With advances in surgical techniques and greater understanding of
immunosuppressive management, abdominal transplants are becoming a more
widespread definitive treatment for otherwise end-stage diseases. The
most common abdominal transplants include hepatic, renal, pancreatic,
and islet-cell transplants. Implementing ultrasound as a diagnostic tool
in the immediate post- and perioperative periods provides an accurate
assessment of allograft viability that obviates the need for additional
exams, which could subject the patient to unnecessary radiation and
contrast exposure or the risks of invasive procedures.
6,000 hepatic transplants are performed annually in the United States
(U.S.) and, as of December 2011, > 16,000 patients were awaiting
transplantation.1 Postoperative ultrasound evaluation can
accurately and effectively detect complications that will affect
long-term morbidity and mortality. With increasing demand for liver
transplants and for reduction of wait-list mortality rates, the
available donorpool has been expanded by the advent of the split-liver
transplant technique from cadaveric donors and lobar (right or left)
grafts from living related donors in addition to whole liver
transplants. It is imperative to recognize and understand the anatomy,
variant anatomy, and functionality of these special cases.
transplants increase the recipient pool by dividing a donor liver
between an adult and pediatric recipient. Adults most often receive the
right lobe segments 5-8 (Figure 1). In larger patients, the medial
segment of the left hepatic lobe may be included along with the right
lobe (segments 4-8). Pediatric recipients can then be transplanted with
the remaining left hepatic lobe (segments 2-3 or 1-4).2 Split-liver
transplants may employ vascular conduits and reconstruction, which
increases the risk of postoperative complications.2 It is advisable to consult with the surgical team to better understand potentially complicated reconstruction anatomy.
evaluation of the hepatic allograft should begin with grayscale imaging
of the type of transplant, transplant size, echotexture,and location
within the abdomen. Special attention should be paid to the biliary
tree. Routine Doppler interrogation of the hepatic vessels should
include, when present, the main, right and left hepatic arteries and
portal veins, as well as the middle, right, and left hepatic
veins.Perihepatic collections are common in the immediate postoperative
state, but should decrease over time and exhibit no mass effect to the
hepatic parenchyma and vessels.
the anatomy or variant anatomy of the various types of hepatic
transplants will help focus examination of the anastomotic channels as
well as reveal the complications associated with each and prevent
erroneous diagnoses. Approximately 50% of transplant recipients will
endure a postoperative complication, 10% of those being vascular
complications.3,4 With its accuracy in detecting hepatic artery complications in nearly 92% of cases,5 ultrasound
becomes an essential and imperative diagnostic exam. Most often, the
donor hepatic artery is anastomosed in an end-to-end fashion to the
recipient hepatic artery or between the donor celiac axis and
bifurcation points (right and left hepatic orGDA and PHA) of the
recipient.2,6,7 A Carrel patch, an aortic patch containing
the donor’s aorta, including the origin of the celiac axis, may also be
used as an anastomotic channel.8 Oftentimes, a “fish mouth”
anastomosis must be performed to overcome size discrepancy between a
small-caliber donor artery and a larger-caliber recipient artery.7,8
Alternatively, an interposition graft, often using the donor’s iliac
artery, may connect the donor hepatic artery to the recipient
supraceliac or infrarenal aorta or other tributary.2,6,7 The
discrepancy in size may increase the risk of hepatic artery
complications, including stenosis and thrombosis, in the postoperative
period, or it may mimic a pseudostenotic appearance.2 It is not uncommon to have the donor celiac artery anastomosed to the recipient hepatic artery at the bifurcation.
