Keywords
liver transplantation - thrombosis - biliary strictures - interventional radiology
Introduction
The world's first successful liver transplant was performed by Dr. Thomas Starzl in
the 1960s.[1] In the current era, an increasing number of surgeries are performed for various
liver pathologies which improve life expectancy. Liver transplant, being the last
resort for the treatment of end-stage chronic liver disease as well as acute liver
failure, requires strict vigilance for assessing long-term graft survival. Since acute
rejections are diagnosed only by liver biopsy, noninvasive imaging techniques are
used to rule out other vascular and nonvascular complications. After rejection, vascular
complications are the second most common cause of graft dysfunction.[2] Therefore, imaging plays an important role in the surveillance of post-liver transplantation
(LT). Posttransplantation complications are classified as vascular and nonvascular
complications, which in turn are again divided into biliary, intraparenchymal, and
intra-abdominal complications. In this pictorial essay, we demonstrate a spectrum
of findings using various imaging techniques like B-mode ultrasound (USG), Doppler
imaging, computed tomography (CT), and magnetic resonance imaging (MRI) for diagnosing
these complications. Tremendous improvement and wide acceptance of interventional
management using minimally invasive procedures is the current trend in treating various
vascular complications.
Surgical Techniques
While deceased donor LT utilizes the whole liver graft from the donor, in live donor
transplantation most commonly right liver lobe from the donor is implanted in the
recipient. In right lobe donor hepatectomy, the middle hepatic vein is left with remnant
left lobe in the donor. In smaller adults and older children, left lobe of the liver
with middle and left hepatic vein drainage can be utilized as a viable graft .The
most frequent procedure is a right hepatectomy with a resection plane just to the
right (about 1 cm) of the middle hepatic vein.[3] The alternate method is a left hepatectomy, in which the liver is often divided
into two parts in a similar plane which is reserved for those where the small-sized
liver graft is adequate. For smaller pediatric patients, left lateral segmentectomy
is specifically used.[4] The most common hepatic arterial anastomosis is end-to-end between donor common
hepatic artery and recipient proper hepatic artery in deceased donor transplantations[5] and donor right (or left) hepatic artery and the recipient right/left hepatic arteries
in case of live donor LTs. Hepatic vein anastomosis may be performed by either end-to-side
cavo-caval “piggyback technique” or side-to-side cavo-caval anastomosis as per surgeon's
preference. Portal vein is also anastomosed with end-to-end technique between the
donor and recipient vessel. Biliary anastomosis is usually performed end-to-end between
the donor and recipient common bile ducts.
Imaging Modalities
Ultrasound
This is the first-line imaging modality used to assess postliver transplant patients
in the immediate postoperative period.[6] USG is a widely available noninvasive imaging modality for quick evaluation of the
liver parenchyma. B-mode imaging, color Doppler, spectral evaluation, and elastography
are the diverse techniques to assess the graft function. Being a nonionizing and cheaply
available modality, it can be repeated multiple times in appropriate clinical settings
at the bedside without the need for radiating or shifting the patients. It is done
daily during the first week of the postoperative period and as and when required in
the rest of the postoperative period. B-mode is usually done to screen the hepatic
parenchymal echotexture and look for any obvious intra- and perihepatic collections,
biliary radicle dilatation, or periportal cuffing ([Fig. 1]). Color Doppler is used to determine the presence of blood flow and its direction
with respect to the liver. Any absence of flow warrants immediate further assessment
by triple-phase CT to exclude thrombosis of the culprit vessel. Spectral waveform
acquisition gives information about the peak systolic velocity (PSV), resistive index
(RI), acceleration time, and acceleration index. Hepatic artery is usually assessed
intrahepatically which shows rapid upstroke with an acceleration time of less than
0.08 seconds. The presence of a forward diastolic component with an RI value of 0.55
to 0.7 in hepatic arteries is essential for adequate perfusion of the graft. RI value
of more than 0.8 is a nonspecific finding which indirectly indicates various causes
of graft dysfunction as well as could also be a normal finding in the immediate postoperative
period in view of graft edema. The PSV is usually within 200 cm/s at the anastomotic
site and less than 103 cm/s in the intrahepatic branches. Portal vein is assessed
extrahepatically which demonstrates hepatopetal, monophasic, and continuous phasic
spectrum. Sainz-Barriga et al reported that portal flow volume of less than 180 mL/min
per 100 g liver weight (LW) showed poor survival rates.[7] Asencio et al proposed that portal flow volume exceeding 250 mL/min per 100 g LW
is indicated for controlling portal venous pressure.[8] Normal hepatic veins show a normal triphasic pattern of flow which can be demonstrated
in the inferior vena cava (IVC) also.[9] Using newer techniques like shear wave elastography, the parenchymal stiffness can
be evaluated for follow-up patients. Limitations of USG include poor acoustic window
secondary to postoperative scars and dressing and it is operator-dependent.
