摘要
Ascites is the most common complication related to cirrhosis and is associated with increased morbidity and mortality.Ascites is a consequence of the loss of compensatory mechanisms to maintain the overall effective arterial blood volume due to worsening splanchnic arterial vasodilation as a result of clinically significant portal hypertension.In order to maintain effective arterial blood volume,vasoconstrictor and antinatriuretic pathways are activated,which increase overall sodiumand fluid retention.As a result of progressive splanchnic arterial vasodilation,intestinal capillary pressure increases and results in the formation of protein-poor fluid within the abdominal cavity due to increased capillary permeability from the hepatic sinusoidal hypertension.In some patients,the fluid can translocate across diaphragmatic fenestrations into the pleural space,leading to hepatic hydrothorax.In addition,infectious complications such as spontaneous bacterial peritonitis can occur.Eventually,as the liver disease progresses related to higher portal pressures,loss of a compensatory cardiac output and further splanchnic vasodilation,kidney function becomes compromised fromworsening renal vasoconstriction as well as the development of impaired solute-free water excretion and severe sodium retention.Thesemechanisms then translate into significant clinical complications,such as refractory ascites,hepatorenal syndrome and hyponatremia,and all are linked to increased short-termmortality.Currently,liver transplantation is the only curative option for this spectrumof clinical manifestations but ongoing research has led to further insight on alternative approaches.This review will further explore the current understanding on the pathophysiology andmanagement of ascites as well as expand on two advanced clinical consequences of advanced liver disease,refractory ascites and hyponatremia.
腹水是肝硬化最常见的并发症,会增加肝硬化患者的并发症发生率和病死率。腹水的形成是由于临床显性门脉高压症引起内脏动脉血管舒张不断加剧、继而导致全身有效动脉血容量的代偿机制丧失。为了维持有效动脉血容量,血管收缩和抗利钠系统被激活,以增加血钠浓度,促进液体潴留。随着内脏动脉血管进行性舒张,肠道毛细血管压力增高,加之肝窦高压所继发的毛细血管渗透压增高,最终导致腹腔内低蛋白液形成。在部分患者中,液体能通过膈膜窗进入胸腔从而形成胸水。此外也会出现一些感染性并发症,如自发性细菌性腹膜炎。最终,随着肝硬化的进展、门脉压力的不断增高、心输出量代偿功能的丧失及内脏血管舒张的进一步恶化,肾功能也会因肾脏血管收缩、自由水排泄受损及严重的钠潴留而受损,从而出现顽固性腹水、肝肾综合征和低纳血症等并发症,这些并发症都会增加短期病死率。目前,肝移植是惟一的根治方法,但最近的研究结果也使我们看到了一些替代治疗方案的曙光。本文将对腹水、顽固性腹水和低钠血症的病理生理及治疗策略进行深入探讨。
