In this chapter, we review the history of HCV infection in patients with liver cirrhosis. Selection of appropriate regimens for HCV-infected patients with cirrhosis, consistent with approved indications, practice guidelines, and emerging data is presented. Finally, this chapter explains individualization of therapy to maximize SVR rates in HCV-infected patients with cirrhosis and to critically appraise the role of newer agents and regimens in the management of HCV-infected patients with cirrhosis.
Part of the book: Advances in Treatment of Hepatitis C and B
Ascites is a pathological accumulation of fluid in the peritoneal cavity. Cirrhosis is the most common cause of ascites, representing for 85% of cases. More than one cause may be responsible for the development of ascites (multifactorial). Development of ascites is a poor prognostic event in the natural history of cirrhosis, with approximately 15 and 44% of patients with ascites succumbing in 1 and 5 years, respectively. Patients with cirrhosis need referral for liver transplantation after development of ascites. Proper history and physical examination are important in diagnosing the cause of ascites. Diagnostic paracentesis and abdominal sonogram should be performed during initial evaluation. Low salt diet and diuretic are the initial treatment option, and large volume paracentesis is an option for non‐responder to diuretics. Transjugular intrahepatic portosystemic stent‐shunt (TIPS) is highly valuable in properly selected patients.
Part of the book: Liver Cirrhosis
Diuretics are considered the first-line pharmacological treatment option for ascites. Diuretic treatment begins with spironolactone and furosemide. Non-pharmacological options include salt restriction, large-volume paracentesis (LVP), transjugular intrahepatic portosystemic shunt (TIPS), and peritoneovenous shunt. Ascites can be mobilized if renal sodium excretion tops 78 mmol daily (88 mmol–10 mmol daily) after restricting sodium intake to 88 mmol/day (about 2000 mg/day). The majority of patients with cirrhotic ascites respond to a combination of sodium restriction and diuretics such as spironolactone and furosemide (90%). Ascites that does not respond to sodium restriction and high-dose diuretic treatment (400 mg/day of spironolactone and 160 mg/day of furosemide) or following paracentesis is labeled refractory. Refractory ascites can be managed with large-volume paracentesis or transjugular intrahepatic portosystemic shunt. Peritoneovenous shunting is considered as a third-line treatment option after all other measures such as diuretics, large-volume paracentesis, or transjugular intrahepatic portosystemic shunt deemed unsuccessful or contraindicated. It has a high rate of shunt obstruction.
Part of the book: Ascites
Ascites refer to accumulation of fluids in the peritoneal cavity. Ascites is caused by multiple causes, among which liver cirrhosis is the commonest. Confirming the etiology is the first and most important step toward proper management. Assuming that ascites is always caused by cirrhosis can lead to unnecessarily sending patients with different etiologies for liver transplantation, particularly patients with non-cirrhotic portal hypertension. Calculating serum albumin ascitic gradient is important in differentiating ascites due to portal hypertension from other etiologies. The first-line therapy for ascites in cirrhosis is low salt diet and diuretics. It is important to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) and nephrotoxic medications in these patients.
Part of the book: Ascites
Liver cirrhosis is associated with a wide range of systemic and pulmonary vascular abnormalities. Cardiac dysfunction also occurs in patients with advanced liver disease (cirrhotic cardiomyopathy). The circulation in cirrhosis is hyperdynamic, which is typically characterized by hypotension resulting from the associated vasodilatation and reflex tachycardia. The circulatory dysfunction in cirrhosis is the proposed pathophysiological mechanism leading to sodium and water retention in patients with liver cirrhosis. Hyperdynamic circulation is triggered by increased intrahepatic resistance due to cirrhosis, leading to a progressive increase in portal venous pressure. As portal hypertension worsens, local production of vasodilators increases due to endothelial activation, leading to splanchnic and systemic arterial vasodilation. Nitric oxide (NO) is considered one of the most important vasodilator molecules in the splanchnic and systemic circulation. The reduction in the effective arterial blood volume results in diminished renal arterial blood flow and subsequently triggers the rennin-angiotensin-aldosterone system (RAAS), antidiuretic hormones (ADHs) and sympathetic nervous system (SNS), leading to renal artery vasoconstriction. All these changes lead to sodium retention and volume expansion, manifested as ascites and peripheral edema. Furthermore, disease progression is associated with various degrees of renal dysfunction.
Part of the book: Ascites