This document discusses multimodality imaging of livers after transplant. It begins with an introduction to liver transplantation and its increasing prevalence. It then provides an overview of imaging techniques used, focusing on Doppler ultrasound and CT/MR angiography. The document describes normal postoperative findings for the hepatic artery, portal vein, and hepatic veins. It identifies hepatic artery thrombosis and stenosis as important complications and provides details on their ultrasound and CT/MR imaging appearances. The goal is to help radiologists recognize critical diagnoses that can affect the health and survival of transplant recipients.

1. Multimodality Imaging after
Liver Transplant
Capt. Soe Moe Htoo
Radiology Dept., DSLH

2. Introduction
• Liver transplant remains the only treatment option for those with end-
organ failure.
• Liver transplant is the second most common type of organ transplant.
• With continued improvement in graft survival, more patients are living with
liver allografts.
• As a result, radiologists are performing imaging of transplanted livers in
their day-to-day practice.
• It is vital that radiologists recognize critical diagnoses that affect the
health and survival of the hepatic graft and graft recipient.

3. Overview of Imaging Techniques
• The surgical notes should be reviewed at the time of imaging to
understand the vascular and biliary surgical anastomoses and
ensure that all surgical anastomoses have been evaluated.
• Doppler US is the initial imaging examination following transplant
because it can be performed at the bedside and allows evaluation
of the vasculature (Table 2).

5. Normal Postoperative Findings
Normal Hepatic Artery
• The normal hepatic artery displays continuous diastolic flow with a
resistive index (RI) of 0.5–0.8.
• Sharp upstroke with an acceleration time shorter than 0.08 second.
• A wide range of hepatic artery peak systolic velocity (PSV) values,
ranging from 13 to 367 cm/sec, have been documented in the early
postoperative period.
• An elevated PSV may be caused by transient self-resolving anastomotic
edema or persistent portal hypertension.

6. Normal Hepatic Artery Waveform

7. • An elevated RI (>0.8) or transient absence of diastolic flow in the
hepatic artery is very common in the early postoperative period,
occurring in up to half of liver allograft recipients
• Risk factors include older age of the donor and prolonged ischemic
time.
• This usually normalizes within 4 days after the surgery.
• In contrast, a low RI (<0.6) in the early postoperative period is
associated with an increased risk of vascular complications, with
approximately 80% specificity, and should be closely monitored.

8. Transient elevated RI in a 44-year-old man immediately following liver transplant.
(A) Postoperative day 0 shows an elevated RI (1.0) in the hepatic artery
(B) Findings of CEUS performed at the bedside confirm the patency of the
hepatic artery at the porta hepatis (white arrow).

9. Normal Portal Vein
• The portal vein has continuous hepato-petal flow with mild cardiac and
respiratory variations (Fig 1).
• The surgical anastomosis may have a small caliber change of up to 5 mm, which
is often insignificant.
• In the early postoperative period, the portal venous velocity often increases to
greater than 50 cm/sec with turbulent flow.
• This is believed to be due to compression of the portal vein by postoperative
edema or fluid collections, or it may result from a transient reactive increase in
splanchnic flow.
• A mismatch in size between the donor and recipient portal veins also may be
responsible for the increased velocity and turbulence in the early postoperative
period, and it usually normalizes over several weeks.
• In addition, portal vein gas can be a normal finding in the first few weeks after the
transplant.

10. Normal Potovenous Waveform

11. Normal Hepatic Vein
• The normal hepatic venous waveform is triphasic owing to the
cardiac cycle of the right heart chambers.
• Loss of phasicity may occur in the early postoperative period as a
result of edema of the graft.

12. Normal Hepatic Venous Waveform

13. Important Complications
Hepatic Artery Thrombosis
• most common and potentially devastating vascular complication
after liver transplant. (overall incidence of 4.4%)
• common cause of graft loss (53% of patients undergo repeat
transplant) and has a high mortality rate (33%) in the early
postoperative period.
• The clinical picture varies from fulminant graft failure to biliary
sepsis.
• The median time to detection is 6.9 days.

14. • With refinement of surgical techniques, the incidence has decreased
during the past few decades.
• Early hepatic artery thrombosis is treated with revascularization if it is
diagnosed early, repeat transplant, or observation if the clinical
manifestations are mild.
• After liver transplant, the hepatic artery is the sole supplier of blood to the
biliary tree.
• Early thrombosis results in potentially catastrophic consequences of
extensive biliary necrosis and graft infarction.

