formation between the aneurysm and biliary tree or portal vein can occur. Surgical correction is usually required, but there have been reported cases treated successfully with stent placement (34,35).
US reveals a periportal or intrahepatic cystic structure usually in juxtaposition to the course of the hepatic artery (Fig 5). Our experience suggests that all newly diagnosed cystic masses in or around the liver transplant should undergo both color and spectral Doppler analysis to avoid mistaking a pseudoaneurysm for a benign collection. Doppler examination demonstrates a disorganized arterial flow pattern. Intrahepatic arterial tardus-parvus waveforms may be present. Within a large pseudoaneurysm, the predominant flow pattern may be monophasic due to the slow turbulent flow within the cavity. These appearances should not be mistaken for a venous varix (36).
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Figure 5a. Hepatic artery pseudoaneurysm in a 58-year-old woman with worsening results on liver function tests 23 days after orthotopic liver transplantation. (a) Gray-scale US image obtained through the porta hepatis shows a focal cystic structure (arrow) alongside the hepatic artery. (b) Color Doppler image shows that the cystic structure (arrow) is vascular, an appearance consistent with a pseudoaneurysm. (c) Color and spectral Doppler image of the right intrahepatic artery shows a tardus-parvus waveform. (d) Corresponding contrast-enhanced CT image shows the pseudoaneurysm (arrow).
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Figure 5b. Hepatic artery pseudoaneurysm in a 58-year-old woman with worsening results on liver function tests 23 days after orthotopic liver transplantation. (a) Gray-scale US image obtained through the porta hepatis shows a focal cystic structure (arrow) alongside the hepatic artery. (b) Color Doppler image shows that the cystic structure (arrow) is vascular, an appearance consistent with a pseudoaneurysm. (c) Color and spectral Doppler image of the right intrahepatic artery shows a tardus-parvus waveform. (d) Corresponding contrast-enhanced CT image shows the pseudoaneurysm (arrow).
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Figure 5c. Hepatic artery pseudoaneurysm in a 58-year-old woman with worsening results on liver function tests 23 days after orthotopic liver transplantation. (a) Gray-scale US image obtained through the porta hepatis shows a focal cystic structure (arrow) alongside the hepatic artery. (b) Color Doppler image shows that the cystic structure (arrow) is vascular, an appearance consistent with a pseudoaneurysm. (c) Color and spectral Doppler image of the right intrahepatic artery shows a tardus-parvus waveform. (d) Corresponding contrast-enhanced CT image shows the pseudoaneurysm (arrow).
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Figure 5d. Hepatic artery pseudoaneurysm in a 58-year-old woman with worsening results on liver function tests 23 days after orthotopic liver transplantation. (a) Gray-scale US image obtained through the porta hepatis shows a focal cystic structure (arrow) alongside the hepatic artery. (b) Color Doppler image shows that the cystic structure (arrow) is vascular, an appearance consistent with a pseudoaneurysm. (c) Color and spectral Doppler image of the right intrahepatic artery shows a tardus-parvus waveform. (d) Corresponding contrast-enhanced CT image shows the pseudoaneurysm (arrow).
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Portal Vein Complications.—
Portal vein complications include thrombosis and stenosis.
Portal vein thrombosis and stenosis occur in 1%–2% of transplant recipients (21,22,24). Contributing causes include faulty surgical technique, misalignment or excessive vessel length, hypercoagulable states, or previous portal vein surgery. The clinical presentation includes portal hypertension, hepatic failure, edema, and massive ascites. Treatment options range from balloon angioplasty, thrombolysis, or stent placement to surgical correction with thrombectomy, placement of a venous jump graft, or creation of a portosystemic shunt (37–41).
US of portal vein thrombosis shows vessel narrowing or an echogenic luminal thrombus with no Doppler flow (Fig 6). Occasionally, an acute thrombus is anechoic. In these cases, gray-scale images of the vessel appear normal and the abnormality is evident only at color flow and spectral Doppler analysis. This emphasizes the necessity for careful assessment of the portal vein throughout its entire length with both gray-scale and spectral US. In portal vein stenosis, there is focal color aliasing with more than a three- to fourfold increase in velocity at the stenosis relative to that at the prestenotic segment (Fig 7) (42).
