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\begin{document}

\title{Splenic artery steal syndrome after liver transplantation: A case series
and review of literature}



\author[1]{Assim Saad Eddin}%
\author[2]{Abhiram kamaraju}%
\author[3]{Umar Ramzan}%
\author[2]{Jay Yu}%
\author[2]{Surbhi Dadwal}%
\author[2]{Sandeep Laroia}%
\affil[1]{University of Iowa Hospitals and Clinics}%
\affil[2]{University of Iowa Health Care}%
\affil[3]{Northwestern University Feinberg School of Medicine}%


\vspace{-1em}



  
  \date{June 17, 2024}


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\emph{Splenic artery steal syndrome after liver transplantation: A case
series and review of literature}

Assim Saad Eddin, MD\textsuperscript{1} ;Abhiram Kamaraju,
MBBS\textsuperscript{1}; Umar Ramzan, BS\textsuperscript{2}, Jay Yu,
MD\textsuperscript{1} ;Surbhi Dadwal, MBBS\textsuperscript{1}; Laroia
Sandeep, MD\textsuperscript{1}

1.University of Iowa Hospitals and Clinics, Department of Radiology,
Iowa city, Iowa, United States

2.Northwestern University Feinberg school of medicine, Chicago,
Illinois, United States

Corresponding author:

Dr. Assim Saad Eddin

Department of Radiology, University of Iowa hospitals and clinics

Email: assim-saadeddin@uiowa.edu

\emph{Keywords: Radiology and Imaging}

\emph{Word count:} \textbf{2648}

\emph{Key Clinical Message:}

Splenic steal syndrome (SASS) represents a challenge to interventional
radiologists after orthotopic liver transplantation. In this case
series, we present three cases of patients who developed SASS after
their liver transplants.

\emph{Introduction:}

Hypoperfusion of the hepatic artery includes two subtypes, which are
SASS and gastroduodenal steal syndrome. It is a nonocclusive disease of
the hepatic artery that often presents within 60 days of liver
transplantation (1). In addition to hypoperfusion of the hepatic artery,
SASS presents with blood flow being diverted to splenic parenchyma
through the splenic artery, and this syndrome may be an under-recognized
contributor to graft ischemia (2). Although most cases of SASS are
discovered within 60 days of liver transplantation, SASS can present up
to 5.5 years post-transplantation (3). The incidence of SASS ranges from
0.6\% to 10.1\% in liver transplant recipients (4). This wide range in
incidence is due to no fixed objective diagnostic criteria (4). It is
mainly a diagnosis of exclusion, and two important alternate diagnoses
often considered are hepatic artery stenosis and hepatic artery
thrombosis. Some studies have placed importance on pre-transplant
evaluation for risk factors and potential subsequent intervention to
reduce the risk of SASS (5,6). However, studies that have sought out
potential risk factors such as spleen-liver ratio, splenomegaly, and
pre-transplant splenic and hepatic artery size have had mixed results
(7,8,9).

\emph{Clinical manifestations:}

The hepatic artery hypoperfusion leads to a nonspecific hepatic
dysfunction which is detected by elevated liver enzymes in the acute
stage (less than 2 months) (7). However, patients often present with
other complications such as ascites 2 months after the procedure, which
is considered an overt sign of hepatic dysfunction (2). Cholestasis,
biliary ischemia, and hypersplenism are also possible complications of
SASS (1,4,10). Overall, the clinical features of SASS are not
consistent, and patients can range from being asymptomatic to having
acute liver failure (3).

\emph{Histology:}

Histologically, SASS has been noted to demonstrate cholestasis,
epithelial ductal regressive changes, and centrilobular zone necrosis
(1,11,12,13). If transplant biopsy were performed, SASS generally
demonstrates mild inflammation, which contrasts with the overt findings
seen during acute rejection (1). Potential consequences of SASS feature
early graft dysfunction and biliary ischemia, potentially leading to
re-transplantation (2,4).

Some institutions perform either prophylactic or post-transplant
treatment procedures in up to 25\% of all transplant patients (4). The
outcome of SASS depends on the time since the hepatic artery suffered
ischemia. Therefore, it is necessary to diagnose and treat the
complication as soon as possible (14). The diagnosis of SASS is
particularly challenging as it has nonspecific signs such as elevated
LFTs, cholestasis and graft dysfunction (14).

\emph{Case history/examination:}

Case 1:

A70-year-old white female with a history of arthritis was evaluated for
preop surgical clearance by her PCP prior to scheduling left knee
replacement. Blood work at the hospital revealed elevated LFTs.