hepatic artery waveforms include the presence of a brisk systolic
upstroke with presence of diastolic flow, a resistive index range of 0.5
to 0.7.2,6 (Figure 2). The acceleration time of the peak systolic velocity should be < 80 milliseconds.2,6 It
is common to demonstrate decreased diastolic flow and high resistive
indices in the immediate postoperative period attributed to edema or
vasospasm.2,6,9 These high-resistive indices are not only
detected in the main hepatic artery, but parenchymal branches as well,
and are apparent within 72 hours of the postoperative period and should
be transient, resolving by 2 weeks.6,9
The most common
site of significant hepatic artery stenosis is at the donor-recipient
anastomotic site, occurring in up to 11% of cases.3,4,8 It
often is difficult to visualize, due either to the small caliber of the
vessels or to overlying bowel gas. If seen, a focal area of color
Doppler aliasing may direct the diagnostician to the site of a subtle or
obscured stenosis. Targeted Doppler evaluation of a hemodynamically
significant stenosis would demonstrate an angle corrected peak systolic
velocity > 2 m/s or a twofold velocity increase when compared to the
prestenotic segment.2,3,8 Waveform findings distal to the
site of stenosis may reveal a “tardus-parvus” waveform, witha prolonged
PSV acceleration time > 80 milliseconds, or diminished resistive
indices < 0.5 (Figure 3).2,3,8
The most common
postoperative arterial complication is hepatic artery thrombosis, often
detected within the first 3 months, and occurs at an even higher rate if
arterial reconstruction or grafts are employed.2 The rate of
hepatic artery thrombosis is as high as 5% to 12% with one-year
reconstruction or graft viability at approximately 73%.2,7,8 The rate is even higher in the pediatric population, with prevalence as high as 42%.4 Hepatic
artery thrombosis is associated with significant morbidity and
mortality, with mortality rates as high as 58%, and is the
second-leading cause of graft failure in the immediate postoperative
period.6,7,10 Delayed-hepatic arterial thrombosis can occur
many years after transplant, accounting for the majority of vascular
complications, and is associated with chronic rejection, pediatric
transplants,and sepsis.2 The lack of arterial flow within the porta hepatitis or within the liver parenchyma is the most striking finding.3 Low-resistance
arterial waveforms may be detected within the liver despite the
presence of a main-hepatic artery thrombosis due to small collateral
vascular tributaries.3, 7
pseudoaneurysms are a less common vascular complication. They are
classified as either intrahepatic or extrahepatic.3 Intrahepatic
pseudoaneurysms usually arise as sequelae of infection or postbiopsy
complication in a patient with suspected rejection.7
Extrahepatic pseudoaneurysms typically develop at the site of the
hepatic-artery anastomosis either from surgical or mycotic etiology.2,7,8
Grayscale imaging will demonstrate an anechoic cystic-appearing
structure with the typical color and Doppler findings of the “yin-yang”
color swirl and the “to-and-fro” spectral velocity pattern seen in
pseudoaneurysms of any cause.2,3 If the recipient hepatic
artery or celiac artery is stenosed, an aortohepatic jump graft (usually
the donor iliac artery) may be required.2
The portal vein anastomosis is usually performed via an end-to-end anastomosis between donor and recipient.6-8
Similar to hepatic arterystenosis, portal vein stenosis occurs at the
anastomotic site and can be identified by a focal area of luminal
narrowing (< 2.5 mm) on grayscale orby focal-color aliasing on color
imaging.2 Doppler interrogation of a hemodynamically
significant stenosis will reveal a peak systolic velocity> 150 cm/s
at the anastomosis, or a 3- to 4-fold peak systolic velocity increase
when compared to the prestenotic segment.2,3,8 Portal-vein
thrombosis can also often occur at the site of anastomosis and can be
seen as an echogenic or isoechoic (acute) intraluminal-filling defect on
grayscale with absent or partial flow on color Doppler imaging.3 With
chronic thrombosis, revascularization or cavernous transformation may
be seen inthe adjacent porta hepatis. Additional secondary signs of
portal vein thrombosis include ascites, edema, splenomegaly, and
collateralization of shunts.7,8 If the portal vein is
completely thrombosed, an SMV or splenic vein jump graft using the donor
iliac vein, superior mesenteric vein, or splenic vein may be used as a
The IVC has traditionally been anastomosed in an end-to-end fashion,
but with increasing frequency an end-to side or side-to-side anastomosis
known as the “piggyback” technique is performed. This technique
connects by anastomosis the donor supra-hepatic IVC to the recipient
hepatic venous confluence while the donor infra-hepatic IVC, if present,
is tied off (Figure 1).2,6-8 This method obviates the need
for veno-venous bypass and caval reconstruction. “Piggyback”
reconstruction is often employed in split-liver transplants and is
required for left lateral segment transplants (segments 2-3), since the
donor IVC does not accompany the allograft.2 When evaluating
an end-to-end anastomosis, Doppler evaluation of venous velocities and
waveforms should include both supra- and infrahepatic anastomoses.2
and hepatic venous waveforms should demonstrate the normal triphasic
pattern reflecting the dynamics of blood flow during the cardiac cycle.6 The
normal waveform demonstrates 2 hepatofugal peaks reflecting right
atrial filing during ventricular systole and diastole,followed by a
hepatopetal peak from retrograde flow into the hepatic veins during
atrial contraction. (Figure 4).11
are rare, but include stenoses and thromboses at the anastomotic site,
and occur more commonly in pediatric populations, retransplantation, and
when end-to-end anastomoses rather than “piggyback” anastomoses were
employed.2,8 Grayscale depiction of IVC stenosis, which more
commonly occurs at the suprahepatic anastomosis, will demonstrate an
area of focal narrowing and color aliasing.2,3 A
hemodynamically significant stenosis will demonstrate a 3- to 4-fold
increase in peak systolic velocity when compared to the prestenotic
cava.2,8 Downstream intrahepatic venous waveforms will lose
phasicity and demonstrate flattening of the normal triphasic waveform.
