title: Influence of spontaneous portosystemic collateral pathways on portal hemodynamics in living-related liver transplantation in children. Doppler ultrasonographic study.
abstract: We investigated the influence of spontaneous portosystemic collateral pathways on the portal hemodynamics and examined the necessity for ligating these vessels in pediatric liver transplantation from living donors. We assessed portal blood flow before, during, and after surgery in 82 pediatric recipients (mean age, 4.2 years), using Doppler ultrasonography. When blood flow in the reconstructed portal vein was decreased (< 10 ml/min/kg body weight) and portosystemic collaterals persisted during surgery, those vessels were ligated and Doppler flowmetry was examined again. Spontaneous portosystemic collaterals were detected at one or more sites in 67 patients before transplantation. These collaterals had been ligated in 17 patients before intraoperative flowmetry. Among the remaining 50 patients, initial Doppler studies revealed a decrease in portal blood flow in 22 patients. Nine patients had hepatofugal splenic venous flow and 6 had no significant flow signals from the intrahepatic portal vein. Ligation of collaterals resulted in a remarkable increase in portal blood flow in 20 patients, all of whom are alive. The remaining 2 patients died of graft failure due in part to portal hypoperfusion. On the other hand, the collaterals were not ligated in 24 patients because adequate portal blood flow was confirmed by intraoperative flowmetry. Postoperatively, flow signals from the unligated collateral vessels gradually diminished, but they still persisted in 3 patients at 12 months after transplantation. Hepatofugal blood flow through the portosystemic collateral pathways may persist after implantation of a normal graft. If the patent collaterals significantly reduce the effective portal blood flow, these vessels should be ligated in order to avoid graft failure.
authors.affiliation: First Department of Internal Medicine, Kyoto University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fujimoto
authors.forename: F
authors.initials: F
authors.lastname: Moriyasu
authors.forename: T
authors.initials: T
authors.lastname: Nada
authors.forename: Y
authors.initials: Y
authors.lastname: Suginoshita
authors.forename: Y
authors.initials: Y
authors.lastname: Ito
authors.forename: K
authors.initials: K
authors.lastname: Nishikawa
authors.forename: H
authors.initials: H
authors.lastname: Someda
authors.forename: M
authors.initials: M
authors.lastname: Okuma
authors.forename: Y
authors.initials: Y
authors.lastname: Inomata
authors.forename: N
authors.initials: N
authors.lastname: Ozaki
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D005260:Female; D006085:Graft Survival; D006439:Hemodynamics; D006801:Humans; D007223:Infant; D008099:Liver / Q000098:blood supply*; D016031:Liver Transplantation; D008297:Male; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D011168:Portal System / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D014463:Ultrasonography