Ultrasound of the abdomen revealed cholelithiasis with intra- and
extrahepatic duct dilatation. She underwent ERCP with sphincterotomy and
biliary and pancreatic stent placement. However, the patient continued
to have jaundice and elevated LFTs. She underwent a repeat ERCP with
placement of biliary stent and removal of pancreatic stent. The patient
eventually developed abdominal pain after stent placement and then
presented to the emergency room.

A CAT scan of the abdomen and pelvis revealed severe dilatation of
intrahepatic bile ducts of both right and left hepatic lobes with abrupt
cutoff of the hepatic ducts just above the confluence suggesting
high-grade obstruction from tumor. Patient was referred to our
institution where she was found to have intrahepatic biliary ductal
dilation with suggestion of obstruction from the mass at the hilum. She
was subsequently evaluated with MR cholangiopancreatography and was
noted to have marked intrahepatic biliary dilation with cutoff of the
right and left ducts at the porta hepatis which is unchanged raising the
question of possible hilar cholangiocarcinoma. Extrahepatic bile duct
was of normal caliber. Labs at that time revealed a mild elevation of
CEA at 7 and CA-19-9 at 103. The patient had ERCP with sphincterotomy,
spyglass with biopsy, and 2 biliary stents placed. Bile duct biopsy
revealed atypical epithelial cells suspicious for carcinoma. Subsequent
blood work revealed elevated total bilirubin of 10. Pathology was
reviewed at the hospital and the diagnosis of adenocarcinoma was
confirmed. Over the next three months, patients complained of a loss of
appetite and had significant weight loss. She also started complaining
of upper abdominal pain after stent placement. She complained of nausea
with dry heaves. She complained of weakness, lightheadedness, itching,
and insomnia. Since the jaundice began, a severe rash developed on her
abdomen and legs. Patient then underwent right hepatic lobectomy,
periportal lymph node dissection, bile duct resection, roux-en-y
hepatico-jejunostomy for the diagnosed Klatskin's tumor. She was
eventually transferred to the SNICU, as planned, post operatively. She
tolerated the procedure well, but her post operative course has been
complicated by liver failure, likely SFSS complicated by SBP and further
decompensation including encephalopathy and hepatorenal syndrome.

She eventually underwent proximal splenic artery coil embolization to
decrease portal hypertension. She has been on broad spectrum antibiotics
and caspofugin for enterobacter and C. glabrata SBP as well as fungemia.
The patient was transferred to the hospital floor where she slowly
improved, but her liver function remained poor. The patient had
worsening confusion and lactulose was restarted with subsequent
improvement.

She eventually experienced diarrhea, so the lactulose was discontinued.
The patient subsequently developed hypernatremia and had ascites
requiring multiple paracenteses. She continued taking antibiotics for
bacterial and fungal infections (UTI, pneumonia, and bacterial
peritonitis). Despite the medications, her labs continued to show liver
dysfunction with evidence of hepatorenal syndrome. She was readmitted to
the SNICU due to difficulty with hypotension, and where she was
restarted on CRRT.

She continued to have difficulty with sepsis/ongoing infections with
some isolates growing resistant organisms, sepsis, liver failure, fluid
collections requiring IR drainage, hypotension with pressor requirement,
renal failure with persistently low urine output, and lactic acidosis.

Case 2:

A74-year-old white female with a history of end stage liver disease from
alcoholic cirrhosis complicated by portal hypertension, ascites,
esophageal varices and hepatic encephalopathy. The patient underwent
orthoptic liver transplantation and was able to cope with the procedure
well. Post transplantation, the patient was transferred to SNICU, and
liver function tests (LFTs) were monitored. The liver numbers were
elevated, particularly AST and ALT.

There was a slight elevation in the creatinine post transplantation,
which was indicative of Acute Kidney Injury (AKI). Preoperative US
showed diminished diastolic flow (Figure 1A). Post operative liver US
(Figure 1B) demonstrated reversal of diastolic flow in the hepatic
artery with high resistivity index and high portal vein velocity
concerning for hepatic arterial hypoperfusion.

The IR team was consulted to evaluate SASS. A celiac angiogram (Figure 2
A and B) was performed which demonstrated findings consistent with SASS.
The patient underwent successful embolization of splenic artery with Amp
Latzer plug. Post procedural ultrasound demonstrated improved flow in
the hepatic artery with improved peak velocities and forward diastolic
flow (Figure 2B). After the procedure, there were no complications, and
the patient was transferred to the hospital floor. The liver numbers
improved post embolization and were within normal range after 2 days.
There was a spike in the liver enzymes that raised concern for acute
rejection. The patient underwent liver biopsy showing mild to moderate
acute rejection, which was treated with pulse dose steroids. Post
treatment, the liver numbers decreased gradually.

