Dr. Piyasena is a 4th-year Radiology Resident and Dr. Allison is the Director of the Radiology Residency Program and the Director of Ultrasound, Department of Radiology, Georgetown University Hospital, Washington, DC.
Prolonged graft survival as a result of improvements in surgical
techniques and immunosuppressive drugs has led to an increased number of
organ transplantation surgeries. Data from the Organ Procurement and
Transplant Network shows that 16,481 kidney and 6443 liver transplants
were performed in the United States in 2006 alone.1 Given
this development, there is an increased need for accurate methods of
evaluating suspected postoperative complications. Several of the major
complications after liver and renal transplantation can rapidly lead to
graft loss or further patient morbidity or mortality.
complications can be detected by ultrasound imaging, thus often making
ultrasound the ﬁrst-line method of diagnosis. Ultrasound is often the
modality of choice for primary evaluation, as it is noninvasive,
relatively inexpensive, does not require intravenous contrast, can be
obtained at the bedside, and can often rapidly and accurately depict
many common complications, most notably those of vascular etiology.
Computed tomography, magnetic resonance imaging, and angiography are
often reserved for cases in which ultrasound is inconclusive or the
extent of a ﬁnding cannot be fully appreciated by ultrasound alone. It
is essential that the radiologist is able to recognize these
complications so that proper management, including further diagnostic
workup or surgical/radiologic intervention, can ensue.
article, the basic postsurgical anatomy of liver and renal transplants
is presented, as well as the sonographic appearance of several of the
complications that can often be detected by ultrasound, with emphasis on
surgical techniques have been developed to increase the number of
available organs for transplantation, including the use of living donor
transplants or split cadaveric organ transplants. Liver splitting
involves the division of a donor cadaveric liver in order to transplant
the left lateral segment into a small child and the extended right
segment into a larger child or adult.2,3 The sonographer must
know the type of procedure that was performed in order to correctly
identify and assess the involved vasculature, particularly when variant
or suboptimal anatomy is identiﬁed or when a premorbid condition
necessitates alteration of the routine transplant procedure, as in the
case of an interposition graft.
Basic whole-liver transplantation
involves 1 biliary and 4 vascular anastomoses and routine
cholecystectomy. The preferred biliary anastomosis is end-to-end from
the donor common bile duct to the recipient common hepatic duct.
However, if the recipient common hepatic duct is diseased, too short, or
otherwise inadequate for anastomosis, a choledochojejunostomy or
hepaticojejunostomy with a Roux-en-Y limb is constructed.
hepatic arterial anastomosis is typically an end-to-end ﬁsh-mouth
anastomosis where the donor common hepatic artery and splenic artery
branch point or the origin of the celiac artery with an aortic Carrel
patch (small portion of the adjacent aorta surrounding the celiac artery
origin) is connected to the recipient right and left hepatic artery
bifurcation or the proper hepatic– gastroduodenal artery bifurcation. If
the recipient has a dual blood supply to the native liver (for example,
a replaced right hepatic artery from the superior mesenteric artery),
then the larger of the arterial inﬂow vessels is used in the
anastomosis. When the donor liver has a replaced right hepatic artery,
the donor celiac artery with the Carrel patch is harvested and an
anastomosis is created between the re-placed right hepatic artery and
the proximal stump of the donor splenic artery, thus essentially
recreating a single origin for the hepatic arterial inﬂow.4 At
times, it may be necessary to use a donor iliac artery interposition
graft attached directly to the supraceliac or infrarenal aorta to ensure
adequate arterial inﬂow as in the case of stenosis or small caliber of
the more distal native artery.5
The portal vein
anastomosis is also an end-to-end anastomosis. In the case of portal
vein thrombosis or previous portal vein surgery, a donor iliac vein jump
graft may be interposed between the recipient superior mesenteric vein
or splenic vein and the donor portal vein.6
inferior vena cava (IVC) is typically transected immediately above and
below the intrahepatic portions and the supra- and infra-hepatic
anastomoses are performed in an end-to-end fashion (Figure 1A). A
variation of this procedure involves an end-to-side (piggyback
technique) or side-to-side anastomosis, thereby leaving the recipient
IVC intact (Figure 1B).7
Liver transplant complications
after liver transplantation can be subdivided into vascular and
nonvascular. For the purpose of this article, emphasis will be placed on
Nonvascular complications–– Small
perihepatic ﬂuid collections are common immediately after surgery and
typically represent small hematomas or seromas. These collections should
resolve within a few days or weeks after surgery. Although ultrasound
is sensitive to the presence of perihepatic ﬂuid, the speciﬁcity is very
low. Many of the common ﬂuid collections, including blood, pus,
ascites, bile, or lymph, can all have a similar appearance (Figure 2).
