Witte C L, Witte M H
Fed Proc. 1983 Apr;42(6):1685-9.
Bleeding esophagogastric varices and ascites are the most serious complications of portal hypertension. Rupture of varices develops because of progressively rising portal pressure as rapid splanchnic blood flow combines with increasing portal vascular resistance (active congestion). The greater the restriction to transhepatic portal venous flow, the less the increment in splanchnic blood flow required to generate a venous pressure ultimately exceeding the bursting tension of thin-walled varices. Ascites, on the other hand, represents an imbalance of hydrodynamic forces in the microcirculation of the liver and digestive tract. Large amounts of fluid are driven out of the vascular space into visceral tissues. When the rate of lymph return to the systemic venous circulation fails to keep pace with increased capillary filtration, peritoneal transudation ensues. A complex sequence of events is then set into motion leading to renal salt and water retention. Plasma volume is restored, but at the same time hepatosplanchnic lymph formation is aggravated and a vicious cycle is thereby created. Treatment depends on reduction of lymph formation by indirect (dietary restriction of salt and water and diuretic drugs) or direct (portasystemic shunt) portal decompression or, alternatively, on acceleration of an already rapid lymph return (peritoneovenous shunt) to match the high rate of lymph production.
食管胃静脉曲张破裂出血和腹水是门静脉高压最严重的并发症。由于快速的内脏血流与门静脉血管阻力增加（主动充血）相结合，门静脉压力逐渐升高，导致静脉曲张破裂。对经肝门静脉血流的限制越大，产生最终超过薄壁静脉曲张破裂张力的静脉压力所需的内脏血流增量就越小。另一方面，腹水代表肝脏和消化道微循环中流体动力的失衡。大量液体从血管间隙被驱入内脏组织。当淋巴回流入体循环静脉的速度跟不上毛细血管滤过增加的速度时，就会发生腹膜渗出。随后会引发一系列复杂的事件，导致肾脏对盐和水的潴留。血浆容量得以恢复，但与此同时，肝内脏淋巴形成加剧，从而形成恶性循环。治疗方法包括通过间接（限制饮食中的盐和水以及使用利尿药物）或直接（门体分流）门静脉减压来减少淋巴形成，或者通过加速已经很快的淋巴回流（腹膜静脉分流）来匹配高淋巴生成率。