Case 3:

A 68-year-old white male with end stage liver disease (ESRD),
decompensated cirrhosis secondary to alpha-1 antitrypsin deficiency and
nonalcoholic steatohepatitis, complicated by a single episode of
variceal hemorrhage. The patient underwent orthoptic liver
transplantation.

He also had a history of nonocclusive portal and mesenteric vein
thrombosis secondary to antithrombin III deficiency. Intraoperatively, a
large pre-existing portal vein thrombus was removed. He was transferred
to the Surgical Intensive Care Unit (SICU) post transplantation. Post
operative Duplex ultrasound of the liver demonstrated no presence of
thrombus in the hepatic or portal veins. His liver numbers were high
post-transplant but were down trending.

The patient was extubated and then transferred to the hospital floor. He
had a single spike of fever, but his blood and urine cultures were
negative. Ultrasound was performed and showed increased hepatic artery
resistive index, spectral broadening and decreased phaticity of hepatic
vein flow. The patient had no major symptoms. During his stay on the
floor, there was a notable rise in GGT and ALP.

His post-operative course was complicated with an AKI and was managed
with n-acetylcysteine. The patient reported shortness of breath and
chest pain. There was a significant drop in the hemoglobin and blood
pressure. CXR showed right basilar atelectasis, and CT angiogram
demonstrated a large hepatic hematoma with hepatic rupture of the
posterior right lobe and a diffusely narrowed hepatic artery. He was
immediately transferred to the SICU and effectively managed and stable
for the rest of his stay. He suffered diarrhea secondary to laxatives,
Clostridium difficile was ruled out.

The patient was transferred to the floor again, his liver numbers
improved, except for GGT and ALP which remained elevated. The explanted
liver was later found to have granulomas containing Histoplasma.

The patient continued regular follow-up and lab draws post-transplant.
His liver numbers returned to normal after 3 months. However, creatinine
was slightly elevated and was presumed to be due to Calcineurin
inhibitor nephrotoxicity. The liver numbers continued to fluctuate
throughout his follow-up course. On a follow-up liver ultrasound, he was
found to have persistent dilated portal vein and splenomegaly, and
spectral broadening of the hepatic vein waveforms. This was concerning
portal hypertension without portal vein thrombosis. He was then referred
to IR service for a trans jugular biopsy with pressure measurement. The
biopsy demonstrated no liver fibrosis and no rejection, but the portal
vein branch morphology to be abnormal.

The patient underwent a hepatic arteriogram (Figure 3) and a hepatic
venogram with pressure measurement. He was found to have hypoperfusion
to the common hepatic artery secondary to stealing from the splenic
artery. The IR team was consulted for a possible splenic artery
embolization. He underwent 70\% embolization of spleen using
500--700-micron PVA particles. Patient tolerated the procedure well and
the post procedural course was unremarkable. He was discharged a couple
of days later.

There was a sudden spike in the ALP and GGT levels after the procedure,
and the ultrasound demonstrated an enlarged spleen, which was presumed
to be due to necrosis from the recent embolization. The liver numbers
returned to normal levels a few weeks later.

\emph{Methods (Differential diagnosis, investigations and treatment):}

\emph{Diagnosis and Imaging:}

The most frequently relied upon modality for the diagnosis of SASS is
angiography (8). It is defined as a subjective slow flow of blood in the
hepatic artery relative to that in the splenic artery in the absence of
significant artery abnormalities such as hepatic artery stenosis,
thrombosis or kinks (15). Uflacker and coworkers diagnosed SASS when
there is a visualization of hepatic artery during the portal-venous
phase of angiogram (3). However, others have not relied on this
definition or threshold (5). Other modalities for detection of SASS
include regular doppler ultrasonography (US) (14). US is often performed
daily within the first week after OLT. Emergency angiography is
performed when a weakened or decreased signal is detected on US (14). US
findings are nonspecific and are not often used to describe SASS cases
since findings overlap with other conditions such as infection,
transient graft edema, or rejection (16,17,18). The most described US
findings include a high level of arterial resistive index (above 0.8)
(19). Reversal of diastolic flow or low diastolic flow is also often
observed (3,4). Furthermore, arterial velocities are rarely reported
(17). Nevertheless, US findings are not often used for diagnosis of SASS
(14). In fact, only 30 \% percent (34 out of 113) of the SASS cases
reported US findings. Other methods for the diagnosis of SASS include a
splenic volume greater than 830 cm3, which has an almost 75\% accuracy
in diagnosing SASS (7,8). Splenic artery diameter of greater than 4.0 mm
or splenic artery to hepatic artery ratio of greater than 1.5 are
considered indicators of SASS (7,8). Some studies have also indicated a
difference of at least 6mm between hepatic and splenic artery diameters
as being predictive of SASS (6). However, no imaging modality truly
solidifies the diagnosis, and the diagnosis is only confirmed upon
seeing improved graft function and increased hepatic arterial perfusion
after correcting splenic artery perfusion.

