Management of Acute Liver Failure in a Patient with Portal and Hepatic Vein Thrombosis

Moni Stein M.D., Christopher L. Bowlus M.D.,
and Howard Nelson M.D.
University of California Davis Medical Center

Fig. 1. CT of the abdomen shows enlarged main portal vein (see arrow) filled with clot. A rim of contrast is seen around the clot. No cavernous transformation is seen. Also notice large retroperitoneal venous collaterals (see arrowhead). Mild ascites is present.

Fig. 2. CT of the liver shows reconstitution of the right portal vein (see arrow). No normal hepatic veins are seen.

Case Reference No. CC-0100-06

A 62-year-old man with chronic liver disease related to hepatitis B, hepatitis C and alcoholic liver disease presented with acute exacerbation of his liver function and changes in mental status related to encephalopathy. At presentation, his laboratory values were as follows: HCT 26.5%, platelets 200,000, AST 695 U/L, ALT 489 U/L, ALP 194 U/L, total bilirubin 14.1 µg/L, ammonia 136 µg/dl, INR 1.37 and a serum creatinine of 2.3 mg/dl. CT of the abdomen showed a thrombosed main portal vein (figure 1) with reconstitution of the right portal vein intrahepatically (figure 2). There was no cavernous transformation and the rim of contrast around the clot suggested that it was acute. There was no visualization of normal hepatic veins which raised the suspicion of acute hepatic vein thrombosis. The left renal vein was enlarged and retroaortic (figure 3), likely fed by porto-systemic collaterals. A Doppler ultrasound was performed to verify the status of the hepatic veins, in search for a cause of his acute deterioration. It showed flow in the hepatic veins, although it was reported that the scan was difficult. The patient was evaluated for liver transplantation; however, he was rejected because of his ongoing alcoholic consumption.

A discussion took place with the clinical team regarding the management options in this patient. Because he was not a surgical candidate it was decided to first have another look at his hepatic veins and secondly attempt a TIPS procedure. Through the transjugular approach the right hepatic vein was accessed. It contained non-occlusive clot (see figure 4). It was decided to perform TIPS that would provide adequate outflow to the thrombosed portal vein and would help clear the right hepatic vein clot. Portal vein access was created and the portal clot was demonstrated with venography (see figure 4). A TIPS was created and dilated to 10 mm with the lower end positioned at the level of the portal clot. The Amplatz thrombectomy device (Microvena) was used to try and eliminate the clot with little success. Subsequently an infusion catheter was introduced into the clot and 14 mg of tPA were infused. The infusion had to be stopped because of bleeding from the mouth. The portal clot did not resolve and the TIPS was extended beyond the clot in the portal vein (see figure 5).

Fig. 3. CT of the abdomen shows large splenic hilum varices (see arrowhead). The left renal vein is enlarged and retroaortic (see arrow). Porto-systemic collaterals likely fed this vein.

Fig. 4. Portal venogram shows a large round clot in the main portal vein (see arrow) and non-occlusive clot in the right hepatic vein (see arrowhead).

Fig. 5. A TIPS was created with the lower end starting beyond the clot (see arrow) in the main portal vein and the upper end at the margin of the right hepatic vein.

The spontaneous porto-systemic collaterals were embolized with coils to improve flow in the shunt. The patient was transferred to the ICU in stable condition, however his respiratory status deteriorated and his chest X-ray showed diffuse air-space disease. He died the next day from respiratory failure that was thought to be related to aspiration of blood during the procedure.

Questions:
1) What is the etiology of acute liver failure in this patient?

2) Can acute portal vein thrombosis cause exacerbation of liver failure?

3) Is TIPS a reasonable option for this type of patient?

4) Would hepatic vein thrombectomy or thrombolysis without TIPS would have been a safer way to go?

5) If the patient was not an active alcoholic, would liver transplantation be a good management option?

6) Was this patient too sick to intervene on?

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