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Figure 6a. Portal vein thrombosis. (a) Subcostal oblique US image shows the bifurcation of the portal vein into right and left branches. Echogenic material is seen in the vessel lumen (arrows). An acute thrombus may be anechoic and identified only at color flow imaging as a flow defect. (b) Subcostal right paramedian US image shows the long axis of the main portal vein (MPV) with a distal thrombus (T).
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Figure 6b. Portal vein thrombosis. (a) Subcostal oblique US image shows the bifurcation of the portal vein into right and left branches. Echogenic material is seen in the vessel lumen (arrows). An acute thrombus may be anechoic and identified only at color flow imaging as a flow defect. (b) Subcostal right paramedian US image shows the long axis of the main portal vein (MPV) with a distal thrombus (T).
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Figure 7. Portal vein stenosis. Gray-scale US (top left), color Doppler (top right), and spectral Doppler (bottom) images of the long axis of the main portal vein show focal color aliasing (second arrow) at the vascular anastomosis. The waveforms show a greater than sixfold velocity in the poststenotic segment (first arrow) relative to the velocity in the prestenotic segment (third arrow), a finding consistent with a significant stenosis.
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IVC Complications.—
IVC complications include thrombosis and stenosis.
IVC thrombosis and stenosis are relatively rare, diagnosed in less than 1% of transplant cases (21). They are more common in cases of retransplantation and in the pediatric population. IVC stenosis occurs acutely secondary to an anastomotic size discrepancy or suprahepatic caval kinking from organ rotation. Delayed caval stenosis may occur secondary to fibrosis, a chronic thrombus, or neointimal hyperplasia. Correlation of the US findings, such as hepatomegaly, ascites, or pleural effusions, with clinical symptoms is required to determine the severity of the stenosis. Treatment includes balloon angioplasty and stent placement (43).
US of IVC thrombosis may reveal obvious vessel narrowing or an intraluminal echogenic thrombus with no Doppler signal (Fig 8). In IVC stenosis, there is a three- to fourfold increase in velocity through the stenosis as compared with that at the prestenotic segment (Fig 9). A significant suprahepatic caval stenosis may result in reversed flow or absence of phasicity in the hepatic veins (42).
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Figure 8a. IVC thrombosis. (a) Subcostal oblique US image obtained through the hepatic confluence shows an echogenic thrombus (arrows) that fills the lumen of the right hepatic vein and extends into the IVC. (b) Right paramedian sagittal US image shows the IVC thrombus (arrows).
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Figure 8b. IVC thrombosis. (a) Subcostal oblique US image obtained through the hepatic confluence shows an echogenic thrombus (arrows) that fills the lumen of the right hepatic vein and extends into the IVC. (b) Right paramedian sagittal US image shows the IVC thrombus (arrows).
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Figure 9a. IVC stenosis. (a, b) Right paramedian sagittal gray-scale US (a) and color Doppler (b) images show focal narrowing of the IVC lumen with associated flow turbulence secondary to a stricture at the distal IVC anastomosis (arrows). (c) Spectral Doppler image shows a twofold increase in velocity between the prestenotic (right arrow) and poststenotic (left arrow) IVC segments with turbulent flow in the poststenotic segment. A satisfactory waveform could not be obtained at the stenosis due to artifact from the surgical sutures. Although the stenosis was significant at gray-scale and Doppler US, the patient was asymptomatic and the referring clinicians decided to monitor the stenosis with US follow-up.