Fig. 1 A 41-year-old male patient who underwent liver transplant 2 weeks back, presented
with history of fever and elevated bilirubin levels with deranged liver function test
(LFT). Ultrasound (USG) abdomen of the liver showed diffuse periportal hyper echogenicity
(A, yellow arrow) with mild right pleural effusion (red arrow). Contrast-enhanced computed
tomography (CECT) abdomen axial (B) and coronal (C) image of the upper abdomen depicted diffuse intrahepatic periportal hypodensity
(green arrow) with diffuse common hepatic duct enhancement (blue arrow) suggestive
of periportal edema with cholangitis.
Computed Tomography
CT remains the confirmatory and complementary noninvasive imaging modality because
of its rapid acquisition, and excellent spatial and temporal resolution. Noncontrast
CT is essential to identify the graft and its bed as well as to identify any hyperdense
hematoma. Fluid density collections can also be identified in the perigraft regions
which can extend to the pelvic cavity. The gross evaluation of the abdominal cavity
is also looked upon to screen for other associated pathologies. Triple-phase contrast-enhanced
study is performed mainly to assess the vascular status of the graft. Any abrupt change
in RI value in the Doppler scan should raise concern for hepatic artery thrombosis
(HAT)/stenosis (HAS), which is evaluated in the arterial phase. Similarly, portal
and venous phases are used to analyze the portal vein and hepatic veins draining to
the IVC. Multiplanar reconstruction can be used to visualize coronal and sagittal
planes for optimal assessment of small vessels in all directions. The virtual reconstruction
technique depicts three-dimensional images of complex anatomic structures.
Magnetic Resonance Imaging
MRI is used only for the assessment of certain pathologies which are inconclusive
by the above-mentioned imaging modalities. It is limited by longer acquisition time,
lack of accessibility, poor patient factors, and lower spatial resolution than CT.
Noncontrast MR techniques can be used to assess the hepatic vessels; however, contrast
administration is necessary for precise evaluation. A noninvasive comprehensive evaluation
of the biliary system is possible only by magnetic resonance cholangiopancreatography
(MRCP). The likelihood of biliary complications in the graft may be increased as a
result of variant anatomy, which may necessitate two separate biliary-enteric anastomoses
or ductoplasty, with the creation of a common ductal opening.[10] Fluid characterizations to differentiate abscess, hematoma, and biloma can be done
using advanced imaging modalities, likely Dixon sequences, diffusion imaging, and
cholangiography technique.
Digital Subtraction Angiography
Digital subtraction angiography (DSA) can be used as a diagnostic as well as a therapeutic
tool. It has a superior temporal resolution as compared to CT or MRI and thus it helps
in assessment of flow characteristics in obstructive lesions to guide further management.
Definite diagnosis of vascular pathologies is made with the help of the DSA, particularly
arterial stenosis or thrombosis, with the added advantage of treating the pathologies
in the same sitting. Postbiopsy or infective pseudoaneurysm (PSA) is also confirmed
by DSA which warrants interventional management. Unique advantages include the elimination
of motion artifacts and providing a superselective angiogram for guiding interventional
treatment.
Vascular Complications ([Table 1])
Vascular Complications ([Table 1])
Table 1
Vascular complications following liver transplantation
|
Vascular complications
|
Clinical features/lab parameters
|
Imaging modality of choice
|
|
Hepatic artery thrombosis
|
• Early postoperative period
• May present with fulminant liver failure
• Elevated liver enzymes, biliary leaks, rarely septicemia
|
Contrast-enhanced CT
|
|
Hepatic artery stenosis
|
• Insidious course with vague abdominal discomfort
• Elevated liver enzymes
|
|
Portal vein thrombosis/stenosis
|
• Deranged LFT in late postoperative period
• Signs of portal hypertension (ascites, gastrointestinal bleeding)
|
|
Hepatic vein/IVC stenosis/thrombosis
|
• Signs of Budd–Chiari syndrome – abdominal distension/pain, ascites, anterior abdominal
wall collaterals, splenomegaly
|
Abbreviations: CT, computed tomography; IVC, inferior vena cava; LFT, liver function
test.