15. • Doppler US findings of impending thrombosis, including low-velocity
high-resistance flow, should prompt urgent evaluation with contrast-
enhanced US or CTA.
• Nolten described a predictable progression of the following US findings:
loss of diastolic flow (elevated RI) followed by dampening of the systolic
peak and finally complete loss of hepatic arterial flow (Figs 4, 5).
• The diagnosis of hepatic artery thrombosis should be confirmed with
contrast-enhanced US, or with CTA, particularly if there is a discrepancy
between the patient’s clinical picture and the Doppler US findings or if the
Doppler US findings are unclear.

16. (A)Duplex US image 1 day after transplant shows absent diastolic flow, with an RI of 1.0 and low velocity
(34.1 cm/sec) in the hepatic artery. Doppler US owing to concern for impending hepatic artery
thrombosis.
(B)Power Doppler US image 3 days after transplant shows a complete loss of flow in the hepatic artery.
(C)Contrast-enhanced MR image shows hepatic artery occlusion
Fourteen days after transplant, the patient underwent repeat liver transplant.
Fig: 4

17. Early hepatic artery thrombosis with hepatic infarct in a 44-year-old man with markedly elevated
liver function test results at routine follow-up 2 weeks after transplant.
(A) Duplex Doppler US image of the region of the hepatic artery at the porta hepatis shows
trace remnant flow with poor arterial pulsatility, suggestive of impending hepatic artery
thrombosis. A strong arterial tracing was seen in the celiac axis, but the hepatic artery origin
could not be found (not shown).
(B) Transverse gray-scale US image of the left hepatic lobe shows a peripheral wedge-shaped
hypoechoic heterogeneous area (arrow) consistent with hepatic infarct.
Fig: 5

18. (C) Axial follow-up CTA image 8 hours later shows complete hepatic artery thrombosis (arrow) with
soft-tissue thickening surrounding the thrombosed artery.
(D) Venous phase CT image shows the same infarct (arrow) in the left hepatic lobe.
The patient required repeat liver transplant 4 days later. Pathologic analysis of the explanted liver
revealed massive panlobular hepatocyte necrosis and bile duct loss, consistent with hepatic artery
occlusion.
Fig: 5

19. • Hepatic artery thrombosis is diagnosed when there is an absence
of Doppler flow in the hepatic artery proper and the intrahepatic
branches.
• US has nearly 100% sensitivity for early hepatic artery thrombosis,
especially in the 1st week after transplant.
• Although US is very sensitive, it is susceptible to false-positive
results due to slow flow.
• Hepatic artery thrombosis can also affect the liver parenchyma.
• Parenchymal infarct and necrosis appear as a peripheral wedge-
shaped area of heterogeneous echotexture on gray-scale US
images and as non-enhancing hypoattenuating areas on CT
images (Fig 5).
• Air may be present within the infarct and can mimic an abscess
(Fig 6).

20. Fig: 6
Hepatic infarct with necrosis and air in a 57-year-old woman with
elevated liver function test results 3 weeks after living-donor
transplant.
Axial NECT image shows a collection of air (arrow) in the right hepatic
lobe, consistent with a large infarct in the hepatic graft.
The hepatic artery was occluded at US (not shown), and hepatic artery
thrombosis was confirmed with catheter angiography.
The patient required repeat liver transplant several days later.

21. • In the early postoperative period, a high RI (>0.8) in the hepatic
artery can be seen in multiple scenarios, including postoperative
edema, vasopressor drug use, impending arterial thrombosis,
splenic arterial steal, and primary graft nonfunction (Fig 7).
• Correlation with the patient’s clinical condition and liver function test
results helps guide further investigations.

23. Hepatic Artery Stenosis
• Hepatic artery stenosis usually affects the anastomosis and is the most
common arterial complication after liver transplant.
• The clinical manifestations of hepatic artery stenosis overlap with those of
delayed thrombosis.
• Hepatic artery stenosis is amenable to endovascular therapy, so imaging plays
a vital role in differentiating these two conditions.

