Pasternak B M, Cohen H
Angiology. 1978 May;29(5):367-73. doi: 10.1177/000331977802900503.
The notorious predilection for rupture of splenic artery aneurysms in women of childbearing age is once more stressed by this case report. Although such ruptures usually result in a catastrophic interabdominal bleeding, in rare instances they lead to the formation of an arteriovenous fistula and consequent portal hypertension. Arterialization of the portal vein results in a progressive development of intrinsic hepatic morphologic changes and hepatoportal sclerosis, which further elevate the pressure in the portal system. This combination of pathophysiologic hemodynamic features closely resembles the original concept of Banti. He postulated that portal hypertension began with pathologic changes within the spleen which were associated with an increased blood flow through this organ. This led to increased flow and pressure in the portal venous system and ultimately cumulated in cirrhosis of the liver. This concept of the pathophysiology of portal hypertension has been universally abandoned, but it could serve as a model of the sequelae of an arteriovenous communication within the portal system.
本病例报告再次强调了育龄女性脾动脉瘤破裂的臭名昭著的倾向。尽管此类破裂通常会导致灾难性的腹腔内出血,但在极少数情况下,它们会导致动静脉瘘的形成并继而引发门静脉高压。门静脉的动脉化导致肝脏内在形态学变化和肝门静脉硬化的渐进性发展,这进一步升高了门静脉系统的压力。这种病理生理血液动力学特征的组合与班替氏病的最初概念极为相似。他推测门静脉高压始于脾脏内的病理变化,这与通过该器官的血流量增加有关。这导致门静脉系统内的血流和压力增加,并最终累积导致肝硬化。门静脉高压病理生理学的这一概念已被普遍摒弃,但它可作为门静脉系统内动静脉交通后遗症的一个模型。