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Figure 9b. IVC stenosis. (a, b) Right paramedian sagittal gray-scale US (a) and color Doppler (b) images show focal narrowing of the IVC lumen with associated flow turbulence secondary to a stricture at the distal IVC anastomosis (arrows). (c) Spectral Doppler image shows a twofold increase in velocity between the prestenotic (right arrow) and poststenotic (left arrow) IVC segments with turbulent flow in the poststenotic segment. A satisfactory waveform could not be obtained at the stenosis due to artifact from the surgical sutures. Although the stenosis was significant at gray-scale and Doppler US, the patient was asymptomatic and the referring clinicians decided to monitor the stenosis with US follow-up.
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Figure 9c. IVC stenosis. (a, b) Right paramedian sagittal gray-scale US (a) and color Doppler (b) images show focal narrowing of the IVC lumen with associated flow turbulence secondary to a stricture at the distal IVC anastomosis (arrows). (c) Spectral Doppler image shows a twofold increase in velocity between the prestenotic (right arrow) and poststenotic (left arrow) IVC segments with turbulent flow in the poststenotic segment. A satisfactory waveform could not be obtained at the stenosis due to artifact from the surgical sutures. Although the stenosis was significant at gray-scale and Doppler US, the patient was asymptomatic and the referring clinicians decided to monitor the stenosis with US follow-up.
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Biliary Complications
Biliary complications are seen in up to 25% of transplants (44). Eighty percent occur within the first 6 months after transplantation, and the vast majority of these occur within the first 3 months (45). Complications include leaks, strictures, stones or sludge, dysfunction of the sphincter of Oddi, and recurrent disease.
Leaks at the end-to-end biliary anastomosis, although rare, are associated with significant morbidity and occasional mortality (18). If a T tube has been inserted, the leak most often occurs at the site of T-tube entry into the duct. Nonanastomotic leaks, remote from the T-tube entry point, are associated with hepatic artery thrombosis in 89% of cases (42). The bile extravasates freely into the peritoneal cavity or forms a perihepatic fluid collection. The clinical presentation is variable, ranging from mild abdominal symptoms to septicemic shock. Treatment includes biliary stent placement and drainage of collections. Most bile leaks are sterile. Cholangiography is the standard test.
Strictures can occur at anastomotic and nonanastomotic sites. Anastomotic strictures are secondary to scar tissue causing retraction and narrowing of the common bile duct at the suture site. They often require surgical or radiologic intervention. US typically shows dilated intrahepatic ducts with dilatation of the proximal common bile duct to the level of the anastomosis (Fig 10). The common bile duct distal to the anastomosis is of normal or near-normal size.
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Figure 10a. Anastomotic stricture of the bile duct. (a) Right paramedian sagittal US image shows focal narrowing of the middle portion of the common bile duct (arrow) at the surgical anastomosis. (b) Corresponding image from endoscopic retrograde cholangiopancreatography shows the narrowing (arrow). (c) Color and spectral Doppler image of the main hepatic artery shows a normal waveform.
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Figure 10b. Anastomotic stricture of the bile duct. (a) Right paramedian sagittal US image shows focal narrowing of the middle portion of the common bile duct (arrow) at the surgical anastomosis. (b) Corresponding image from endoscopic retrograde cholangiopancreatography shows the narrowing (arrow). (c) Color and spectral Doppler image of the main hepatic artery shows a normal waveform.
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Figure 10c. Anastomotic stricture of the bile duct. (a) Right paramedian sagittal US image shows focal narrowing of the middle portion of the common bile duct (arrow) at the surgical anastomosis. (b) Corresponding image from endoscopic retrograde cholangiopancreatography shows the narrowing (arrow). (c) Color and spectral Doppler image of the main hepatic artery shows a normal waveform.
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Nonanastomotic strictures are most often secondary to ischemia caused by hepatic artery compromise. The blood supply to the distal common bile duct (recipient) is rich because of collateral flow, whereas the vascularity of the more proximal duct (donor) and of the intrahepatic ducts is more tenuous and solely derived from the reconstructed hepatic artery. The clinical presentation consists of deranged liver function test results or progressive obstructive jaundice. Treatment includes balloon dilation with or without percutaneous transhepatic biliary drainage. The strictures often commence at the hepatic hilum and extend peripherally or may be intrahepatic and multiple. US shows focal segmental intrahepatic or hilar ductal dilatation without an obvious obstructing mass or stone. If intrahepatic dilatation is identified in the posttransplantation liver, the hepatic artery should be carefully examined, with particular attention paid to the color and spectral signal to determine if there is any arterial compromise.