24. • The Doppler US findings in the intrahepatic and main arteries
include classic parvus tardus and an RI lower than 0.5.
• Broadening the criteria to include a mild parvus tardus waveform in
the main hepatic artery improves the sensitivity of Doppler US for
detecting hepatic artery complications (Fig 9)
• Criteria have been suggested:
• an RI lower than 0.4 and a systolic acceleration time longer than
0.12 second
• a classic parvus tardus waveform
• PSV higher than 200 cm/sec at or just beyond the stenosis
• PSV lower than 48 cm/sec in the hepatic artery distal to the
stenosis in association with abnormal liver function test results.

25. • Owing to the deep location of the hepatic artery anastomosis, this
can be quite challenging.
• If the proximal segment of the hepatic artery is obscured by bowel
gas, a deep location, or tortuosity of the hepatic artery, then CTA or
MR angiography should be performed.

26. Hepatic artery stenosis in a 58-year-old man with new increasing alkaline phosphatase and
transaminase levels 5 weeks after liver transplant.
(A) Duplex US image of the main hepatic artery at the porta hepatis shows a borderline low RI and mild
parvus tardus waveform, with blunting of the systolic peak. This subtle change in waveform prompted
close evaluation of the intrahepatic arteries and proximal main hepatic artery for possible arterial
complications.
(B) Duplex US image of the intrahepatic artery shows a classic parvus tardus waveform and low RI,
suggestive of hepatic artery stenosis.

27. (C) On the duplex US interrogation image of the proximal main hepatic artery, the stenosis is
directly visualized, with color aliasing and a PSV of 593 cm/sec.
(D) Catheter angiographic findings confirm the stenosis (arrow). The patient was treated with
angioplasty, and his liver function test results dramatically improved the week following treatment.

28. Splenic Artery Steal
• Splenic artery steal syndrome, also called nonocclusive hepatic
artery hypoperfusion, is a cause of graft ischemia.
• The reported incidence ranges from 0.6% to 10.1%, although the
true incidence may be higher owing to under recognition and under
reporting.
• Splenic artery steal syndrome occurs predominantly in the early
post-operative period, within 2 months after transplant.
• Quintini et al suggested that it is due to primary portal hyper
perfusion with compensatory hepatic artery hypoperfusion
secondary to the hepatic artery buffer response.

29. • The clinical manifestation of splenic artery steal syndrome is
nonspecific.
• Most patients have elevated transaminase levels.
• Less common findings include graft dysfunction, graft failure,
recurrent ascites, and findings of hypersplenism such as
splenomegaly and thrombocytopenia.
• Doppler US findings include an elevated RI (>0.8), hepatic artery
systolic velocities lower than 35 cm/sec, and portal hyper perfusion
with elevated portal venous velocity.

30. • CT findings of splenic steal (Non-specific)
• splenic artery size larger than 4 mm or greater than 150% of the
diameter of the hepatic artery
• splenomegaly with a splenic volume greater than 829 mL
• Catheter angiography shows reduced blood flow to the hepatic
artery and preferential flow to the splenic artery, gastroduodenal
artery, or left gastric artery (Fig 11).
• The most common treatment for splenic artery steal is splenic
artery embolization.
• Post treatment US often reveals normalization of the hepatic artery
systolic velocity.

31. Splenic steal syndrome in a 58-year-old man after liver transplant.
(A) Doppler US image 4 days after transplant shows a persistently low PSV and an
elevated RI in
the hepatic artery, which prompted further evaluation with catheter angiography.
(B) Catheter angiogram of the celiac artery shows preferential flow toward the spleen
(arrow) and away from the hepatic artery. The patient was treated with splenic artery coil
embolization.
(C) Catheter angiogram shows improved flow toward the hepatic graft (white arrow) after
splenic artery embolization.

32. Portal Vein Thrombosis
• Portal vein thrombosis is the most common portal venous complications.
• Risk factors include a hyper-coaguable state, increased downstream
resistance, decreased portal venous inflow, prior portal venous surgery
(eg, transjugular intrahepatic portosystemic shunt), prior portal vein
thrombosis, and surgical technical problems (eg, significant difference in
caliber between recipient and donor portal veins).
• Portal vein thrombosis appears as a filling defect in the portal vein on
contrast-enhanced images and color Doppler US images and may be
hyperechoic or anechoic at gray-scale US (Fig 13).