(Figure 4).3,8 In severe cases, there may be flow reversal in the intrahepatic veins.3,8
Pseudostenosis is often caused by kinking at the vascular pedicle and
can mimic a hemodynamically significant stenosis; however, maneuvers
such as scanning in expiration, or in the standing position may
differentiate between the two.2 IVC thrombosis is uncommon,
but when present, also occurs at the sites of anastomosis. Grayscale
will demonstrate isoechoic to echogenic intraluminal clot with color
images demonstrating partial or absent venous flow.3 Additional secondary signs indicating IVC occlusion include ascites, hepatomegaly, edema, and pleural effusions.2,7 Full
liver transplants require evaluation at the site of anastomosisas well
as individual interrogation of the right, middle, and left hepatic
veins. Normal hepatic venous waveforms demonstrate a triphasic pattern
reflecting the various phases of the cardiac cycle. Similar to the IVC,
loss of normal phasicity should prompt a search for a suprahepatic IVC
Approximately 15% to 25% of liver transplant
recipients will experience a biliary complication, and usually within
the first 3 months.3,7,8 While cholangiography remains the gold standard for diagnosing biliary complications, sonography is a vital screening tool.
The gallbladder is removed during transplantation; however, it may be common to visualize a cystic duct remnant.3,8 The
biliary anastomosisis usually performed in an end-to-end fashion
connecting the donor common bile duct to the recipient common hepatic
duct, a choledochocholedochostomy, in an attempt to preserve the
functionality of the sphincter of Oddi, thus decreasing the risk of
enteric reflux.6,7 In instances where the recipient’s common hepatic duct is diseased, absent, or too short, a choledochojejunostomy is performed.6-8 This is also the preferred biliary anastomosis in pediatric patients, in which case resultant pneumobilia is often present.
leaks are the most common biliary complications and often present as
peritransplant anechoic or hypoechoic fluid collections.8 Biliary strictures most often occur at the site of anastomosis.8 A
common duct diameter measuring > 4 mm should raise high clinical
concern for a downstream stricture, whether it be from ischemia,
rejection, or infection.3 The biliary system in a transplanted liver is dependent purely on the arterial system for vascular supply.7,8 Therefore,
areas of bile-duct strictures, dilatation (Figure 5), and leaks,
especially remote from the anastomotic site, may indicate biliary
ischemia and should prompt a careful survey of the hepatic artery,
particularly at the anastomotic site.7,8 It is then imperative to focus the exam to uncover the underlying etiology resulting in the biliary abnormality.
Postoperative fluid collections
It is common to have
several small peritransplant fluid collections or hematomas (Figure 6),
which are expected to gradually shrink and resolve within days to weeks.7,8 A transient small right pleural effusion is also a common finding.7 Bilomas, lymphoceles, and abscesses are other considerations.
Due to chronic immunosuppression of liver
transplant recipients, posttransplantation lymphoproliferative disorder
(PTLD), which is often associated with infection from Epstein-Barr virus
(EBV), and non-Hodgkin’s lymphoma are becoming more common.3,7
Autoimmune hepatitis and Langerhans cell histiocytosis have been
suggested as posing an increased risk of PTLD. The anatomic distribution
of PTLDis related to the type of allograft itself. A common spectrum of
findings in the liver is focal intraparenchymal masses (Figure 7),
ill-defined infiltrative pattern and heterogeneous porta hepatis masses
(Figure 8).12 Differential diagnoses for intrahepatic masses
in a posttransplant recipient includes abscess, infarction, postsurgical
hematoma or contusion, biloma, lymphoma, or carcinoma.
