PMC4005056_01
(a) Axial and (b) coronal contrast-enhanced CT of the upper abdomen obtained at admission shows a liver of cirrhotic morphology and nodular contours with mild diffuse heterogeneous enhancement. Splenomegaly, partly visualized ascites, and gastroesophageal varices are also noted. These findings were consistent with cirrhosis and sequela of portal hypertension. Numerous surgical clips about the porta hepatis represent changes of orthotopic liver transplantation.
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A 46-year-old female with medical history of cryptogenic cirrhosis, status postorthotopic liver transplantation done 9 years ago, presented to the tertiary care hospital with end-stage liver disease, hepatic encephalopathy, and abdominal distension secondary to recurrent ascites, requiring frequent paracentesis (Figure 1).
(a) Portovenogram performed during TIPS procedure shows a radioopaque graduated pigtail catheter in place, maintaining the tract created between the middle hepatic vein (thin arrow) and the inferior branch of the right portal vein (thick arrow). (b) Portovenogram with TIPS stent in place (arrow). The proximal uncovered portion was within the inferior branch of the right portal vein and the distal end was within the middle hepatic vein just before joining the inferior vena cava.
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Successful creation of TIPS was performed using 8 cm long and 1 cm wide Viatorr stent graft from the middle hepatic vein to the inferior branch of the right portal vein (Figure 2).
(a) Axial contrast-enhanced CT of the upper abdomen during the portal-venous phase demonstrates thrombosed left and middle hepatic veins (thin arrows). The proximal end of the TIPS stent is seen within the IVC which is occluding ostia of the left and middle hepatic veins (black arrow). The right hepatic vein is patent and adequately opacified with IV contrast (thick arrow). A wedge-shaped hypodense area in hepatic segments V and VIII (asterisk) representing hepatic infarction. (b) Coronal MIP image of the upper abdomen shows the position of the TIPS stent, communicating the right portal vein and the mid hepatic vein with its most cranial tip within the IVC (arrowhead).
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Also noted was the TIPS stent terminating in the inferior vena cava overlapping the ostia of the left and middle hepatic veins and associated thrombosis of left and middle hepatic veins (Figure 3).
(a) Axial contrast-enhanced CT of the upper abdomen shows a well-defined nonenhancing hypodense area liquefaction necrosis of infarcted liver parenchyma in hepatic segments V and VIII (asterisk). Again noted is the hypodense material within the left hepatic vein, consistent with hepatic vein thrombosis. (b) Ultrasound of the right lobe of the liver demonstrates a heterogeneous collection that corresponds to hepatic infarction.
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Ten days later, a follow-up CT of the abdomen and ultrasound was performed showing interval development of a fluid collection at the site of the previously documented liver hypoattenuation, consistent with hepatic abscess formation (Figure 4), which was later drained via percutaneous approach using ultrasound guidance.