Diagnostic ultrasound ( PDFDrive )

CHAPTER 18 Organ Transplantation 631
FIG. 18.8 Bile Duct: Sludge. Oblique sonogram shows intraluminal
sludge, secondary to ascending cholangitis, in the CBD (arrow), with
extension into the right hepatic duct (arrowhead).
Hepatic Artery Thrombosis
Hepatic artery thrombosis is the most important vascular
complication of liver transplantation, with an incidence of 2.5%
to 6.8% and mortality as high as 35%. 28 If retransplantation is
not performed for these patients, mortality can increase to 73%. 29
he pathophysiology is oten diicult to decipher. Risk factors
include patients requiring complex vascular reconstruction
(caused by multiple arterial supply to the liver or small donor
and recipient vessels), rejection, severe stenosis, increased cold
ischemic time of the donor liver, and ABO blood type
incompatibility. 8,30
Ater transplantation, the donor bile duct is entirely dependent
on the transplanted hepatic artery, particularly the right, for its
arterial blood supply. herefore patients with hepatic artery
thrombosis can present clinically with delayed biliary leak,
fulminant hepatic failure, or intermittent episodes of sepsis
thought to be secondary to liver abscess formation within infarcted
tissue. 30 However, the clinical presentation, imaging indings,
and patient outcomes are related to the timing of thrombosis
of the hepatic artery. Hepatic artery thrombosis occurring within
1 month of transplantation can be classiied as early hepatic
artery thrombosis. his is oten associated with biliary tract
necrosis, bacteremia, acute fulminant hepatic failure, and a high
patient morbidity rate. 29 Gray-scale sonography may show the
hepatic artery at the porta hepatis; however, no low is detected
on color or spectral Doppler in the hilum or parenchyma.
Hepatic artery thrombosis occurring ater 1 month of transplantation
can be classiied as late hepatic artery thrombosis.
his is usually associated with a milder clinical course, with
patients remaining either asymptomatic for months to years or
showing an insidious course eventually involving biliary tract
complications, relapsing fevers, or bacteremia. It is thought that
the development of collateral arterial vessels, as early as 2 weeks
ater surgery, accounts for the survival of the transplant in these
patients. Although resection of all vascular connections in the
transplant can hinder development of collateral circulation, arterial
collateral vessels could develop from the angiogenic potential
of the omentum and mesentery. On ultrasound, a tardus-parvus
arterial waveform (RI < 0.5; AT > 100 ms) is detected within
the hepatic parenchyma (Fig. 18.10). Within the hilum, no arterial
low is demonstrated, or if periportal arterial collaterals are
present, a tardus-parvus waveform may be detected. herefore
demonstration of arterial low in the hepatic parenchyma does
not exclude the presence of hepatic arterial thrombosis, and
meticulous inspection of the parenchymal waveform is warranted
29,30 (see Fig. 18.10).
Occasionally, a false-positive diagnosis of hepatic artery
thrombosis can occur with severe hepatic edema, systemic
hypotension, and high-grade hepatic artery stenosis. 8 In situations
with poor visibility of the porta hepatis because of abdominal
girth or overlying bowel gas, lack of detectable low within the
hepatic artery should be viewed with caution and conirmed on
computed tomography angiography (CTA).
Hepatic Artery Stenosis
Hepatic artery stenosis has been reported in up to 11% of
transplant recipients and most oten occurs at or within a few
centimeters of the surgical anastomosis. Risk factors for development
of stenosis include faulty surgical technique, clamp injury,
rejection, and intimal trauma caused by perfusion catheters. 27
Clinically, patients have biliary ischemia and/or abnormal LFT
values.
Doppler ultrasound can provide direct and indirect evidence
of hepatic artery stenosis. Direct evidence involves identifying
and localizing a hemodynamically signiicant narrowing within
the vessel. he porta hepatis should be initially screened with
color Doppler ultrasound to detect a focal region of color aliasing
within the hepatic artery, which indicates high-velocity turbulent
low produced by the stenotic segment. If the stenosis is hemodynamically
signiicant, spectral tracing will reveal peak systolic
velocity (PSV) of greater than 2 to 3 m/sec, with associated
turbulent low distally. Indirect evidence of hepatic artery stenosis
includes a tardus-parvus waveform anywhere within the hepatic
artery (RI < 0.5; AT > 100 ms). his waveform suggests the
presence of a more proximally located stenotic region. 27 Indirect
evidence of stenosis is much more common in clinical practice
than documentation of the stenosis itself (Figs. 18.11 and 18.12).
he presence of an intraparenchymal tardus-parvus waveform
indicates alterations in the intrahepatic arterial bed from impaired
arterial perfusion of the liver. Although it is detected most oten
in patients with hepatic artery stenosis, tardus-parvus waveform
may also result from collateral vessels arising from hepatic artery
thrombosis or, less frequently, from severe aortoiliac atherosclerosis.
herefore an intraparenchymal tardus-parvus waveform
cannot distinguish between hepatic artery stenosis and thrombosis
if the hepatic arterial trunk is not visualized and meticulously
investigated. 31
Mild degrees of hepatic artery narrowing may also be present
without Doppler abnormalities. herefore if clinical suspicion
is high, a normal Doppler study should not preclude further