Grayscale evaluation of the renal allograft
should begin with size and position of the transplant within the
abdomen. Due to its superficial location within the abdomen, fine detail
may be more apparent than retroperitoneal native kidneys, such that
visualization of cortico-medullary differentiation may be a normal
The most common location for the renal allograft is
extraperitoneal in the right iliac fossa; however, intraperitoneal
(pediatric patients)and contralateral transplants may also be
encountered. Cadaveric transplants are often harvested with a portion of
the donor aorta, which is anastomosed in an end-to-side fashion to the
recipient’s external iliac artery.13 Living related donor
transplants are often anastomosed in an end-to-side fashion, which
ligates the donor main renal artery to the recipient external iliac
artery or an end-to-end fashion to the recipient internal iliac artery
(Figure 9). The venous anastomosis is usually an end-to-side connection
between the donor main renal vein recipient external iliac vein. The
donor ureter is often times implanted into the dome of the recipient
bladder, uerteroneocystostomy.13 Variations of these surgical techniques exist in which it becomes important to consult with the surgical team.
pediatric cadaveric kidney transplants are termed pediatric en bloc
(EBK) and are an alternative type of transplantation intended to
increase the number of available donors. The donor aorta and inferior
vena cava are anastomosed end-to-side to the recipient iliac vessels or
in-line with an end-to-end anastomosis between the recipient aorta and
IVC and the divided ends of the recipient external iliac artery and
veins (Figure 10). Despite higher rates of graft thrombosis than
standard adult cadaveric donors (5% versus 1.8%), graft survival rates
A small amount of fluid within the
renal pelvis can also be expected (Figure 11), allowing for incompetence
at the ureterovesicular junction anastomosis and increased urine
production by the sole transplant kidney, ultimately producing the same
volume of urine produced by two native kidneys.15 When
imaging with a full bladder, and fluid is present within the renal
pelvis, it is important to reimage the kidney after having the patient
void. Fluid that persists extends and distends the infundibula and
calyces should prompt a careful survey for the cause of obstruction.
Mechanical obstruction most often occurs within the first 6 months and
usually involves the distal third of the ureter near the bladder
implantation site.13 The possible causes of ureteral
strictures or obstruction are numerous and include ischemia, rejection,
faulty surgical technique, pelvic fibrosis, extrinsic compression by a
pelvic fluid collection, or intrinsic obstruction caused by fungus
balls, clot, calculi, and papillary necrosis among others.13
Peritransplant fluid collections are a common postoperative finding, reported in up to 50% of cases.13 The differential diagnosis includes hematoma, seroma, abscess, urinoma, or lymphocele.3 Hematomas
and seromas usually present in the immediate postoperative period
andare often sonolucent, although internal complexity is common in
hematomas. Abscesses usually occur within days 7-10, while lymphoceles
develop within months.3,15 Urinomas are rare, but usually
occur within the first few weeks and result from the breakdown of the
ureterovesicular junction and may form near the bladder apex or cause an
intraperitoneal leak.13,15 Regardless of the etiology of the
fluid collection,it is important to discern whether there is
significant interval increase in size or mass effect upon the allograft
and if vascular compromise is evident warranting emergent interventional
or surgical exploration and evacuation.