Hepatic Artery
Exclusive knowledge about the vascular anastomosis is necessary to optimally assess
the vessel status. In orthotopic LT, the donor coeliac artery is anastomosed with
the right or left hepatic artery. In the case of a diseased hepatic artery, a graft
interposition is done between the anastomosis. The hepatic artery being the sole blood
supply for biliary ducts, vigilant surveillance is necessary to rule out biloma or
biliary strictures which could indirectly represent HAS/occlusion.
The most common and most dangerous vascular complication following LT is HAT which
usually occurs between 2nd and 15th weeks.[9] It can occur in 4.8 to 9% of patients postliver transplant patients. Risk factors
include prolonged cold ischemia time, graft rejection, ABO incompatibility, and pediatric
population.[11] Hepatic artery is vital as it is the sole supply to the biliary tree. Untreated
HAT will lead on to biliary ischemia and strictures with adverse outcomes. USG is
the initial modality of choice which has high sensitivity and specificity for HAT.
It is identified as the absence of flow in the visualized hepatic arteries in the
Doppler study ([Fig. 2]). Reduced diastolic component and peak systolic velocities are predictors of imminent
HAT. False positive findings may be secondary to diffuse severe spasm of the hepatic
arteries or due to reduced cardiac output.[9] The absence of flow in Doppler evaluation warrants contrast-enhanced CT (CECT) which
can accurately determine the length and extent of thrombosis of hepatic arteries.
MR angiography can also depict similar findings in cooperative patients. Most patients
need surgical exploration or endovascular thrombectomy in the event of an early posttransplant
HAT. In case the attempts to salvage the hepatic artery fail, retransplantation is
indicated. Delayed HAT is usually managed conservatively.[12]
Fig. 2 A 37-year-old male patient post DDLT (deceased donor liver transplantation) - postoperative
day (POD) 4. Routine ultrasound (USG) Doppler surveillance (A) showed absent color flow (yellow arrow) in the intrahepatic portions of hepatic
artery, raising the possibility of thrombosis. Contrast-enhanced computed tomography
(CECT) abdomen coronal maximum intensity projection image (B) shows nonopacification of hepatic artery (red arrow) consistent with vascular thrombosis.
CECT coronal multiplanar reconstruction images (C) show diffuse body wall edema with mild ascites.
Stenosis of the hepatic arteries usually occurs within the first 3 months of surgery
with a median time of 100 days.[2]
[13] The incidence is around 4 to 11%. It usually occurs due to clamping injury, graft
rejection, and vasa vasorum disruption. Increased velocity of more than 200 cm/s at
the site of suspected stenosis or anastomosis with aliasing in color Doppler suggests
HAS. Indirect findings distal to the stenosis are an increase in diastolic component
with reduced resistance index to less than 0.55, a delayed acceleration peak (more
than 80 ms) together producing the characteristic parvus et tardus pattern of flow.[14]
[15] Other ancillary findings in Doppler evaluation include an anastomotic to the preanastomotic
ratio of 3:1. Three-dimensional reconstruction of CECT depicts focal stenosis of the
hepatic artery and its branches ([Figs. 3] and [4]). HAS can predispose to thrombosis and thereby pose a risk to the liver. As mentioned
in the previous section, HAS can impair blood supply to the biliary tree resulting
in strictures and ischemic cholangiopathy. Early posttransplant HAS is usually related
to a surgical issue and surgical correction is preferred; angioplasty is likely to
pose a risk of rupture at the anastomotic site. An interventional procedure like percutaneous
transluminal balloon angioplasty is the treatment of choice in late HAS, occurring
after the first 30 days of LT. In cases where there is recoil or flow limiting dissection,
stent placement may be considered.