\emph{Treatment:}

All our patients were managed with splenic artery embolization.
Embolization in the first case was with coils. However, embolization in
the second and third cases were done with Amplatzer plug and
500--700-micron PVA particles respectively. Our treatment methods were
consistent with the modalities at other institutions. Many institutions
have considered splenic artery coil embolization as the primary
treatment for SASS (15,17). Patients with SASS often have a thick
splenic artery with a diameter that is often thicker than 5.0 mm or 1.5
times that of the hepatic artery (14). Therefore, fast arterial flow can
push the coil into the branch of splenic artery leading to ischemic
necrosis of the spleen and possibly septicemia (10). Furthermore, the
incidence of infection after coil embolization was reported to be as
high as 50 \% (15).

\emph{Conclusion and results:}

Splenic artery embolization was the most common treatment modality for
our SASS patients. Our patients had significant clinical improvement
after their treatment. However, more novel treatments need to be
investigated in the future. Imaging modalities such as ultrasound,
arteriogram and venograms with pressure measurements were used to
diagnose this syndrome. An angiogram can be used after the procedure to
ensure prompt flow in successful cases.

\emph{Discussion:}

Currently, the treatments for SASS range from interventional
radiological ones to surgical ones such as splenic artery ligation,
proximal and distal embolization, banding and splenectomy
(13,14,21,22,23). Despite the wide range of possibilities, proximal
splenic artery embolization remains the most popular and preferred
intervention because it is less invasive than surgical options with less
risk of both intra and postoperative bleeding (11). It is also known
that proximal embolization is much more likely to maintain collateral
flow to the spleen than distal embolization (3). Table 1 summarizes the
most common methods for managing SASS. To explore hepatic artery
perfusion after embolization, an angiogram should be performed, and in
successful cases, this angiogram demonstrates increased, prompt flow in
the hepatic artery. In addition, it demonstrates increased enhancement
of the liver parenchyma during the late arterial phase (3).

Other treatments such as temporary splenic artery blockage have also
been reported in the literature (14,24,25). This method can lead to
decreased splenic artery flow without irreversible local ischemic
necrosis of the spleen. More studies are needed to investigate this
intervention. Nevertheless, it appears to be a promising therapeutic
intervention to SASS. Our case series highlights the fact that proximal
splenic artery embolization, either with coils or plugs, is the most
common treatment for SASS after orthotopic liver transplantation. It
also sheds light on relatively new and effective treatments such as
temporary blockade of splenic artery. Furthermore, it shows how imaging
modalities such as hepatic arteriogram and venograms with pressure
measurement can facilitate the diagnosis of this syndrome. Table 1 shows
most common treatments and their clinical outcome for SASS patients at
other institutions.

As research moves forward and more risk factors are found to be
associated with SASS, a greater importance may be placed upon
prophylactic treatment, such as pre-operative splenic artery
embolization. Mogl et al. demonstrated reduced risk of SASS
complications after SAS prophylaxis compared to post-operative treatment
(5). A randomized control trial by Umeda et al. also demonstrated that
preoperative embolization in patients who had severe portal hypertension
resulted in reduced hepatic hypoperfusion along with lower operative
time and blood loss (17). Other interventions such as splenic artery
ligation or banding are often used as prophylactic measures and can be
used if the diagnosis of SASS is made posttransplant (33).

Statement of funding:

There are no financial sources to disclose

Informed consent:

Written informed consent for publication of the case report was taken
from the participants

Authors contributions:

Assim Saad Eddin, MD: Original draft, review \& editing

Abhiram Kamariju, MBBS: Original draft, review \& editing

Umar Ramzan Bsc: Review \& editing

Jay Yu, MD: Supervision, review \& editing

Surbhi Dadwal, MBBS: Review \& editing

Sandeep Laroia, MD: Conceptualization, Supervision, review \& editing

Conflict of Interest statement:

The authors hereby agree that there are no conflicts of interest to
disclose.

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2001;173(10):908-913. doi:10.1055/s-2001-17592\selectlanguage{english}
\begin{figure}[H]
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