Vascular complications of renal transplants are not uncommon, occurring up to 12% of all cases.3 Normal
Doppler interrogation of the intrarenal arteries should demonstrate
sharp systolic upstrokes with a slow decay during diastole, and
resistive indices < 0.7 (Figure 11).15,16 The acceleration time of the peak systolic velocity should measures < 0.07 sec, with a pulsatility index of < 1.15 The
main renal vein should demonstrate a monophasic waveform with lower
velocities and minimal respiratory variation (Figure 11).16
artery stenosis is usually a late complication and most often occurs at
the site of anastomosis or just distal to it and often demonstrates an
area of turbulence as well as peak systolic velocities > 2 m/s or a
peak systolic velocities> 2 times the peak systolic velocity measured
in the external iliac artery, proximal to the anastomosis.3,13,15 Spectral
waveform findings in the downstream interlobar arteries will often show
a tardus-parvus waveform with prolonged acceleration time (> 0.07
sec) (Figure 12) and low resistive indices (< 0.56).13
vein thrombosis is a rare, but serious complication, usually occurring
within the first 4 weeks of the postoperative period.3,15
Characteristic findings include visualization of thrombus and absent
flow in the main renal vein with swelling of the allograft.3,13 However,
secondary signs, such as increased resistance in the arterial waveform,
diastolic flow reversal, with preservation of a brisk systolic
upstroke,may be the main finding to suggest renal vein thrombosis.3, 13,15-16
renal artery thrombosis is also a rare, but serious complication (<
1%) occurring in the immediate postoperative period and can lead to
graft loss, if not recognized in a timely manner.16 Grayscale imaging may demonstrate segmental infarcts as ill-defined peripheral hypoechoic areas without detectable color flow.13 Global
infarcts will manifest as diffuse swelling of the allograft, which will
often appear abnormally hypoechoic and without detectable color flow.13
to hepatic allografts, renal pseudoaneurysms can be either
intraparenchymal, often a complication of a prior percutaneous biopsy,
or extrarenal, usually at the site of anastomosis or sequelae of
infection.3 Color Doppler will demonstrate the “yin-yang” and “to-and-fro” flow at the pseudoaneurysm neck (Figure 13).15
fistulas are another postbiopsy complication. These are almost
exclusively diagnosed on color Doppler imaging with the presence of
aliasing color flow, high velocity, low-resistance arterial spectral
waveforms, and arterialization of the venous waveform, which persists
even on high Doppler scale settings (Figure 14).3,13,15-16
diagnosis of allograft rejection on ultrasound is often an elusive one
and may be deferred to the clinical history as well as a percutaneous
biopsy. However, certain sonographic grading criteria exists in the
attempt to elucidate the potential of transplant rejection based on
grayscale and color Doppler findings, such as allograft swelling, loss
of renal sinus fat, prominence of medullary pyramids, pelvi-infundibular
wall thickening (Figure 15), and elevated resistive indices.17 In addition, Doppler analysis may reveal elevated resistive indices > 0.8, and sometimes even reversal of diastolic flow.13 These
Doppler findings can also be seen in the setting of vascular
thrombosis, acute tubular necrosis (ATN), and drug nephrotoxicity. Lack
of arterial or venous flow will confirm the diagnosis of vascular
thrombosis. ATN is common in the early postoperative period and almost
exclusively occurs with cadaveric allografts. A differentiating feature
from acute rejection is that ATN gradually resolves over the first few
weeks, whereas acute rejection often peaks within the first 3 weeks of
the postoperative period. Tissue sampling is necessary to distinguish
between these 2 entities.
Prolonged immunosuppression often places
the recipient at risk for development of malignancy, including renal
cell carcinomas and urothelial malignancies, as well as lymphoma and
post transplant lymphoproliferative disease (PTLD).13 The
development of a suspicious solid intrarenal mass (Figure 16) should
raise concern for any one of these complications. PTLD in renal
transplant populations will often manifest as pathologic
lymphadenopathy; however, PTLD can infiltrate the allograft parenchyma
or present as a heterogeneous mass surrounding vessels in the renal
hilum, which can lead to vascular compromise.13
More than 35,000 pancreas transplants had been performed worldwide as of December 201018 in
diabetic patients. Pancreas transplants are categorized as simultaneous
pancreatic kidney transplant (SPK) in those with concomitant end-stage
renal nephropathy (75%), pancreas transplantation after previous kidney
transplant (PAK) (18%), and pancreas transplant alone (PTA) (7%).18
evaluation of the pancreatic transplant begins with grayscale imaging
of the allograft and is usually the first-line modality in the
evaluation for clinically suspected graft dysfunction. The pancreatic
allograft is typically placed in the extraperitoneal right iliac fossa
and renal allograft placed in the extraperitoneal left iliac fossa for
SPK (Figure 17).
