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.