Rarely, partial or complete sloughing of the biliary epithelium occurs due to necrosis of the biliary tree (46). This serious complication should be suspected if US reveals marked dilatation of the intrahepatic biliary tree with accompanying echogenic intraluminal debris (Fig 11). The debris consists of a variable combination of the sloughed epithelium and biliary stones. Generalized ductal change does occur in the absence of obstruction or leakage and is associated with acute rejection, ischemia, or cholangitis. US may demonstrate irregularity of the intrahepatic bile ducts with lack of normal tapering and increased periductal echogenicity (47).
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Figure 11a. Sloughing of biliary epithelium in a liver transplant recipient with known hepatic artery thrombosis and biliary necrosis. (a) Transverse US image shows distention of the common bile duct by echogenic intraluminal material (arrows), which represents sloughed biliary epithelium. (b) Coronal MR image of the porta hepatis, obtained after administration of a biliary excreting agent, shows a filling defect within the biliary tree confluence (arrows), which represents the sloughed epithelium. (c) Contrast-enhanced CT image shows the "cutoff" of the main hepatic artery (large arrow). Short arrows = surgical sutures of the hepatic artery anastomosis. (d) Color Doppler image obtained at the porta hepatis shows no flow in the hepatic artery. Only portal vein flow is seen (red areas). (Fig 11b courtesy of K. Khalili, MD, Princess Margaret Hospital, Toronto, Ontario, Canada.)
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Figure 11b. Sloughing of biliary epithelium in a liver transplant recipient with known hepatic artery thrombosis and biliary necrosis. (a) Transverse US image shows distention of the common bile duct by echogenic intraluminal material (arrows), which represents sloughed biliary epithelium. (b) Coronal MR image of the porta hepatis, obtained after administration of a biliary excreting agent, shows a filling defect within the biliary tree confluence (arrows), which represents the sloughed epithelium. (c) Contrast-enhanced CT image shows the "cutoff" of the main hepatic artery (large arrow). Short arrows = surgical sutures of the hepatic artery anastomosis. (d) Color Doppler image obtained at the porta hepatis shows no flow in the hepatic artery. Only portal vein flow is seen (red areas). (Fig 11b courtesy of K. Khalili, MD, Princess Margaret Hospital, Toronto, Ontario, Canada.)
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Figure 11c. Sloughing of biliary epithelium in a liver transplant recipient with known hepatic artery thrombosis and biliary necrosis. (a) Transverse US image shows distention of the common bile duct by echogenic intraluminal material (arrows), which represents sloughed biliary epithelium. (b) Coronal MR image of the porta hepatis, obtained after administration of a biliary excreting agent, shows a filling defect within the biliary tree confluence (arrows), which represents the sloughed epithelium. (c) Contrast-enhanced CT image shows the "cutoff" of the main hepatic artery (large arrow). Short arrows = surgical sutures of the hepatic artery anastomosis. (d) Color Doppler image obtained at the porta hepatis shows no flow in the hepatic artery. Only portal vein flow is seen (red areas). (Fig 11b courtesy of K. Khalili, MD, Princess Margaret Hospital, Toronto, Ontario, Canada.)
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Figure 11d. Sloughing of biliary epithelium in a liver transplant recipient with known hepatic artery thrombosis and biliary necrosis. (a) Transverse US image shows distention of the common bile duct by echogenic intraluminal material (arrows), which represents sloughed biliary epithelium. (b) Coronal MR image of the porta hepatis, obtained after administration of a biliary excreting agent, shows a filling defect within the biliary tree confluence (arrows), which represents the sloughed epithelium. (c) Contrast-enhanced CT image shows the "cutoff" of the main hepatic artery (large arrow). Short arrows = surgical sutures of the hepatic artery anastomosis. (d) Color Doppler image obtained at the porta hepatis shows no flow in the hepatic artery. Only portal vein flow is seen (red areas). (Fig 11b courtesy of K. Khalili, MD, Princess Margaret Hospital, Toronto, Ontario, Canada.)