Prior to 1995, 90% of all pancreas transplants
had pancreatic exocrine drainage via the bladder. Exocrine bladder
drainage has the advantage of being able to follow urine amylase as a
nonspecific rejection marker especially for solitary pancreatic
transplants, PAK and PTA, where serum creatinine cannot be followed for
rejection as in SPK. However, alkaline pancreatic excretions can result
in metabolicacidosis in addition to urologic complications such as graft
pancreatitis from reflux and urinary tract infections. The more
physiological enteric pattern of exocrine drainage is currently the most
commonly used whereby the allograft exocrine duct drains via an
end-to-side or side-to-side anastomosis between donor duodenum and
The arterial anastomosis involves creating a
donor iliac Y-graft to the donor splenic and superior mesenteric
arteries which are the anastomosed in an end-to-side fashion to the
recipient right common iliac artery or external iliac artery (Figure
The predominant method of pancreatic venous drainage utilizes
systemic venous drainage (SVD) with forming an anastomosis of the donor
portal vein in an end-to-side fashion to the recipient right external
iliac vein.19 The distal aspects of the donor splenic and
superior mesenteric vessels are blind ending. Alternative portal venous
drainage (PVD) connects the donor portal vein to the recipient superior
mesenteric vein or its major branch vessel, which creates a more
physiologic efflux of insulin towards the liver. No significant
long-term differences have been seen in SVD versus PVD.20
there is a living donor segmental graft, it comprises the pancreatic
body and tail. The donor splenic artery and vein are anastomosed to the
recipient external iliac vessels. Exocrine drainage can be done via
bladder anastomosis or enteric Roux-en-Y loop to the graft.21 The
normal pancreatic allograft is homogeneous and hypoechoic to the
surrounding fat (Figure 19). Color Doppler and power Doppler increase
detection of intraparenchymal and anastomotic vasculature. The majority
of graft failures in the first 6 months are due to technical factors,
such as vascular thrombosis, infection, anastomotic leak, or bleeding.
Acute rejection typically occurs between 6 and 12 months and chronic
rejection12 months after transplantation.22
can be seen as a swollen allograft and parenchymal heterogeneity.
Ultrasound has a limited role in the diagnosis of acute rejection due to
a wide range of sensitivities, 13% to 82%.23-24 These
imaging features are nonspecific, as they can also be seen with
pancreatitis and vascular thrombosis. No specific serum marker has yet
to be found which can distinguish between these entities. And unlike
renal transplantation, no reliable resistive index measurement has been
established for acute rejection in pancreatic transplantation.
Sonographically-guided pancreatic allograft biopsy has been shown to be
superior to both grayscale and spectral Doppler findings in the
diagnosis of rejection.23
The most common cause of vascular-transplant dysfunction is vascular thrombosis, venous slightly greater than arterial.25-26
Clinically,patients may have hyperglycemia, graft pain, and
hyperamylasemia. The blind-ending distal splenic and superior mesenteric
stumps are prone to thrombosis, which necessitates careful
documentation of patency or evaluation for extent of clot burden, since
thrombosis is the most common cause for early graft failure.25 The
lack or decrease of color flow, absence of appropriate spectral
tracings, and visualization of echogenic intraluminal thrombus (Figure
20) lead to the diagnosis of vascular occlusion. Reversal of diastolic
flow in the pancreatic transplant arteries is highly specific for venous
thrombosis.27 Venous clots can propagate to occlude draining
vessels and can be treated with anticoagulation, catheter-directed
pharmacologic thrombolysis/mechanical thrombectomy, or surgical
thrombectomy. Slow flow in the splenic vein through the graft can cause a
pseudothrombosis appearance. Recognition of this entity and further
evaluation with Doppler or delayed contrast-enhanced CT can help avoid
this pitfall.28 Short-segment peripheral thrombi can be seen and do not necessarily require treatment.
MRA has had some promising results for diagnosing vascular
complications. However, the role of MRI may be limited as the pancreas
transplant population with its high rate of concomitant renal morbidity
is at risk for gadolinium-induced nephrogenic systemic fibrosis.
Additional vascular complications include anastomotic turbulent flow or
elevated velocities indicative of stricture, pseudoaneurysm with
swirling color pattern and turbulent to-and-fro spectral tracing, and
postbiopsy arteriovenous fistulas.
fluid collections may represent hematomas, pseudocysts, abscesses,
seromas, urinary leaks, ascites, or anastomotic leaks. These appear as
anechoic or complex fluid collections.
Long-term PTLD in pancreas
transplants is associated with Epstein Barr virus infection and ranges
from benign B-cell hyperplasia to malignant lymphoma. The incidence is
highest in the first year and seen in up to 6% of patients from a series
of 212 recipients.29 The greatest number affected were those
who underwent solitary pancreas transplant, PAK or PTA, over SPK.
Patients present with nonspecific symptoms, including malaise, fevers,
chills, mild elevation of pancreatic enzymes, nausea, and vomiting. The
findings of PTLD typically manifest in the allograft, either alone or
with additional extra-allograft findings, and rarely extra-allograft
only. PTLD may manifest as diffuse or focal allograft enlargement,
extra-allograft lymphadenopathy, and rarely or ganomegaly.30 These findings are nonspecific as they can are also seen in rejection and overlap temporally in presentation.
