Harada N, Ito T, Taura S, Tsuchiya R, Koga Y
Jpn J Surg. 1975 Sep;5(3):145-52. doi: 10.1007/BF02469395.
A case of portal hypertension secondary to traumatic hepatoportal arteriovenous fistula with portal fibrosis was successfully treated by ligation of the afferent hepatic arteries which decreased significantly portal pressure and corrected the abnormal blood inflow to the portal vein via A-V fistula resulting in a recovery of the disturbed liver function. Collateral blood supply from the left hepatic artery into the right hepatic lobe was found to be quite satisfactory after the ligation of the hepatic artery. Hemodynamic data and clinical findings of the present case suggest that the mechanism responsible for the portal hypertension is the inflow block resulting from the interruption of portal venous flow by the inflow of arterial blood via A-V fistula and the subsequent increased blood pressure in portal vein radicals.
一例继发于创伤性肝门静脉动静脉瘘伴门静脉纤维化的门静脉高压症患者,通过结扎肝动脉输入支成功治愈,门静脉压力显著降低,纠正了经动静脉瘘进入门静脉的异常血流,肝功能紊乱得以恢复。结扎肝动脉后发现,左肝动脉向右肝叶的侧支血液供应相当充足。本病例的血流动力学数据和临床发现表明,门静脉高压的机制是动脉血经动静脉瘘流入导致门静脉血流中断,进而引起门静脉分支血压升高,造成血流受阻。