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.