Fig. 3 A 44-year-old male patient post deceased donor liver transplantation (DDLT) - postoperative
day (POD) 5. Coronal contrast-enhanced computed tomography (CECT) image (A) shows linear filling defect (yellow arrow) in the proximal hepatic artery with luminal
irregularity s/o dissection in the recipient common hepatic artery and focal narrowing
at the anastomotic site (red arrow). Virtual reconstructed image (B) demonstrates the same findings (yellow and red arrows).
Fig. 4 In the same patient, virtual reconstructed image (A) shows infrarenal aorto-hepatic jump graft (yellow arrow) after ligating the native
hepatic artery. Contrast-enhanced computed tomography (CECT) axial sections (B) of the upper abdomen show linear contrast opacification of aorto-hepatic jump graft
(yellow arrow). Mild ascites with mesenteric haziness is also noted. Following deranged
lab parameters repeat CECT images in coronal and axial planes (C and D) showed nonopacification of the jump graft (green arrow) consistent with complete
thrombosis of the extrahepatic portions of jump graft.
(.) Hepatic artery pseudoaneurysm
PSAs are abnormal focal outpouching of the arteries which are lined only by the tunica
adventitia. It can occur extrahepatically at the vascular anastomotic site or intrahepatically
secondary to needle biopsy or local infection. Though PSAs are silent, intrahepatic
rupture or erosion into the biliary tree are dreaded complications of hepatic PSAs.
B-mode USG shows anechoic focus along the course of the hepatic artery which on color
Doppler shows a characteristic bidirectional yin-yang pattern (to and fro). A bidirectional
or sometimes slow monophasic pattern of flow is seen in spectral Doppler.[16] In CT/MRI there is contrast distribution within the lesion similar to that of the
arterial vessels. Peripheral PSAs can be managed with superselective embolization
of the feeding artery close to the PSA with coils/glue. More central PSAs arising
in nonexpendable vessels can be managed with stent graft placement if feasible.
Portal Vein
Portal vein complications are usually less frequent as compared to those in the hepatic
artery with a prevalence of 1 to 2%. Early-onset portal vein thrombosis (PVT) is often
due to rapidly progressing graft dysfunction whereas late-onset PVT is due to chronic
graft rejection. Clinical features range from abdominal pain, ascites, splenomegaly
(signs of portal hypertension), varices, or liver failure.
PVT may occur at the site of anastomosis (extrahepatically) or intrahepatically. Various
risk factors include previous PVT, small-sized portal vein (< 5 mm), hypercoagulable
states, prior portal vein surgery (transjugular intrahepatic portosystemic shunt),
and interposition of grafts for portal vein reconstruction.[13]
[17] B-mode USG shows an echogenic thrombus within the portal vein reflecting chronic
thrombosis whereas acute thrombosis is seen as anechoic intraluminal focus. Lack of
venous flow in the Doppler imaging and focal filling defect at the anastomotic site
or beyond in triple-phase CT is the corresponding finding ([Fig. 5]). Partial filling defect can later evolve to complete chronic occlusion ([Fig. 6]). PVT can occur in the perioperative period (< 72 hours after transplant), early
(< 30 days), or late (> 30 days) periods after LT. Perioperative PVT is associated
with a high rate of graft loss (75%) irrespective of treatment. Early PVT also has
a poor prognosis and must be managed aggressively. Catheter-directed thrombolysis
combined with endovascular thrombectomy or surgical thrombectomy are the treatment
options. For thrombolysis, the portal vein can be accessed through transhepatic, transjugular,
or transsplenic routes. Late PVT can be managed conservatively with anticoagulation
if asymptomatic.[12]
Fig. 5 A 44-year-old male with living donor liver transplantation (LDLT) 1 year back. Color
Doppler images (A and B) show absence of wall-to-wall color in the main portal vein (yellow arrow) secondary
to eccentric echogenic thrombus. Reduced flow volume in main portal vein was documented
with spectral analysis. Contrast-enhanced computed tomography (CECT) axial and coronal
images (C and D) depict partial eccentric hypodense thrombus in the extrahepatic portions of main
portal vein (red arrow), respectively.
Fig. 6 A 63-year-old male patient with orthotopic liver transplant after 5 months. Ultrasound
(USG) images of the porta hepatis shows absent color uptake in the main portal vein
(A, yellow arrow) with hypertrophied and tortuous hepatic artery (B, red arrow)—consistent with thrombosis in main portal vein and compensatory increase
in hepatic artery flow. Contrast-enhanced computed tomography (CECT) coronal image
(C) of the upper abdomen shows nonopacification of main portal vein (green arrow), s/o
thrombosis of main portal vein.
