Ascites Pathogenesis The activation of neurohumoral factors as described in the "Pathophysiology" section results in a high volume state due to sodium and water retention. Additionally, with cirrhosis, there is increased
hydrostatic pressure and decreased production of
albumin, which lead to decreased
oncotic pressure. Combined, this leads to leakage of fluid into the peritoneal cavity.
Management The management of ascites needs to be gradual to avoid sudden changes in systemic volume status, which can precipitate hepatic encephalopathy, kidney failure, and death. The management includes
salt restriction in diet, diuretics to urinate excess salt and water (
furosemide,
spironolactone),
paracentesis to manually remove the ascitic fluid, and
transjugular intrahepatic portosystemic shunt (TIPS).
Spontaneous bacterial peritonitis Pathogenesis In cirrhosis, there is bacterial overgrowth in the intestinal tract and increased permeability of the intestinal wall. These bacteria (most commonly E. coli & Klebsiella) are able to pass through the intestinal wall and into ascitic fluid, leading to an inflammatory response.
Management Antibiotic treatment is usually with a third generation cephalosporin (ceftriaxone or cefotaxime) after a diagnostic paracentesis. Patients are also given albumin.
Management Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin such as
terlipressin) and endoscopic (banding ligation) treatment have similar results. TIPS (
transjugular intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding. The management of active variceal bleeding includes administering vasoactive drugs (somatostatin, octreotide), endoscopic banding ligation, balloon tamponade and TIPS.
Management A treatment plan may involve
lactulose,
enemas, and use of antibiotics such as
rifaximin,
neomycin,
vancomycin, and the
quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.
Hepatorenal syndrome Pathogenesis Activation of neurohumoral factors (discussed in the Pathophysiology section) leads to renal vasoconstriction, which results in decreased blood supply to the kidneys and therefore, a decreased glomerular filtration rate. This can be an acute kidney injury (HRS type 1) or a slowly progressive kidney failure (HRS type 2). This use of splanchnic vasoconstrictors increases mean arterial pressure, which increases the amount of blood supplied to the kidneys. ==Treatment==