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Stones and sludge, although infrequent after transplantation, are associated with high morbidity (48). Cyclosporine can alter the bile composition, inducing crystal formation in the common bile duct, resulting in biliary sludge and stone formation (46). Other causes include retained stones within the graft or stones secondary to bile stasis from biliary strictures (Fig 12).
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Figure 12a. Biliary stone. (a) Right paramedian sagittal US image shows a distended common bile duct and a focal echogenic calculus (arrow) with distal acoustic shadowing. (b) Corresponding CT image shows the calculus (arrow).
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Figure 12b. Biliary stone. (a) Right paramedian sagittal US image shows a distended common bile duct and a focal echogenic calculus (arrow) with distal acoustic shadowing. (b) Corresponding CT image shows the calculus (arrow).
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Dysfunction of the sphincter of Oddi causes hepatic dysfunction in a minority of transplant recipients. It is thought to be secondary to devascularization or denervation of the ampulla of Vater, leading to dysfunction of the sphincter. US shows diffuse dilatation of both the extrahepatic donor duct and the native duct without evidence of an anastomotic bile duct stenosis. After sphincterotomy, there is usually reversal of both the ductal dilatation and the deranged liver function test results.
Recurrence of primary sclerosing cholangitis occurs in up to 20% of cases with a mean interval of 350 days after transplantation (49). Definitive US diagnosis may be difficult with gray-scale evaluation, as the findings of mural biliary tree irregularity and diverticulumlike outpouchings are similar to those caused by severe hepatic artery compromise. Recurrent disease should be suspected in patients who have undergone transplantation for end-stage primary sclerosing cholangitis and who demonstrate biliary ductal dilatation or ductal wall thickening in the setting of a normal Doppler arterial waveform (Fig 13). Often, the diagnosis of recurrence relies on histologic findings.
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Figure 13a. Recurrent sclerosing cholangitis 1 years after orthotopic liver transplantation. (a) Right paramedian sagittal US image shows mural thickening of the common bile duct (arrows). However, the arterial Doppler waveform was normal. (b) Magnified view shows the abnormality (arrows).
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Figure 13b. Recurrent sclerosing cholangitis 1 years after orthotopic liver transplantation. (a) Right paramedian sagittal US image shows mural thickening of the common bile duct (arrows). However, the arterial Doppler waveform was normal. (b) Magnified view shows the abnormality (arrows).
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Neoplastic Complications
Neoplastic disease in the transplanted liver may represent recurrent neoplasia or posttransplantation lymphoproliferative disorder. Hepatocellular carcinoma recurs most commonly in the form of lung metastases, followed by multifocal lesions in the liver graft (Fig 14) (50).
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Figure 14a. Recurrent hepatocellular carcinoma in a 49-year-old man 10 months after transplantation for alcoholic cirrhosis. Pathologic analysis of the liver explant at the time of transplantation revealed previously undiagnosed multiple microscopic foci of hepatocellular carcinoma. (a) Median sagittal US image shows a large mass of mixed echogenicity in the right hepatic lobe (arrows). (b) Corresponding contrast-enhanced CT image shows the mass (arrows).
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Figure 14b. Recurrent hepatocellular carcinoma in a 49-year-old man 10 months after transplantation for alcoholic cirrhosis. Pathologic analysis of the liver explant at the time of transplantation revealed previously undiagnosed multiple microscopic foci of hepatocellular carcinoma. (a) Median sagittal US image shows a large mass of mixed echogenicity in the right hepatic lobe (arrows). (b) Corresponding contrast-enhanced CT image shows the mass (arrows).