Islet cell transplantation
Islet cell transplantation
has an emerging role in the treatment of type I diabetes in those with
severe recurrent hypoglycemia associated with unawareness and early
secondary complications refractory to medical management. Between 1999
and 2008, there were 412 recipients of islet cell transplantations.31 The
most successful islet cell transplantation with respect to insulin
independence is the Edmonton protocol,whereby highly purified cadaveric
donor islet cells are infused through a cannula into the main portal
vein via a percutaneous anterior or midaxillary puncture of a branch
right portal vein performed under fluoroscopy. After delivery, the
hepatic tract is embolized with a variety of materials, including coils,
fibrin glue, and gelatin sponge, to minimize the risk of hemorrhage.
Posttransplant imaging demonstrates anechogenic linear tract along the
embolization path (Figure 21). The protocol also calls for a potent
steroid-free immunosuppression protocol of dacluzimab, sirolimus, and
The most common early complication is
hemorrhage, either hepatic subcapsular or parenchymal, or bleeding into
the peritoneal or pleural spaces. Second most common complication is
portal venous thrombosis, which is seen as echogenic thrombus, typically
in a right portalvein branch, with decreased or lack of color flow and
absent venous spectral pattern. Less common complications include
arteriovenous fistulas, trauma to the adjacent biliary system, and
interruption of the pleura.33
Interestingly, a late
complication seen after 6 months is the development of periportal
hepatic steatosis without steathohepatitis.34-35 Periportal
echogenities (Figure 22) develop representing microvesicular fat and are
seen on MR as signal drop off on opposed-phase imaging. It is thought
to be a benign local effect of insulin from grafted islet cells and is
not associated with graft dysfunction. Long-term immunosuppression afte
rislet transplantation has also resulted in a significant percentage of
premenopausal females (70%) developing sirolimus-associated ovarian
cysts with a mean ovarian cyst size of 6 cm.36 Some of these
cysts can be symptomatic leading to pelvic pain from torsion or rupture.
Withdrawal of sirolimus results in regression of cyst size.
As the number of abdominal transplants
increases, knowledge of transplant anatomy and timely recognition of
complications are imperative to increase transplant survival and
decrease unnecessary procedures. Ultrasound remains the modality of
choice in most institutions and determines the need for intervention or
further evaluation with CT or MRI.
US Department of Health and Human Resources. Organ procurement and
transplantation network website. http://optn.transplant.hrsa.gov.
Accessed December 20, 2011.
- Vaidya S, Dighe M, Kolokythas O, Dubinsky T. Liver transplantation: Vascular complications. Ultrasound Q. 2007;23:239-253.
- Little AF, Dodd G. Postoperative sonographic evaluation of the hepatic and renal transplant patient. Ultrasound Q. 1995;13:111-119.
- Wozney P, Zajko AB, Bron KM, et al. Vascular complications after liver transplantation: A 5 year experience. AJR Am J Roentgenol. 1986; 147: 657-663.
- Flint EW, Sumkin JH, Zajko AB, Bowen A. Duplex sonography of hepatic artery thrombosis after liver transplantation. AJR Am J Roentgenol. 1988;151: 481-483.
- Brody M, Rodgers SK, Horrow MM. Spectrum of normal or near-normal sonographic findings after orthotopic liver transplantation. Ultrasound Q. 2008;24:257-265.
S, Sebastia MC, Margarit C, et al. Complications of orthotopic liver
transplantation: Spectrum of findings with helical CT. Radiographics. 2001;21:1085-1102.
- Nghiem HV, Tran K, Winter TC, et al. Imaging of complications in liver transplantation. Radiographics.1996;16:825-840.
W, Facciuto ME, Rocca JP, et al. Doppler ultrasonographic findings on
hepatic arterial vasospasm early after liver transplantation. J Ultrasound Med. 2006;25:631-638.
J, Colina I., Demetris AJ, et al. Cause and timing of first allograft
failure in orthotopic liver transplantation: A study of 177 consecutive
patients. Hepatology. 1991;14:1054-1062.
- Shin D, Jeffrey R., Desser T. Pearls and pitfalls in hepatic ultrasonography. Ultrasound Q. 2010;26: 17-25.
AA, Hosseinzadeh K, Almusa O, et al. Imaging of posttransplantation
lymphoproliferative disorder after solid organ transplantation. Radiographics. 2009;29:981-1000.