Stenosis of the portal vein usually occurs at the site of the vascular anastomosis
with an incidence of less than 1%.[13] Early portal vein stenosis within the first 6 months is usually due to poor iatrogenic
anastomosis whereas late stenosis occurs secondary to neointimal hyperplasia. Abrupt
focal narrowing is seen with PSV of > 125 cm/s. The anastomotic to preanastomotic
PSV ratio is 3:1.[18] CT/MR depicts similar imaging findings in the form of focal significant narrowing
at the anastomotic site. Mild “waisting” of the portal vein is a common finding which
should not be mistaken for stenosis. This often occurs due to discrepancies in the
size of the donor and recipient vein anastomosis. Invasive diagnostic modalities likely
transhepatic portography can also be used to diagnose portal vein stenosis with a
cutoff of > 5 mm Hg gradient.[19]
[20] CT/MR angiography can also be used to identify flow-limiting stenosis in the extra-
and intrahepatic portal veins. Endovascular treatment in the form of a percutaneous
transhepatic portal vein angioplasty with or without stenting is the mainstay of treatment.
Primary stent placement is favored due to the increased risk of hemorrhagic complications
with repeated transhepatic access.
Hepatic Veins and IVC
Several surgical techniques can be used to anastomose donor IVC to the recipient.
End-to-end anastomosis of donor and recipient IVC following resection of the recipient
retrohepatic IVC is the most commonly used technique. Anastomosis of the donor IVC
to the stump of the recipient hepatic vein without resection of retrohepatic IVC is
called the “piggyback” technique. The usual site of stenosis occurs at the anastomotic
site and hence the technique of surgical anastomosis must be known prior.
Just like the other vessels, the most common site for stenosis is the anastomotic
junction. They are rare complications which usually occur late (more than 6 months).
Various risk factors include size discrepancy between donor and recipient IVC, suprahepatic
IVC kinking from organ rotation, intimal hyperplasia or fibrosis compression by graft
edema, or the adjacent collection and hypercoagulable states.[5]
[13] Doppler parameters show an increased velocity at the site of stenosis with focal
aliasing. CT/MR venography demonstrates focal narrowing/stenosis of the IVC with background
features of Budd–Chiari syndrome (hepatomegaly, ascites, pleural effusion) ([Fig. 7]). Percutaneous angioplasty and stenting have become the preferred treatment providing
symptom relief and early clinical outcomes.
Fig. 7 A 48-year-old male patient who underwent orthotopic liver transplantation had high
urine output with deranged renal parameters on 6th postoperative day (POD). Contrast-enhanced
computed tomography (CECT) sagittal images of the upper abdomen shows focal critical
stenosis (A, yellow arrow) in the superior aspect of inferior vena cava (IVC). Axial and coronal
images of the same patient show eccentric hypodense nonocclusive filling defect in
IVC (B and C, green arrow)—consistent with partial IVC thrombosis.
Hepatic vein thrombosis may occur in the early postoperative period secondary to twisting
of the veins, tight anastomosis, and size discrepancy; however, it occurs late in
the course of the postoperative period due to intimal hyperplasia and perivascular
fibrosis. Echogenic thrombus ([Fig. 8]) with loss of triphasicity and decrease in velocity of less than 10 cm/s confirms
hepatic vein stenosis. A pulsatility index of less than 0.45 is also indicative of
hepatic vein stenosis.[2]
[21]
[22] Transstenotic pressure gradient of more than 5 mm Hg warrants treatment. CT/MR venography
can also be used to diagnose hepatic vein stenosis/thrombosis. Early presentation
often requires a surgical revision of the anastomosis while late presentation is usually
managed with percutaneous transhepatic/transjugular angioplasty with or without stenting.[12]
Fig. 8 A 62-year-old male patient—post-deceased donor liver transplantation (DDLT) on 6th
postoperative day (POD) routine Doppler surveillance. Ultrasound (USG) B-mode image
(A) shows iso- to hyperechoic intraluminal thrombus (white arrow) within the right hepatic
vein with no color uptake in Doppler image (B). Contrast-enhanced computed tomography (CECT) axial and coronal sections (C and D) of the upper abdomen of the same patient shows nonopacification in the right hepatic
vein (white arrow) in the venous phase.