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Posttransplantation lymphoproliferative disorder may complicate any organ transplantation. The estimated frequency in adults after liver transplantation is 2%–8.4% (51); it most typically manifests within the first year, often 4–12 months after transplantation (52). The chronic immunosuppression required to prevent organ rejection causes unregulated lymphoid expansion, usually of the B-cell lineage. There is a range of severity of disease from benign mononucleosis to fulminant lymphoma. It is strongly associated with the Epstein-Barr virus. Any organ can be involved, including the lymph nodes, lungs, and gastrointestinal tract. Involvement of the liver may be extra- or intrahepatic. Extrahepatic disease, the more common type, is identified as a poorly defined hypoechoic soft-tissue mass that often encases or narrows the hilar structures (Fig 15). Intrahepatic disease may manifest as a solid focal hypoechoic mass or more commonly as a diffuse infiltrative process (52,53).
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Figure 15a. Posttransplantation lymphoproliferative disease. (a) Transverse US image shows a large, heterogeneous, echogenic mass (arrows) that effaces and displaces the porta hepatis. Biopsy demonstrated posttransplantation lymphoproliferative disease. (b) Contrast-enhanced CT image obtained at a different level shows the mass (arrows), which encases the vasculature at the porta hepatis.
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Figure 15b. Posttransplantation lymphoproliferative disease. (a) Transverse US image shows a large, heterogeneous, echogenic mass (arrows) that effaces and displaces the porta hepatis. Biopsy demonstrated posttransplantation lymphoproliferative disease. (b) Contrast-enhanced CT image obtained at a different level shows the mass (arrows), which encases the vasculature at the porta hepatis.
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Parenchymal Complications
Parenchymal disease may take the form of a focal mass or a diffuse parenchymal abnormality. The differential diagnosis for a focal mass in the transplanted liver is wide and includes infarct, abscess, preexisting donor disease, biloma, metastatic disease, or posttransplantation lymphoproliferative disorder.
Of particular importance is recognition of the parenchymal manifestations of hepatic artery thrombosis and stenosis: infarcts and abscesses. The morphologic appearance of infarcts after transplantation is variable. They may manifest as round or geographic lesions, which are often solid and contain central hypoechoic areas reflecting liquefaction and necrosis (Figs 16–18). Intraparenchymal gas may be identified within the infarct as small highly echogenic flecks, which display dirty shadowing posteriorly secondary to reverberative artifact. There should be accompanying supportive Doppler evidence of arterial compromise. The US appearance of abscesses varies with abscess maturation. Classically, abscesses have thick walls with central hypoechoic areas and, as with infarcts, may contain gas (Fig 19).
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Figure 16. Infarct in a 56-year-old woman with hepatic artery thrombosis 9 days after orthotopic liver transplantation. US (top left) and CT (top right) images show a peripheral parenchymal infarct (*) in segment 6 of the liver. Doppler spectrum for the intrahepatic artery (bottom) shows an abnormal tardus-parvus waveform (arrow); this flow originates from collateral pathways.
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Figure 17a. Infarct in a 42-year-old woman with fatigue 5 years after liver transplantation. The fatigue was secondary to delayed hepatic artery thrombosis, which led to extensive infarction of the liver. (a) Transverse US image of the liver shows a large area of heterogeneous parenchyma with central hypoechoic areas (arrows), which represent necrosis. (b) Corresponding contrast-enhanced CT image shows the infarct (arrows).
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Figure 17b. Infarct in a 42-year-old woman with fatigue 5 years after liver transplantation. The fatigue was secondary to delayed hepatic artery thrombosis, which led to extensive infarction of the liver. (a) Transverse US image of the liver shows a large area of heterogeneous parenchyma with central hypoechoic areas (arrows), which represent necrosis. (b) Corresponding contrast-enhanced CT image shows the infarct (arrows).
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Figure 18a. Biopsy-proved infarct in a 35-year-old patient 4 months after orthotopic liver transplantation for fibrolamellar carcinoma. (a) Midline transverse US image shows an echogenic focus with a hypoechoic rim (arrow) in the left hepatic lobe. (b) Corresponding contrast-enhanced CT image shows the lesion (arrow).