The differential diagnosis will depend on the speciﬁc appearance and
timing of its development related to surgery. The signiﬁcance of a
perihepatic ﬂuid collection often depends on the size of the collection
(whether or not there is resultant mass effect) and the clinical
Posttransplant liver parenchymal abnormalities may be
focal or diffuse. Focal lesions may represent pre-existing donor disease
(such as a hepatic cyst or hemangioma), infarct, abscess, biloma, or
metastatic disease. Particular attention should be paid to the hepatic
artery when a liver abscess or infarct is suspected, as they may be the
result of hepatic arterial thrombosis or stenosis. Evaluation of the
liver parenchyma may reveal recurrent hepatic disease, as has been well
documented in cases of viral hepatitis, primary biliary cirrhosis,
primary sclerosing cholangitis, and malignancy, such as hepatocellular
carcinoma and cholangiocarcinoma. Other diffuse parenchymal
abnormalities include rejection, ischemia, hepatitis, or cholangitis,
but these may show only nonspeciﬁc heterogeneity of the liver
parenchyma. The hepatic artery resistive index has been shown to be
unreliable in the assessment of transplant rejection.7-9
Posttransplantation lymphoproliferative disorder (PTLD) complicates 2% to 8.4% of adult liver transplants.10 This
disease process can involve the lymph nodes, lungs, bowel, and
abdominal organs. Extrahepatic disease appears as a poorly deﬁned
hypoechoic hilar mass, while intrahepatic disease may appear as a focal
solid hypoechoic mass or a diffuse inﬁltrative parenchymal process11 (Figure 3).
Biliary complications are common and are seen in up to 25% of transplants.12 The
vast majority of these complications are made up of biliary leaks. Bile
leaks may occur at the T-tube insertion site after its removal several
months after surgery, and at the anastomosis. Anastomotic strictures may
result from scarring secondary to surgical manipulation and can result
in intrahepatic biliary ductal dilatation. The native duct will often be
normal in caliber. Nonanastomotic leaks and strictures are often the
result of ischemia secondary to hepatic artery compromise.13 Intra- or extrahepatic bilomas can collect as a result of a bile leak, which can then become infected.14
common biliary complications include biliary sludge and stones.
Generalized bile duct abnormalities in the absence of obstruction or
leakage can be seen in cases of rejection, ischemia, or cholangitis.
complications from liver transplantation can result in signiﬁcant
compromise to the graft, often in the early postoperative period.11 Gray-scale,
color, and spectral Doppler is performed on all of the major vessels in
order to exclude thrombosis or stenosis. The authors must emphasize the
importance of knowing the exact postsurgical anatomy, as it is
essential that all vascular anastomoses are evaluated. The majority of
vascular complications occur at or adjacent to an anastomosis.
