is an Assistant Professor of Abdominal Imaging and
is an Associate Professor and the Chief of Abdominal Imaging in
the Department of Radiology, University of California, San
In the United States, more than 300,000 organ transplants have
been performed, more than 250,000 of which were abdominal organs.
The number of transplants performed each year continues to rise,
and the radiologist plays a key role in monitoring and diagnosing
disease in this special patient population. This article will
discuss radiologically evident complications associated with solid
abdominal organ transplants.
The most commonly transplanted abdominal organ is the kidney.
More than 14,000 renal transplants were performed in the United
States in 2003, and 86,000 patients are on the kidney transplant
Common indications for renal transplants are medical renal disease
(36%), diabetic nephropathy (21%), and hypertensive nephropathy
While renal transplantation is not a life-saving procedure, it
greatly improves quality-of-life and is more cost-effective in the
long term compared with chronic hemodialysis.
Assessment of a renal transplant recipient must also include
evaluation for complications of the patient's underlying disease.
If the patient has diabetes or continues to smoke, atherosclerosis
may persist or progress. Bowel paresis or ischemia and arterial
stenoses may still occur and must not be overlooked as a cause of
abdominal pain (Figure 1). Furthermore, renal allograft recipients
may have ongoing sequelae from prior peritoneal dialysis, such as
bowel adhesions or sclerosing peritonitis,
a thickening of the peritoneum that may be associated with prior
peritoneal infection (Figure 2).
The typical renal allograft is placed in an extraperitoneal
location protected posterolaterally by the iliac bone. The donor
renal artery and vein are anastomosed to the recipient external or
internal iliac vessels, and the ureter is tunneled into the bladder
near the trigone to minimize reflux but may be anastomosed
elsewhere in the bladder.
Two kidneys may be transplanted en bloc into an adult iliac fossa
if the donor is a child.
In the first few weeks after transplantation, perinephric fluid
collections may be seen, usually in the extraperitoneal space
(Figure 3). These fluid collections tend to displace adjacent
structures such as the bowel, and may surround the bladder or
retroperitoneal vessels. A high-attenuation collection may be due
to hematoma, possibly indicating a leaking vascular anastomosis,
requiring urgent surgical revision. Careful evaluation for active
extravasation of intravenous contrast is imperative. If the
collection is of fluid density, delayed computed tomographic (CT)
images revealing filling of this collection with dense contrast
material at CT is diagnostic of a urinoma secondary to a leak or
rupture of the ureter. Rim-enhancing fluid collections, especially
if gas-containing, suggest abscess, and percutaneous or surgical
drainage should be performed.
More benign collections, such as seromas or lymphoceles, may
also occur, but these collections may also become secondarily
infected. In general, seromas tend to shrink spontaneously with
time, while lymphoceles can grow. Lymphoceles are particularly
common around renal transplants as compared with other abdominal
transplants, and occur in up to 20% of patients
(Figure 3). The development of lymphoceles is due to both
disruption of lymphatic channels draining the kidney during organ
procurement and the posttransplantation medical regimen.
Renal vascular complications are feared because they may cause
loss of the allograft. CT and magnetic resonance (MR) angiography
may be helpful to delineate patency of the renal arteries and
veins. The most common vascular complication in renal transplants
is renal artery stenosis, which occurs in 1% to 23% of patients.
This complication most commonly occurs soon after transplantation
but may occur several years afterwards. Stenosis is most common at
the anastomotic site and is often amenable to dilatation by
Renal parenchymal abnormalities, such as wedge-shaped infarcts,
poor perfusion on venous-phase imaging or on prolonged nephrogram,
may be also be associated with renal artery stenosis (Figure
Arteriovenous fistula and pseudoaneurysms may occur in a renal
allograft as a result of prior percutaneous biopsy and may cause
hematuria, hypertension, or decreased renal function.
Doppler ultrasound (US) may show a characteristic enlarged vascular
space with, in the case of an arteriovenous fistula, decreased
resistance of the arterial waveform, and arterialization of the
venous waveform. At CT or MR angiography (Figure 5), a prominent
vascular cavity may be seen, possibly with enlargement of the
draining renal vein. Although smaller lesions may be monitored
closely for progression or resolution, larger fistulae may be
treated effectively with transarterial embolization.
The ureter of a renal allograft becomes strictured in up to 10%
most commonly due to insufficient blood supply. In more severe
cases, ureteral necrosis and urine leak may develop, particularly
in patients undergoing high-dose steroid treatment. Ureteral stent
placement or balloon dilatation is helpful to relieve obstruction,
but ureteral revision may be required.
Renal parenchymal complications, such as infarcts and
pyelonephritis, may be seen in the early posttransplant period
(Figure 6). Pyelonephritis may also occur some time after the time
of transplantation, and the risk of infection may be increased with
the presence of ureteral reflux. Ill-defined parenchymal perfusion
abnormalities, perinephric fat stranding, and urothelial thickening
of the renal pelvis and ureter are signs of possible infection.