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Figure 18b. Biopsy-proved infarct in a 35-year-old patient 4 months after orthotopic liver transplantation for fibrolamellar carcinoma. (a) Midline transverse US image shows an echogenic focus with a hypoechoic rim (arrow) in the left hepatic lobe. (b) Corresponding contrast-enhanced CT image shows the lesion (arrow).
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Figure 19a. Abscess in a 57-year-old man with fever and rigor 6 months after orthotopic liver transplantation for primary sclerosing cholangitis. (a) Transverse US image shows a focal mass in the left hepatic lobe. The mass demonstrates highly echogenic air (arrows) and posterior dirty shadowing, which could easily be mistaken for gas in an adjacent bowel loop. (b) Corresponding CT image shows the lesion (arrows).
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Figure 19b. Abscess in a 57-year-old man with fever and rigor 6 months after orthotopic liver transplantation for primary sclerosing cholangitis. (a) Transverse US image shows a focal mass in the left hepatic lobe. The mass demonstrates highly echogenic air (arrows) and posterior dirty shadowing, which could easily be mistaken for gas in an adjacent bowel loop. (b) Corresponding CT image shows the lesion (arrows).
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Benign lesions such as hemangioma or liver cysts are relatively commonplace in the transplanted liver and have the same range of US appearances as in native livers. If the donor was involved in a motor vehicle accident, a focal mass identified at initial US of the implant may represent a hematoma (Fig 20). Bilomas are usually focal hypoechoic round lesions with thin walls. There is often an accompanying history of recent percutaneous biopsy. Focal lesions may be due to metastatic disease from a distant primary tumor such as a colon or lung tumor or, as described earlier, may represent focal posttransplantation lymphoproliferative disorder.
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Figure 20a. Preexisting lesion in a liver implant. Transverse US images show a round hematoma in segment 4b as a focal, well-defined cystic structure with dependent internal echoes, which delineate a fluid-fluid level (arrowheads in b). The donor had been in a motor vehicle accident.
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Figure 20b. Preexisting lesion in a liver implant. Transverse US images show a round hematoma in segment 4b as a focal, well-defined cystic structure with dependent internal echoes, which delineate a fluid-fluid level (arrowheads in b). The donor had been in a motor vehicle accident.
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The differential diagnosis for diffuse parenchymal abnormality in the transplanted liver is also wide and includes rejection, ischemia, hepatitis, and cholangitis. Narrowing the differential diagnosis is dependent not only on the US appearances of the liver transplant but also on the timing and symptoms of clinical presentation. Often, histopathologic analysis provides the final answer.
The US appearances of rejection are nonspecific, and often the only identifiable abnormality is heterogeneity of the liver parenchyma. There is no correlation with the Doppler waveforms, resistive index, or acceleration time of the transplant (54–56). Ischemia also causes diffuse parenchymal heterogeneity, but there is usually supportive Doppler evidence of arterial compromise. If hepatitis recurs in the transplanted liver, there is accompanying biochemical evidence. Reinfection with the hepatitis C virus occurs in nearly all patients who have undergone liver transplantation for hepatitis C virus cirrhosis. In the majority of patients (80%–85%), the infection appears to be benign at short-term and medium-term follow-up, with survival rates comparable with those of patients who undergo transplantation for nonviral chronic liver diseases. Whether progression to cirrhosis will occur in the majority of patients with longer follow-up remains uncertain. However, a small subset of patients who receive transplants for hepatitis C will develop fibrosing cholestatic hepatitis and progress rapidly to liver failure (3). Autoimmune hepatitis also recurs after liver transplantation. These patients are often maintained at a higher level of immunosuppression to prevent recurrence. Cholangitis may cause diffuse parenchymal change with accompanying biliary abnormalities (57).
