Complex Care Exam 1 Practice

Ascites in cirrhosis mainly results from portal hypertension driving fluid from the blood into the peritoneal cavity, compounded by reduced albumin production by the damaged liver. The high hydrostatic pressure in the portal system pushes plasma water (and some protein) across the peritoneal capillaries, while low albumin decreases oncotic pressure to reabsorb fluid back into vessels. In response to perceived low effective circulating volume, the body activates neurohumoral systems (RAAS and sympathetic pathways), promoting sodium and water retention that increases overall fluid in both the vascular and third spaces, worsening ascites. That combination is best captured by saying portal hypertension causes leakage of protein and water into the peritoneal cavity. The other ideas—ammonia-driven encephalopathy, splenic sequestration reducing plasma volume, or gastric mucosal fluid shifts—do not directly explain the accumulation of fluid in the abdomen.