Nonvascular Complications
Nonvascular Complications
Biliary Complications
The second most common complication after graft dysfunction is biliary complication.[23] This can be due to biliary leak, biliary anastomotic strictures, stone casts, and
sludge ([Table 2]).
Table 2
Biliary complications following liver transplantation
|
Biliary complications
|
Clinical features/lab parameters
|
Imaging modality of choice
|
|
Biliary stricture
|
• Abdominal pain, yellowish discoloration, elevated bilirubin levels
|
MRCP
|
|
Biliary sludge/calculus
|
• Obstructive jaundice
• Increase in alkaline phosphatase, SGOT, and SGPT
|
|
Biloma/biliary abscess
|
• Fever, abdominal pain, raised total counts
|
Abbreviations: MRCP, magnetic resonance cholangiopancreatography; SGOT, serum glutamic-oxaloacetic
transaminase; SGPT, serum glutamic pyruvic transaminase.
Biliary leaks usually occur in the early postsurgical period (within first month)
commonly associated with HAS/HAT which is typically seen involving the distal biliary
radicles. The bile leak is most commonly from the biliary anastomosis[13]; other possible sites are bile leaks from the cut surface of the graft and caudate
lobe biliary radicals which are left unsutured. Other rare causes include immunological
and cytotoxic injury. Bile can leak into the peritoneal cavity or form an organized
collection in the form of a biloma. Intrahepatic anechoic cystic focus with no evidence
of internal vascularity could represent biloma. Hepatobiliary-specific contrast-enhanced
MRCP can demonstrate the exact anatomical site as well as active leakage of contrast
into the collections.[24]
[25] Nonanastomotic leaks secondary to HAT usually require retransplantation. Cholescintigraphy
(hepatobiliary nuclear imaging) is a sensitive and specific test for biliary leakage.
A bile leak is indicated by the gradual accumulation of radiotracer in the abdomen
that does not match the morphologic features of the intestine.[26] A diagnostic pitfall that can happen in patients who have a Roux-en-Y limb placed
after hepaticojejunostomy is when normal radiotracer build-up in the limb's blind
end is confused with a bile leak.[27] Bile duct leaks are usually treated by placing stents across the site of leakage.
Biliary obstruction is the most common nonvascular complication occurring mostly as
anastomotic site structures. It is due to intimal hyperplasia and scarring of perianastomotic
tissues. Nonanastomotic sites occurring intrahepatically should raise concern for
HAT or HAS. Other causes of nonanastomotic strictures include pretransplant biliary
diseases (primary sclerosing cholangitis) and focal infections.[13] Biliary radicle dilatation caused by strictures is suspected when bilirubin levels
are elevated. However, in a few cases, CT may not demonstrate dilatation of bile ducts.
In such a case, MRCP or endoscopic retrograde cholangiopancreatography or transhepatic
cholangiography should be performed to determine strictures since even in severe stenosis
biliary radicles may not be dilated ([Fig. 9]). Extrahepatic biliary strictures may be treated with simple dilatation or rendezvous
procedure whereas intrahepatic strictures are usually treated by percutaneous transhepatic
biliary drainage. Serial dilatation with periodic upsizing of the drainage tube may
be needed for opening the stricture.
Fig. 9 A 47-year-old male patient, living donor liver transplantation (LDLT) 4 years ago
came with h/o elevated bilirubin levels during routine yearly follow-up. Maximum intensity
projections of biliary system shows focal short segment tight stricture (A and B, yellow arrow) involving the anastomotic site.
Casts and sludge are usually seen within 1 year of transplantation but choledocholithiasis
is seen after 1 year. It usually occurs due to biliary stasis from preexisting chronic
strictures or alteration of the composition of bile following transplantation. On
MRCP this is usually seen as a well-defined T2 hypointense filling defect in the case
of stones but shows irregular margins for biliary casts ([Fig. 10]). This is typically seen in donation after cardiac death cases where significant
warm ischemic times might lead to ischemic necrosis of the intrahepatic biliary tree.