artery thrombosis is the most common and most devastating vascular
complication, accounting for 60% of all vascular complications and
occurring in 4% to 12% of adult transplants.15,16 Hepatic artery thrombosis is the second leading cause of graft failure in the early postoperative period after acute rejection.7 Patients
with hepatic arterial thrombosis may present with fulminant liver
necrosis, bile leak due to bile duct necrosis, or relapsing bacteremia.17
Ultrasound correctly identiﬁes 92% of thrombosed hepatic arteries.18 Spectral
Doppler evaluation of a thrombosed hepatic artery shows absent extra-
and intrahepatic arterial ﬂow (Figure 4). False-positive ﬁndings of
hepatic artery thrombosis are often attributed to technical factors such
as large patient size or marked ascites. Occasionally, the arterial ﬂow
may be below the level of detection for the ultrasound probe because of
hepatic edema, systemic hypotension or proximal stenosis.5,19 In
the acute postoperative period, impending thrombosis may present with a
typical pattern of progression on serial Doppler examinations (Figure
4). Sonograms show normal hepatic arterial ﬂow on day 1, then a
progressive decrease of diastolic ﬂow, followed by a dampening of
systolic ﬂow, and ﬁnally the total loss of the hepatic arterial
Hepatic artery stenosis has been reported
to occur in 11% of orthotopic liver transplant patients, most often at
the anastomotic site.19,20 Contributory factors may include
faulty surgical technique, clamp injury, vessel ischemia due to
disrupted vasa vasorum, or rejection. Doppler ultrasound of the hepatic
artery in the region of the stenosis will show a focal increase in
velocity greater than 2 to 3 m/sec with associated turbulence and
spectral broadening distally (Figure 5A). Distal to the stenosis, a
tardus-parvus waveform may be seen, consisting of a prolonged systolic
acceleration time (>0.08 seconds) and a resistive index <0.5
(normal 0.5 to 0.7) (Figure 5B). If technical factors do not allow
direct visualization of the hepatic artery anastomosis, a tardus-parvus
pattern alone in the more distal hepatic artery is approximately 75%
sensitive and speciﬁc for hepatic arterial stenosis.19
commonly, liver transplantation may be complicated by a pseudoaneurysm,
most often mycotic and occurring at the anastomosis. An intrahepatic
pseudoaneurysm may result from a focal infection or a percutaneous
procedure. On ultrasound, the pseudoaneurysm typically appears as an
intrahepatic or periportal cystic structure with disorganized turbulent
ﬂow along the course of the hepatic artery.7
Portal vein thrombosis or stenosis is a less common complication, occurring in 1% to 2% of patients.15,20 Possible
risk factors include faulty surgical technique, hypercoagulable states,
vessel size discrepancies that lead to increased turbulence, excessive
vessel length or previous portal vein surgery. Ultrasound of portal vein
thrombosis may show an echogenic or hypoechoic intraluminal thrombus
(Figure 6A) and an absence of Doppler ﬂow (Figure 6B). A focal area of
narrowing at the portal venous anastomosis may be normal, particularly
in cases of size discrepancy between donor and recipient; however, a
greater than 3- to 4-fold increase in velocity at the stenosis relative
to the prestenotic segment is compatible with a signiﬁcant stenosis.
Inferior vena cava thrombosis and stenosis are the least common vascular complications (found in <1% of transplant cases)15,20 and more frequently involve the anastomosis.5 With
gray-scale ultrasound, IVC thrombus appears as an intraluminal
echogenic structure (Figure 7A). Absence of ﬂow can be conﬁrmed with
color and spectral Doppler imaging (Figure 7B). Inferior vena cava
stenosis may show a focal narrowing of the IVC with color aliasing on
Doppler imaging (Figure 8A) that should be differentiated from potential
donor-recipient size discrepancy. A greater than 3- or 4-fold velocity
increase at the stenosis relative to the prestenotic IVC is considered
signiﬁcant (Figure 8B and C). With IVC thrombosis or severe stenosis,
there may be a reversal of ﬂow of the hepatic veins and a loss of the
normal phasicity of the venous waveforms of the hepatic veins and IVC
proximal to the thrombosis/stenosis7 (Figure 8D).
transplanted kidney is usually placed in an extraperitoneal location in
the right or left iliac fossa. Kidney transplants are identiﬁed by the
source of the donor organ, including a cadaveric renal transplant (CRT)
(with the donor organ from a cadaver), a “living” renal transplant (LRT)
(with the donor organ from a living relative) or a living nonrelative
renal transplant (LNRT) (with the donor organ from a living nonrelated
person). With CRT, a Carrel patch (a small portion of surrounding aorta)
is acquired and anastomosed to the recipient external iliac artery in
an end-to-side fashion. Both LRT and LNRT procedures often involve an
end-to-side anastomosis of the donor renal artery to the recipient
external iliac artery or an end-to-end anastomosis of the donor renal
artery to the recipient internal iliac artery. Variant anatomy with
multiple renal arteries can be anastomosed separately to the external
iliac artery or with a Carrel patch that encompasses all of the origins.
