Portal de Periódicos da CAPES

COMMENTS ON ???ARTERIALIZATION OF THE PORTAL VEIN IN ORTHOTOPIC AND AUXILIARY LIVER TRANSPLANTATION???

1996; Wolters Kluwer; Volume: 62; Issue: 9 Linguagem: Inglês

10.1097/00007890-199611150-00038

1534-6080

Richard Aspinall, John P. Seery, Simon D. Taylor‐Robinson, Nagy Habib,

Renal Transplantation Outcomes and Treatments

Recently, Erhard and colleagues (1) reported three liver transplant recipients who also underwent arterialization of the portal veins. The authors reported that none of their patients developed neurological symptoms. We wish to report a much less favorable outcome after portal vein arterialization. A 53-year-old man with hepatitis B cirhosis received an elective orthotopic liver transplant for poor synthetic function and recurrent encephalopathy. The operation was performed on standard veno-venous bypass and the donor liver was revascularized, with good perfusion of the graft on removal of all clamps. On day 6 after orthotopic liver transplantation, the patient developed a rising prothrombin time of 37 seconds and a lactic acidemia. Subsequent Doppler and angiographic studies confirmed thrombosis of the right and middle hepatic veins, which could not be fully cleared by the use of an occlusive ballon “sweep” at venography. Poor hepatic inflow, owing to widespread retroperitoneal collaterals, was believed to be the most likely cause of the thromboses. The patient's liver function continued to deteriorate. He was therefore listed for urgent retransplantation, with the only available liver proving to be an AB mismatch (donor blood group AB, recipient A). At operation, the new donor organ appeared healthy, with an accessory left hepatic artery originating from the left gastric artery. This was protected by removing the celiac axis with a patch, and the new liver was implanted in an orthotopic position. After surgery, the patient's condition was initially stable, but on the second day his serum aspartate aminotransferase level had climbed from 350 to 4000 IU/L. Doppler studies showed a weak hepatic arterial flow and an absence of flow in the portal vein. Angiography revealed a 50% stenosis at the arterial anastomotic site, and indirect portography demonstrated the portal venous flow emptying into a large splenorenal collateral that drained into the inferior vena cava. No contrast was seen in the portal vein itself. At laparotomy, the hepatic artery was pulsating but there was no flow in the portal vein. Consequently, it was decided to arterialize the portal vein with an aorta-portal jump graft, by fashioning an arterial conduit from the two donor iliac arteries and using this to connect the infrarenal aorta to both the hepatic artery and portal vein. After surgery, there was an improvement in his liver function, with the aspartate aminotransferase level falling from 4000 to 500 IU/L and the bilirubin decreasing from 600 to 230 μmol/L. However, the patient developed severe grade IV hepatic encephalopathy and remained unrousable. An electroencephalogram recording revealed a virtually flat trace, albeit with some low-voltage delta wave activity (frequency 1-3 Hz) and some intermittent theta components (frequency 4-5 Hz), but with no response to painful stimuli. Despite contined improvement in his biochemical parameters of liver function, the patient remained severely encephalopathic for a further 5 weeks after the portal vein arterialization. Unfortunately, he developed overwhelming bacterial and fungal septicemia and died after an asystolic cardiac arrest. Arterialization of the portal vein in conjuction with surgical portocaval shunts has been described previously (2). In this study, there was no increase in hepatic encephalopathy when compared with patients who had received a portocaval shunt alone, although the combined procedure did produce a higher incidence of postoperative ascites. In the setting of liver transplantation, Erhard et al.(1) found no increase in encephalopathy in their three patients. However, our patient's outcome appears to suggest that where there are significant portosystemic collaterals, arterialization of the transplanted portal vein can result in severe hepatic encephalopathy. We agree with Erhard et al.'s assertion that arterialization of the portal vein “should only be performed in life-threatening clinical situations.” Richard J. Aspinall1,2 John P. Seery1 Simon D. Taylor-Robinson1 Nagy Habib3 Departments of Gastroenterology and Hepatobiliary Surgery; Hammersmith Hospital; London W12 OHS, UK