The occurrence of biliary cast syndrome, which is defined as the presence of hard,
black lithogenic material inside the biliary system, is reported to range from 4 to
18% in the literature.[28]
Fig. 10 A 62-year-old male patient living donor liver transplantation (LDLT) 2 years back
with elevated bilirubin. T2 HASTE (Half fourier Single-shot Turbo spin-Echo) axial
image showed focal hypointense filling defect (A, yellow arrow) in the proximal left hepatic duct—may represent calculous/dense sludge.
Maximum intensity projections of biliary system (B, white arrow) show multiple dilated intrahepatic biliary radicles predominantly on
the left side (blue arrow), secondary to short segment stricture involving the junctions
of the left and right hepatic duct confluence. Ultrasound (USG) correlation image
revealed echogenic focus (C, red arrow) with no posterior acoustic shadowing. Corresponding axial computed tomography
(CT) image (D) showed no e/o radiodense focus within the left hepatic duct, s/o dense biliary sludge/cast.
Intra-Abdominal Fluid Collections ([Table 3])
Table 3
Other complications following liver transplantation
|
Complications
|
Clinical features/lab parameters
|
Imaging modality of choice
|
|
Hematoma
|
• Right upper quadrant pain
• Massive bleed leads to acute collapse
|
Contrast-enhanced CT
|
|
Abscess
|
• Fever, abdominal pain, raised total counts
|
Contrast-enhanced CT
|
|
Graft rejection
|
• Deranged LFT, hepatic failure, ascites, encephalopathy
|
Imaging – nonspecific
Biopsy – gold standard
|
Abbreviations: CT, computed tomography; LFT, liver function test.
Perihepatic hematomas are inadvertent complications in the immediate and early postoperative
period. Acute hematomas are echogenic in USG with internal echoes on USG. Subacute
to late hematomas usually appear as less echogenic collections in the perihepatic
and along the paracolic gutters. In the case of acute large hematomas with a significant
drop in hemoglobin, CECT should be done to rule out active extravasation. Any hyperdense
collections (> 40 HU) in CT in the intra- or perihepatic regions with postcontrast
increase in the density confirms recent hematoma with active bleeding ([Fig. 11]). MRI typically shows T1 shortening seen along the hepatic surface, which can produce
a mass effect over the parenchyma in case of very large hematomas. Catheter-directed
embolization of the culprit vessel can be attempted to arrest the bleeding.
Fig. 11 A 41-year-old post-cadaveric liver transplant status (postoperative day [POD] 20)
under routine weekly surveillance. Ultrasound (USG) showed heteroechoic hematoma with
central hypoechogenicity (A, yellow arrow) corresponding to the hyperdensity in computed
tomography (CT) axial images (B).
An abscess can occur due to bacteremia or superadded infection of preexisting collection
or infarcted/ischemic tissue. Since bile acts as an excellent growing medium for bacteria,
superadded infections are much more common in intrahepatic bilomas. It is seen as
thick irregular peripheral rim enhancement on imaging with intrinsic air pockets and
central diffusion restriction on MRI. Any abscess intrahepatically must be treated
with sensitive antibiotics and percutaneously drained to prevent further graft dysfunction.[29]
The expected complication following immediate postsurgery is perihepatic seroma which
may be ill-defined and/or localized with thin perceptible walls. USG shows an anechoic
collection with/without septations. It consists of simple liquid with fluid attenuation
(∼10 HU) in CT and T1 hypo- and T2 hyperintensity in MRI. With time seroma generally
resolves and hence follow-up USGs are generally not necessary.