Although the common pathogens are gram-negative bacteria,
and other fungal infections may occur.
CT and MR evaluation for possible renal transplant rejection is
and percutaneous biopsy is required for accurate diagnosis. Imaging
abnormalities for rejection are nonspecific, and include decreased
perfusion or swelling of the allograft, thickening of the
urothelium, and loss of corticomedullary differentiation.
When renal allograft failure occurs, the allograft is usually
left in place. The appearance of this allograft may range from that
of a normal-appearing kidney to an atrophic or hydronephrotic
kidney to an amorphous heavily calcified mass (Figure 3).
Failed allografts should not be mistaken for pelvic
lymphadenopathy, tumor, or contrast-filled bowel.
More than 5000 patients receive liver transplants each year, and
the demand for liver transplantation is increasing, particularly
with the rising prevalence of hepatitis C. While the most common
indication for liver transplantation is liver failure, patients
with hepatocellular carcinoma and small tumor burden may be cured
by liver transplantation. Currently, 5000 patients die annually on
the waiting list for a liver.
In patients who receive a liver transplant, graft survival is
approximately 80% at 3 years.
Liver transplantation surgery is complex and requires
anastomosis of the donor to recipient bile duct, inferior vena
cava, hepatic artery, and portal vein. Unlike kidney and pancreatic
transplantation, liver transplantation requires resection of the
native organ prior to transplantation of the donor organ. Stigmata
of prior cirrhosis, such as varices and splenomegaly, often persist
after successful liver transplantation (Figure 7). Furthermore,
periportal edema is a common and persistent finding that does not
imply pathology (Figure 8).
Biliary complications occur in up to 30% of liver transplant
and are the most common structural complication of liver
transplantation. Fluid collections in the abdomen in the immediate
posttransplant period are most commonly bilomas, which frequently
appear as fluid- density or fluid-signal structures around the
liver, particularly along the cut edge of the liver in patients
with partial liver transplants. Although many of these collections
resolve spontaneously, persistent or enlarging collections may
indicate a significant leak and may require biliary tract stenting
or percutaneous drainage.
Bile duct leak is more common with bili-enteric anastomosis than
with duct to duct anastomosis,
and more common in living donor liver transplants than in cadaveric
liver transplants. Evaluation of biliary leak may be performed
using percutaneous or retrograde cholangiography, but alternative
methods include scintigraphy or excretory CT or MR cholangiography.
Biliary stenosis may result in elevation of liver enzymes, and
noninvasive imaging with MR or CT cholangiography may be performed
to assess severity (Figure 9). Nonocclusive stenoses may be treated
with percutaneous or endoscopic stenting and balloon dilatation,
but occasionally surgical revision may be necessary. Most biliary
stenoses occur at the anastomosis site, but intrahepatic biliary
stenosis may occur in 10% of
and may be associated with hepatic arterial thrombosis, rejection,
An important point to realize is that occasionally bile ducts in
the liver allograft may need to be sacrificed and ligated if they
do not connect to the main duct. These ligated ducts are expected
to dilate over time, and the associated liver parenchyma will
atrophy. Unless these ducts are known to be infected, percutaneous
drains must not be placed into these dilated ducts, unless a
subsequent internal bilioenteric anastomosis is feasible, otherwise
subsequent removal of the percutaneous drain may not be
Evaluation of vascular anastomoses is important for liver
transplant recipients; ideally both an arterial and portal venous
phase examination should be performed at CT or MRI. The most common
vascular complication of liver transplants is hepatic artery
thrombosis or stenosis, which may occur in up to 15% of recipients
(Figure 10). The outcome of hepatic artery thrombosis is variable,
and may range from elevated liver enzymes to biliary stricture and
necrosis to fulminant hepatic necrosis and loss of the graft.
Intrahepatic bilomas and abscesses due to hepatic artery thrombosis
may be successfully treated with percutaneous drainage.
CT and MR angiography are both useful modalities for evaluating
hepatic arterial complications.
Stenoses or thromboses of the venous structures are less common
complications of liver transplants. Portal vein compromise may
result in ascites, variceal bleeding, and liver failure. Both CT
and MR are useful modalities to assess for severity of portal vein
pathology (Figure 11). It should be noted that the presence of
varices, such as a splenorenal shunt or perigastric varices, is
commonly seen after liver transplantation: The mere presence of
varices does not imply portal venous hypertension (Figures 7 and
Liver transplant recipients are at risk of recurrence of their
pretransplant disease. In particular, since hepatitis C is the most
common indication for liver transplantation in the western world,
progression of viral disease in the allograft may occur.
Furthermore, in patients with hepatocellular carcinoma or other
intrahepatic malignancy prior to transplantation, tumor recurrence
may occur. The most common sites of hepatocellular carcinoma
recurrence are the lung and the liver
Pancreatic transplantations are performed primarily in patients
with diabetes, and are usually placed in tandem with, or after, a
The main motivation for pancreatic transplantation is to address
the endocrine deficiency of patients with diabetes who cannot
produce sufficient insulin. While pancreatic transplantation is not
a life-saving procedure, it may prevent long-term complications of
diabetes, including neuropathy, blindness, and renal failure.