Alternatively, the individual arteries can be anastomosed to the
largest so that there is essentially a single donor vessel supplying the
entire graft. The renal vein is attached in an end-to-side anastomosis
to the external iliac vein. Ureteral drainage is restored, preferably by
means of ureteroneocystostomy. Another procedure sometimes performed
for kidneys obtained from donors <5 years of age involves the
transplantation of both kidneys into a single recipient and using the
donor aorta and vena cava for vascular anastomosis (an “en bloc”
pediatric transplant). As with liver transplants, knowledge of the exact
renal transplant procedure performed is essential for accurate
interpretation of both normal and abnormal ﬁndings.
Renal transplant complications
Complications after renal transplantation can also be subdivided into vascular and nonvascular complications.
Nonvascular complications—Perinephric ﬂuid collections are a common occurrence, found in up to 50% of renal transplants.21 These
include urinomas, hematomas, seromas, lymphoceles, and abscesses.
Although ultrasound is sensitive for their detection, the sonographic
appearance of collections can overlap. The clinical relevance of a ﬂuid
collection depends on its composition, size, location, and whether or
not it is getting larger or exerting signiﬁcant mass effect.
differential diagnosis can be narrowed based on the time of
presentation. Urinomas and hematomas often present in the immediate
postoperative period (up to 2 weeks after surgery), with hematomas
evolving in appearance over time. Lymphoceles are usually delayed,
occurring 4 to 8 weeks after surgery. Unless infected or mixed with
blood, urinomas appear as well-deﬁned anechoic collections without
septations. Perinephric abscesses are uncommon but can occur in the
early postoperative period and are caused by pyelonephritis or bacterial
seeding of a urinoma, hematoma, or lymphocele. The clinical
presentation plays a signiﬁcant role in establishing the diagnosis.
parenchymal abnormalities can be divided into focal or diffuse
processes. A focal area of increased or decreased echogenicity may
represent focal pyelonephritis, infarct, or rejection (Figure 9).
lymphoproliferative disorder complicates approximately 1% of renal
transplant patients, with a spectrum of disease ranging from mild
diffuse polyclonal lymphadenopathy to malignant monoclonal lymphoma.22 The
following can be involved in PTLD: any of the solid organs; hollow
viscera; abdominal, retroperitoneal, and iliac lymph nodes;
retroperitoneal musculature; or peritoneum of the abdomen, with the
extranodal disease predominating. Involvement of the transplant kidney
appears as single or multiple hypo- or mixed echogenic masses.
sonographic appearances of many diffuse renal parenchymal abnormalities
are nonspeciﬁc. Diffuse renal enlargement, cortical thickening,
increased or decreased cortical echogenicity, loss of corticomedullary
differentiation, prominent pyramids, and thickening of the collecting
system can all be seen in the setting of diminished renal function.
Although elevated resistive index obtained at the arcuate arteries was
previously described as an accurate method of detecting acute rejection,23 it
has been subsequently shown that increases in the resistive index can
be seen in various other conditions, including acute tubular necrosis,
renal vein thrombosis, graft infection, compressive perinephric ﬂuid
collections, and obstructive hydronephrosis.24 An elevated
resistive index (>0.8) is now used as a nonspeciﬁc parameter of renal
dysfunction (Figure 10). Ultimate differentiation between acute tubular
necrosis (acute vasogenic nephropathy), acute or chronic rejection, or
drug nephrotoxicity requires a biopsy.
Urologic complications occur in 4% to 8% of patients, including urine leak/ urinoma, urinary obstruction, and urinary calculi.25 Urine
leaks and urinomas often occur in the early postoperative period; the
patient usually presents with pain and swelling at the surgical site and
drainage from the wound. Urinomas appear as nonspeciﬁc, well-deﬁned
anechoic collections without septations.
obstruction occurs in approximately 2% of renal transplants, most often
during the ﬁrst 6 postoperative months. More than 90% occur at the
distal third of the ureter, most commonly at the ureterovesicle
junction.26 Causes of obstruction include edema at the
anastomosis, ischemia or rejection leading to ﬁbrosis and stenosis,
technical error during the ureteroneocystostomy, and kinking of the
ureter. Other, less common causes include calculi, papillary necrosis,
fungus ball, hematoma, and extrinsic compression by perinephric ﬂuid.