Intraparenchymal Complications
Intraparenchymal Complications
An overall most common complication is graft rejection; however, imaging plays a limited
role in its diagnosis. It is divided into acute cellular rejection and chronic ductopenic
rejection. Three weeks after the transplant, cellular rejections can occur, and chronic
rejection starts 6 weeks to 6 months later. CT images show nonspecific findings which
include nonhomogeneity of the liver parenchyma, periportal edema, and differential
parenchymal enhancement. Liver biopsy is the gold standard diagnostic test for identifying
acute/chronic rejection.[30]
Any LT is an immunodeficient state due to the administration of immunosuppressive
drugs which leads to posttransplant lymphoproliferative disorder (PTLD). The liver
is the most common abdominal organ to manifest as PTLD; however, it may affect any
organ with a wide range of spectrum. In the liver, these are seen as hypoechoic nodules
in the liver which appear hypodense on CT. They are T1 and T2 hypointense lesions
without postcontrast enhancement. This may be accompanied by enlarged lymph nodes
in the periportal and para-aortic regions.[31] Neoplasms following LT may be due to the recurrence of primary hepatic malignancy
or metastatic disease from a separate primary malignancy. Transplanted patients are
at high risk for the development of de novo malignancies, Kaposi's sarcoma, skin,
cervical, and breast malignancies. Hepatocellular carcinoma most commonly recurs as
lung metastases or as multiple lesions within the liver graft.[32] Proven tumor-related risk factors for hepatocellular carcinoma recurrence after
LT include elevated alpha-fetoprotein, tumor grade/stage, and vascular invasion.[33]
[34]
Splenic Artery Steal Syndrome
Splenic artery steal syndrome is a very rare entity which occurs in the immediate
postoperative period.[28] On Doppler evaluation there are increased RI values with a reduced diastolic component
in the intra- and extrahepatic arteries accompanied by increased PSV in the portal
and splenic vein ([Fig. 12]). In Angiogram, when the hepatic artery is patent and shows poor sluggish flow with
delayed contrast filling in comparison to the rest of the celiac trunk branches, Splenic
artery steal syndrome is diagnosed. The diagnostic criteria are splenic artery diameter > 4 mm
or 150% of the hepatic artery, enlarged gastroduodenal artery, and sluggish hepatic
artery flow.[35]
[36]
[37] No consensus treatment protocol is there in the literature, however, transcatheter
proximal splenic artery embolization using coils is the most acceptable treatment
followed in many institutions.[38]
[39] Other management options include splenic artery ligation and splenectomy. Redemonstration
of normal hepatic artery flow with an RI value of less than 0.8 indicates successful
management.
Fig. 12 A 45-year-old male patient with living donor liver transplantation (LDLT) had increased
drain output on 3rd postoperative day (POD). Spectral Doppler image (A) shows increased resistive index (RI) values in the hepatic artery with absent diastolic
flow (yellow arrow). Maximum intensity projection showed poor opacification of the
hepatic artery (B, violet arrow) with hypertrophied splenic artery (green arrow) in the arterial phase.
Digital subtraction angiography shows proximal splenic artery embolization (C, orange arrow). Immediate postprocedural Doppler image showed increase in hepatic
artery flow (D, blue arrow).
Conclusion
LT is the definite and final resort for decompensated chronic parenchymal liver disease.
The imaging plays a pivotal role in the prompt diagnosis of various postoperative
complications. USG is the initial modality of choice for screening the hepatic parenchyma
and vasculature, where the alarming findings are reassessed with CT which is more
accurate and has a high spatial resolution. Understanding potential posttransplant
complications as well as the benefits and drawbacks of each imaging technique may
help with early detection and prompt treatment.
Teaching Points
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(1) Complications are divided into vascular and nonvascular complications which in
turn are divided into biliary, infections, and immune response. Hepatic artery thrombosis
is the most common vascular thrombosis.
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(2) Hepatic artery thrombosis occurs usually between 2nd to 15th week. Untreated hepatic
artery thrombosis will lead on to biliary ischemia and strictures with adverse outcomes.
Most patients need surgical exploration or endovascular thrombectomy in the event
of an early posttransplant HAT.
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(3) Hepatic artery stenosis occurs within the first 3 months with median time of 100
days. PSV of more than 200 cm/s is highly suggestive whereas other indirect findings
include increase in diastolic component with reduced resistance index to less than
0.55, a delayed acceleration peak (more than 80 ms) together producing the characteristic
parvus et tardus pattern of flow.
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(4) Biliary strictures are the most nonvascular complications which usually occur
at the anastomotic site. It occurs due to intimal hyperplasia and perianastomotic
site scarring. Nonanastomotic site strictures should raise the suspicion for hepatic
artery thrombosis.
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(5) Splenic artery steal syndrome is a rare complication that occurs in the immediate
postoperative period. Splenic artery diameter of more than 4 mm or more than 150%
of hepatic artery enlarged gastroduodenal artery and sluggish hepatic artery. Transcatheter
proximal splenic artery embolization (SAE) using coils is the most acceptable treatment
followed in many institutions.