33. Portal vein thrombosis involving the main and right portal veins in a 58-year-old man with
abnormal liver function test results 8 months after liver transplant.
(A)Doppler US image shows an echogenic thrombus filling the right portal vein, with a
complete lack of flow. The spectral waveform findings are due to the adjacent right
hepatic artery.
(B)Contrast-enhanced CT image shows a filling defect extending from the portal
confluence (arrow) into the right portal vein (not shown), consistent with thrombus.

34. Portal Vein Stenosis
• less common than portal vein thrombosis
• most commonly due to anastomotic stricture
• US findings
• portal vein peak anastomotic velocity higher than 125 cm/sec
• anastomoticto-preanastomotic velocity ratio of 3:1
• velocity change of 60 cm/sec across the anastomosis (Fig
14).

35. Figure 14. Portal vein stenosis in a 56-year-old man with mildly elevated liver function test
results 6 months after liver transplant.
(A) Doppler US image shows a markedly elevated velocity (206 cm/sec) at the stenotic segment
in the mid main portal vein.
(B) Doppler US image of the more proximal segment of the main portal vein shows a normal
velocity (56.7 cm/sec).

36. Hepatic Vein Outflow Obstruction
• Outflow obstruction occurs with findings of portal hypertension or
graft dysfunction.
• Hepatic vein and IVC complications are rare, with an overall
incidence of 1%.
• Outflow obstruction can be caused by stenosis, thrombosis, or graft
torsion.

37. Hepatic Vein and IVC Stenosis
• Hepatic vein and IVC stenoses are more common in LDLT and pediatric
transplants because of the more complex venous reconstruction (Fig 15),
and the incidence has been reported to be as high as 5% in LDLT.
• US findings include a monophasic venous spectrum, reversal of the flow
direction, and reversal of portal venous flow in severe cases.
• The stenosis is most commonly due to anastomotic stricture.
• Risk factors include pediatric transplant, split transplant, repeat
transplant, size discrepancy between the donor and recipient veins, and
supra caval kinking.
• US findings include a monophasic venous spectrum, which is sensitive
but not specific, and a venous pulsatility index lower than 0.45, which is
95% specific.
• Treatment is typically balloon angioplasty and stent placement.

38. Caval stenosis after three liver transplants in a 15-year-old girl with a history of biliary atresia.
(A) Doppler US image shows narrowing and a markedly elevated velocity (152 cm/sec) in the middle hepatic vein.
Stenosis was suspected, given the multiple repeat pediatric liver transplants, which require a more complex venous
reconstruction.
(B) Findings of catheter venography 1 day later confirmed stenosis, and the elevated right atrium–hepatic vein
pressure gradient was 16 mm Hg. The stenotic segment (arrow) measured 5 mm in diameter.
The patient was treated with angioplasty and stent placement, and the right atrium–hepatic
vein pressure gradient normalized after treatment.

39. Hepatic Vein and IVC Thrombosis
• Risk factors for hepatic vein thrombosis include hyper-coaguable state or
surgical factors, in contrast to the risk factors for stenosis, which is
typically related to the surgical anastomosis.
• US images show an echogenic thrombus in the hepatic veins, and there
may be altered perfusion in the affected liver segments on contrast-
enhanced CT and MR images (Fig 16).
• Thrombosis can occur in the IVC as well.
• The caudal blind-ending portion of the piggyback anastomosis often
becomes thrombosed without adverse clinical consequence.

40. Hepatic vein and IVC thromboses, with elevated liver function test results, 3 weeks after liver transplant in
a 50-year-old woman with a history of antiphospholipid antibody syndrome. ‘
(A)Color Doppler US images at the level of the confluence of the hepatic veins show a nonocclusive
echogenic thrombus extending into the piggyback caval anastomosis (arrows). Note the reversal of
flow in the middle hepatic vein (arrowhead).
(B)Findings on a spectral Doppler US image at the same level confirm the reversal of flow in the middle
hepatic vein (arrowhead) and color blooming artifact (arrow) associated with the thrombus in the IVC.
(C)Contrast-enhanced CT image shows a thrombus extending from the left and middle hepatic veins into
the piggyback anastomosis (white arrow). The patient also had a left portal vein thrombus (not shown)
that caused an infarct (black arrow) and contributed to the hypoperfusion in the left hepatic lobe.