patient with urinary obstruction may not complain of typical renal
colic, as the transplant kidney is denervated. Additionally, this
denervation prevents the transplanted kidney from maintaining any
intrinsic tone, often resulting in a persistent appearance of mild
dilatation. It should also be noted that edema and ﬁbrosis associated
with rejection may prevent the normal dilatation seen with
hydronephrosis.27 Thus, the clinical setting and the use of
further imaging (eg, diuretic renography) may be necessary to determine
the functional signiﬁcance of the appearance of a dilated collecting
system. Secondary infection or pyonephrosis should be suspected when
complex-appearing urine is detected in a dilated collecting system
Renal transplant recipients are at increased risk for developing renal calculi.28 Renal
stones typically appear as echogenic, strongly shadowing structures in
the collecting system. Fungus balls should be suspected when a highly
echogenic mass in the transplanted collecting system exhibits weak
Renal vasculature—Vascular complications occur in 1% to 10% of patients.25,29 Renal
artery thrombosis is a devastating complication and often leads to
graft loss. Doppler ultrasound shows absent intrarenal arterial or
venous ﬂow. It should be noted that markedly diminished blood ﬂow can be
seen in severe rejection and may not be detected on color Doppler.30
vein thrombosis is an early complication that can be secondary to
surgical technique, compression of the renal vein by a ﬂuid collection,
or hypovolemia. The kidney may appear enlarged and hypoechoic with a
lack of Doppler signal in the renal vein. The renal artery shows
increased resistance, often with reversed, plateauing diastolic ﬂow31 (Figure
12). Reversal of diastolic ﬂow can also be seen in the setting of
severe rejection or acute tubular necrosis, but the additional ﬁnding of
absent venous ﬂow is essentially diagnostic for renal vein thrombosis.
artery stenosis usually occurs during the ﬁrst year after surgery and
is the most common vascular complication of renal transplantation.
Approximately half of stenoses occur at the anastomosis due to perfusion
cannula injury, faulty suture technique, or reaction to suture
material, with end-to-end anastomoses having a higher risk of stenosis.
Stenosis can occur proximal to the anastomosis (often due to
atherosclerotic disease) or distal to the anastomosis, secondary to
rejection or turbulent ﬂow. Doppler ultrasound will show a focal area of
color aliasing with velocities >2 m/sec, a velocity gradient between
the stenotic and prestenotic segment of more than 2:1, and poststenotic
spectral broadening (Figure 13A). A tardus-parvus waveform may be
observed in the renal parenchyma32 (Figure 13B).
vein stenosis is less common and usually results from extrinsic
compression by ﬂuid collections or perivascular ﬁbrosis. A focal
aliasing with a 3- to 4-fold increase in velocity on color Doppler
imaging indicates a signiﬁcant stenosis.33
ﬁstulas and pseudoaneurysms may result from percutaneous biopsy of the
transplant kidney. Most of these lesions are small and clinically
insigniﬁcant; however, large shunts may lead to renal ischemia, and
rupture of large arteriovenous ﬁstulas and pseudoaneurysms can cause
hematuria or perigraft hemorrhage. Gray-scale ultrasound may show
ﬁndings similar to simple or complex renal cysts, but with color
Doppler, intense, disorganized ﬂow is identiﬁed (Figure 14A). Larger
arteriovenous ﬁstulas may show a focal ﬂurry of disorganized color ﬂow
thought to be caused by vibration of the tissue surrounding the ﬁstula.
The feeding artery will show a high-velocity, low-resistance waveform,
and the draining vein may show pulsatile, arterialized ﬂow34 (Figure
14). Pseudoaneurysms with a narrow neck show a “to-and-fro” waveform
(forward and reverse ﬂow in the neck). Pseudo-aneurysms can occur at
vascular anastomoses or in association with infection.
is a useful tool in imaging both renal and hepatic transplants.
Knowledge of the surgical anatomy and normal and abnormal appearances of
the transplanted organ permits prompt recognition of complications.
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