- Park SB, Kim J., Cho KS. Complications of renal transplantation ultrasonographic evaluation. J Ultrasound Med. 2007;26:615-633.
- Bhayana S, Kuo YF, Madan P, et al. Pediatric en block kidney transplantation to adult recipients: More than suboptimal? Transplantation. 2010;90:248-254.
- Cosgrove DO, Chan KE. Renal transplants what ultrasound can and cannot do. Ultrasound Q. 2008;24:77-87.
- Gao J, Ng A, Shih G, et al. Intrarenal color duplex ultrasonography: A window to vascular complications of renal transplants. J Ultrasound Med. 2007;26:1403-1418.
Townsend RR, Tomlanovich SJ, Goldstein RB, Filly R. Combined Doppler
and morphologic sonographic evaluation of renal transplant rejection. J Ultrasound Med. 1990; 9:199-206.
AC. 2011 update on pancreas transplantation: Comprehensive trend of
25,000 cases followed up over the course of twenty-four years at the
International Pancreas Transplant Registry (IPTR). Rev Diabet Stud. 2011; 8:6-16.
- Nikolaidis P, Amin RS, Hwang CM, et al. Role of sonography in pancreatic transplantation. Radiographics. 2003;23:939-949.
Lo A, Stratta RJ, Hathaway DK, et al. Long term outcomes in
simultaneous kidney-pancreas transplant recipients with portal-enteric
versus systemic-bladder drainage. Transplant Proc. 2001;33:1684-1686.
- Han DJ, Sutherland DE. Pancreas transplantation. Gut Liver. 2010;4:450-465.
- International pancreas transplant registry. http://www.med.umn.edu/iptr. Accessed November 15, 2011.
J, Krebs T, Klassen D, et al. Sonographic evaluation of acute
pancreatic transplant transplant rejection: Morphology-doppler analysis
versus guided percutaneous biopsy. AJR Am J Roentgenol. 1996;166:803-807.
- Yuh WTC, Wiese JA, Abu-Yousef MM, et al. Transplant imaging. Radiology. 1988;167:679-683.
SP, Kommareddi M, Ojo AO, Luan FL. Early pancreas graft failure with
inferior late clinical outcomes after simultaneous kidney-pancreas
transplantation. Transplantation. 2011;92:796-801.
C, Gruessner AC, Benedetti E, et al. Vascular graft thrombosis after
pancreatic transplantation: univariate and multivariate operative and
nonoperative risk factor analysis. J Am Coll Surg. 1996;182:285-316.
- Foshager MC, Hedlund LJ, Troppmann C, et al. Venous thrombosis of pancreatic transplants: Diagnosis by duplex sonography. AJR Am J Roentgenol. 1997;169:1269-1273.
Gupta R, Rottenberg G, Taylor J. Pseudothrombosis of the iliac vein in
patients following combined kidney and pancreas transplantation. Br J Radiol. 2002;75:692-694.
- Issa N, Amer H, Dean PG, et al. Posttransplant lymphoproliferative disorder following pancreas transplantation. Am J Transplant. 2009;9: 1894-1902.
TL, Krebs TL, Cheong JJ, et al. Imaging features of posttransplantation
lymphoproliferative disorder in pancreas transplant recipients. AJR Am J Roentgenol. 2000;174:121-124.
- Collaborative islet transplant registry. http://www.citregistry.org. Accessed November 15, 2011.
AM, Lakey JR, Ryan EA, et al. Islet transplantation in seven patients
with type I diabetes mellitus using a glucocorticoid-free
immunosuppressive regimen. N Engl J Med. 2000;343: 230-238.
- Low G, Hussein N, Owen RJ, et al. Role of imaging in clinical islet transplantation. Radiographics. 2010;30:353-366.
JF, Rosen M, Siegleman E, et al. Magnetic resonance-defined periportal
steatosis following intraportal islet transplantation: A functional
footprint of islet graft survival? Diabetes. 2003;52:1591-1594.
- Ryan EA, Lakey JR, Rajotte RV, et al. Clinical outcomes and insulin
secretion after islet cell transplantation with the Edmonton protocol. Diabetes. 2001;50:710-719.
E, Koh A, Albaker W, et al. High prevalence of ovarian cysts in
premenopausal women receiving sirolimus and tacrolimus after clinical
islet transplantation. Transpl Int. 2009;22:622–625.