41. • Bridging vein occlusion or stenosis also may cause venous outflow
obstruction and focal graft congestion.
• Bridging veins may serve as important venous outflow tracts along
the surface of a right hepatic lobe graft where the middle hepatic
vein was preserved in the allograft donor.
• Bridging veins can be small in caliber and thus difficult to evaluate
with gray-scale or Doppler US; however, they are often well seen
on contrast enhanced US images.

42. Biliary Strictures
• most common biliary complication, with incidence of 5%–15% after
deceased-donor liver transplant and up to 28 % following LDLT.
• may manifest as cholangitis or asymptomatically with laboratory evidence
of cholestasis (Fig 18).
• Strictures are classified as anastomotic or non-anastomotic.
• Anastomotic strictures are more common, occur in the extrahepatic duct,
and are not associated with decreased graft or patient survival.
• In contrast, non-anastomotic strictures are less common, more likely to
occur at the hilum or multifocally within the intrahepatic ducts, and
associated with decreased graft survival.
• Non-anastomotic structures are most commonly ischemic (Figs E3, E4),
but they may also be due to infection or recurrent sclerosing cholangitis.

43. Anastomotic biliary stricture with elevated liver function test results in a 29-yearold woman with
a history of liver transplant 9 years previously. Her medical history was also notable for aplastic
anemia 1 year after the transplant.
(A) US image shows abrupt narrowin of the midportion of the common bile duct (CBD) (arrow),
with upstream biliary duct dilatation.
(B) MR cholangiopancreatographic (MRCP) image shows an obstructing stricture at the
midportion of the common bile duct, at the site of the anastomosis (arrow).
A dilated cystic duct stump is adjacent to the common bile duct at the porta hepatis
(arrowhead). The patient was treated with balloon dilation of the strictured segment and biliary
stent placement.

44. Bile Leakage
• Bile leaks are common early postoperative complications, occurring in up to 20%
of transplants, and are the second most common biliary complication.
• They are associated with decreased patient and graft survival following liver
transplant.
• Leaks most commonly occur at the anastomosis, although they may also be at
the T-tube exit site if a T-tube is used, from an aberrant duct or cystic duct stump,
or from ischemic injury.
• Bile leakage may manifest as abdominal pain, fever, and/or peritonitis.
• Contrast material leakage is seen at cholangiography or at MRI with hepatocyte
specific contrast media (eg, gadoxetate disodium [Eovist])
• Hepatobiliary iminodiacetic acid scans show radiotracer leakage outside of the
liver, biliary tree, or bowel.
• Leaks are managed surgically or with endoscopic or percutaneous biliary
intervention.

45. Neoplasm
• Liver allograft recipients are at increased risk for malignancy owing
to the immunosuppressive therapy they undergo and preexisting
conditions, such as viral hepatitis or alcohol use, that precipitate
end-stage liver disease.
• Posttransplant lymphoproliferative disorders (PTLDs) include an
Epstein-Barr–associated spectrum of disease ranging from
lymphatic proliferation to lymphoma.

46. • Because liver transplant is offered in select cases of HCC or
cholangiocarcinoma, knowledge of the indications for transplant is critical.
• Any new mass in patients with these cancers should raise suspicion for
recurrent or metastatic disease.
• HCC or cholangiocarcinoma may recur in the hepatic allograft, in adjacent
lymph nodes, or as distant metastases.
• Follow-up imaging with CT or MRI of the abdomen and pelvis for 2–3
years after transplant and following of α-fetoprotein levels are indicated if
HCC was present in the explanted liver.

47. Conclusion
• After liver transplant, complications affecting the hepatic artery and biliary tree are most
likely to threaten the health and survival of the graft.
• Arterial complications are the most common and often the most clinically significant.
• Biliary complications are often related to underlying arterial disease, because the
hepatic artery is the sole vascular supplier of blood to the biliary tree following
transplant.
• Portal venous and hepatic venous complications are much less common overall.
• US is the initial imaging modality of choice; however, abnormal US findings should be
interpreted in conjunction with the clinical picture and liver function test results.
• Additional imaging examinations such as short-interval follow-up US evaluation;
contrast-enhanced US, CTA, or MR angiography; and MRCP are warranted to confirm
critical findings or clarify equivocal results.

48. Thank You