Change in portal flow after liver transplantation: Effect on hepatic arterial resistance indices and role of spleen size

• DOI: 10.1053/jhep.2002.31352
• Publication Date: 2002-08-25T03:46:10Z
• Authors: Massimo Bolognesi; David Sacerdoti; Giancarlo Bombonato; Carlo Merkel; Giovanni Sartori; Roberto Merenda; Valeria Nava; Paolo Angeli; Paolo Feltracco; Angelo Gatta
• Keywords: Adult; Liver Cirrhosis; Male; Liver Failure, Acute; Middle Aged; Liver Transplantation; 3. Good health; Portal System; Hepatic Artery; Regional Blood Flow; Humans; Female; Ultrasonics; Vascular Resistance; Cardiac Output; Blood Flow Velocity; Spleen

Information on changes in splanchnic hemodynamics after liver transplantation is incomplete. In particular, data on long-term changes are lacking, and the relationship between changes in arterial and portal parameters is still under debate. The effect of liver transplantation on splanchnic hemodynamics was analyzed with echo-Doppler in 41 patients with cirrhosis who were followed for up to 4 years. Doppler parameters were also evaluated in 7 patients transplanted for acute liver failure and in 35 controls. In cirrhotics, portal blood velocity and flow increased immediately after transplantation (from 9.1 ± 3.7 cm/sec to 38.3 ± 14.6 and from 808 ± 479 mL/min to 2,817 ± 1,153, respectively, P < .001). Hepatic arterial resistance index (pulsatility index) also augmented (from 1.36 ± 0.32 to 2.34 ± 1.29, P < .001) and was correlated with portal blood velocity and flow. The early changes in these parameters were related, in agreement with the hepatic buffer response theory. Portal flow returned to normal values after 2 years. Superior mesenteric artery flow normalized after 3 to 6 months. Splenomegaly persisted after 4 years, when spleen size was related to portal blood flow. In 7 patients transplanted for acute liver failure, portal flow, and hepatic arterial resistance index were normal after transplantation. In conclusion, a high portal flow was present in cirrhotics until 2 years after transplantation, probably because of maintenance of elevated splenic flow. An early increase in hepatic arterial resistance indices is a common finding, but it is transient and is related to the increase in portal blood flow. A normal time course of portal-hepatic hemodynamics was detected in patients transplanted for acute liver failure.