Perihepatic Complications
Fluid collections and ascites occur commonly after transplantation. Owing to the surgical removal of the normal peritoneal reflections, fluid can accumulate around the bare area of the liver, a location not identified in the preoperative native liver (Fig 21). A right-sided subhepatic hematoma, seen as a complex fluid collection involving the bare area, is an early observation in many transplant recipients. Although US is highly sensitive in detection of fluid collections, it is not specific. Ascites, bile, blood, pus, or lymph may all have a similar appearance of a simple fluid collection. However, there are certain US features that may be more specific. Particulate ascites is seen with blood and pus. Carcinomatosis also gives rise to particulate ascites, but this would be an atypical cause in the setting of recent liver transplantation. In the immediate postoperative period, a hematoma is classically seen as an avascular fluid collection with internal echogenic strands that often involves the bare area of the liver. Acute hemorrhage can appear uniformly echogenic and may mimic a solid mass. Enlargement of the right adrenal gland is often identified at US in the early postoperative period. During surgery, the right adrenal gland undergoes venous ischemia, causing the gland to become hemorrhagic and enlarged (Fig 22).
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Figure 21a. Acute and subacute fluid collections. (a) Transverse US image shows an isoechoic acute hematoma as an echogenic mass (arrows) with echogenicity similar to that of adjacent liver tissue. Acute hematomas can be difficult to detect, as they are often isoechoic relative to adjacent liver tissue. (b, c) Subacute hematoma in a 52-year-old man 10 days after orthotopic liver transplantation. Right paramedian sagittal (b) and corresponding transverse (c) US images show a complex, septated, avascular fluid collection (arrows in b) in the hepatorenal space. The fluid collection extends to the bare area of the liver (B in b), a location not identified in the native liver.
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Figure 21b. Acute and subacute fluid collections. (a) Transverse US image shows an isoechoic acute hematoma as an echogenic mass (arrows) with echogenicity similar to that of adjacent liver tissue. Acute hematomas can be difficult to detect, as they are often isoechoic relative to adjacent liver tissue. (b, c) Subacute hematoma in a 52-year-old man 10 days after orthotopic liver transplantation. Right paramedian sagittal (b) and corresponding transverse (c) US images show a complex, septated, avascular fluid collection (arrows in b) in the hepatorenal space. The fluid collection extends to the bare area of the liver (B in b), a location not identified in the native liver.
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Figure 21c. Acute and subacute fluid collections. (a) Transverse US image shows an isoechoic acute hematoma as an echogenic mass (arrows) with echogenicity similar to that of adjacent liver tissue. Acute hematomas can be difficult to detect, as they are often isoechoic relative to adjacent liver tissue. (b, c) Subacute hematoma in a 52-year-old man 10 days after orthotopic liver transplantation. Right paramedian sagittal (b) and corresponding transverse (c) US images show a complex, septated, avascular fluid collection (arrows in b) in the hepatorenal space. The fluid collection extends to the bare area of the liver (B in b), a location not identified in the native liver.
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Figure 22a. Adrenal hemorrhage. (a) Transverse US image shows a hypoechoic nodule (arrow) in the hepatorenal space. The nodule represents focal adrenal hemorrhage secondary to intraoperative venous infarction. (b) Corresponding CT image shows the nodule (arrow).
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Figure 22b. Adrenal hemorrhage. (a) Transverse US image shows a hypoechoic nodule (arrow) in the hepatorenal space. The nodule represents focal adrenal hemorrhage secondary to intraoperative venous infarction. (b) Corresponding CT image shows the nodule (arrow).
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Conclusions
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Liver transplantation is an accepted and successful form of treatment for a variety of irreversible acute and chronic liver diseases. Comprehensive patient care, advances in surgical technique, and the development of new immunologic agents have all led to a decrease in mortality and morbidity from liver transplantation. Radiologists play a vital role in the postoperative care of transplant recipients. Awareness of both the normal and abnormal US appearances of liver transplants permits prompt recognition and treatment of associated complications.
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Footnotes
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Abbreviation: IVC = inferior vena cava
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References
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