Visual identification of the pancreatic allograft is challenging
if the radiologist is unaware of the anatomy of pancreatic
transplants. The head of the pancreatic allograft is typically in
the right pelvis, with the tail extending superiorly along the
right paracolic gutter. Multiple arterial and venous anastomoses
are typically performed to join the allograft vessels with the
recipient iliac vessels (Figure 13). The donor duodenum, which
drains the pancreatic duct, is anastomosed to either the bladder or
the ileum of the recipent.
Patients with duodenal-to-bladder drainage of the pancreas
allograft are at slightly higher risk for urologic complications
Peripancreatic fluid collections are very common after pancreatic
transplantation, and some degree of allograft pancreatitis is
always noted clinically (Figure 14). Visualization of the
pancreatic allograft at MRI is often best with fat-saturated
T1-weighted sequences after gadolinium administration.
Vascular thombosis is more common in pancreatic transplants than
in renal and hepatic allografts, and may occur in up to 30% of
This predisposition may be due to intravascular stasis caused by
the relatively low volume of blood passing through the pancreatic
parenchyma and due to the discordant caliber of the inflow arteries
(splenic and gastroduodenal arteries) relative to those of the
pancreatic parenchymal arteries. Furthermore, pancreatitis in the
allograft, medical therapy, and prolonged ischemia time may
predispose recipients of pancreatic allografts to vascular
Regardless of the appearance of the pancreatic vessels, the
pancreatic parenchyma must be assessed for enhancement to identify
possible pancreatic necrosis (Figure 15). A pitfall in evaluation
of pelvic veins by CT and MRI is iliac vein pseudo-thrombosis,
which is a laminar flow phenomenon caused by more rapidly enhanced
venous return from the renal allograft than from the lower
extremities. This early venous return from the renal allograft
creates the impression of ipsilateral partial iliac vein
thrombosis, as opacified blood flows adjacent to unopacified blood,
or creates the impression of contralateral iliac vein thrombosis
because the iliac vein opacifies sooner on the renal allograft side
than on the other side.
A new technique for pancreatic transplantation is the injection
of purified insulin-producing islets into the portal vein rather
than the transplantation of the entire donor pancreas. These
injected pancreatic islets embolize into the liver parenchyma and
function to produce insulin. In patients receiving such
transplants, a heterogeneous appearance of the liver parenchyma may
be seen soon after transplantation but, subsequently, its
appearance returns to normal.
General complications of transplantation
Posttransplantation lymphoproliferative disorder (PTLD) is a
feared complication that may occur with any type of allogenic
transplant and affects 2% to 5% of solid-organ transplant patients.
The severity of PTLD may range from local lymphatic tissue
hyperplasia to aggressive systemic lymphoma. Risk factors for PTLD
include an Epstein-Barr virus-negative recipient who receives an
Epstein-Barr virus-positive allograft, history of intensive
immunosuppressive therapy, and hepatitis C. Patients requiring
higher baseline immunosuppressive therapy, such as heart and lung
transplant patients, have a higher risk (up to 15%) for developing
Abdominal PTLD commonly involves extranodal sites, such as the
bowel and liver (Figure 16), but nodal involvement occurs in
While PTLD most commonly occurs within the first year after
transplantation, it may occur remote from the time of
The imaging appearance of PTLD closely mimics that of lymphoma.
Focal masses tend to be homogeneous and hypovascular and tend to
displace rather than occlude the bowel, vessels, and ureters. Also,
PTLD may appear as an infiltrating hilar mass, both in renal and
(Figure 17). Infiltrating tumors may also occur within a transplant
organ and may be difficult to appreciate at imaging. Core or open
biopsy is generally required for diagnosis of PTLD. Patients with
PTLD are treated with a decrease in their immunosuppressive
therapy, and if PTLD is localized to the allograft, resection may
be curative. More aggressive disease may require chemotherapy or
radiation therapy. The overall 5-year survival rate for PTLD is
59%, and a poorer prognosis is associated with onset within the
first year after transplantation.
Due to immunosuppressive therapy, transplant patients are also
at risk for nosocomial and opportunistic infections. Pulmonary
infections are common and are most typically bacterial, but
atypical pathogens (including tuberculosis, aspergillus,
cytomegalovirus, and coccidiomycosis) should also be suspected when
patients do not respond to antibiotic therapy
(Figure 18). Likewise, focal infections of the allograft or colon
may be due to atypical organisms (Figure 19).
For all abdominal transplants, evaluation for possible rejection
remains a difficult diagnosis that largely depends on core or open
As the population of patients with abdominal transplantation
grows, radiologists will increasingly be called upon to assess
these patients for possible complications. Knowledge of the anatomy
and the common complications in this special population is crucial
for making appropriate diagnoses.