The following update to this chapter was made on February 24, 2021:
CHAPTER SUMMARY FROM THE PHARMACOTHERAPY HANDBOOK
For the Chapter in the Schwinghammer, Handbook (not Wells Handbook anymore) please go to Chapter 21, Cirrhosis and Portal Hypertension.
Cirrhosis is a severe, chronic, potentially irreversible disease associated with significant morbidity and mortality. The progression of cirrhosis secondary to alcohol intake, both in those with alcoholic cirrhosis and cirrhosis due to other causes, can be interrupted by abstinence from alcohol. It is therefore imperative for the clinician to educate and support abstinence from alcohol as part of the overall treatment strategy of the underlying liver disease.
Patients with cirrhosis should receive endoscopic screening for varices, and certain patients with varices should receive primary prophylaxis with nonselective β-adrenergic blockade therapy to prevent variceal hemorrhage.
When nonselective β-adrenergic blocker therapy is used to prevent re-bleeding, therapy can be titrated to achieve a goal heart rate of 55 to 60 beats/min or the maximal tolerated dose.
Octreotide is the preferred vasoactive agent for the medical management of variceal bleeding. Endoscopic band ligation is the primary therapeutic tool for the management of acute variceal bleeding.
The combination of spironolactone and furosemide is the recommended initial diuretic therapy for patients with ascites.
All patients who have survived an episode of spontaneous bacterial peritonitis (SBP) should receive long-term antibiotic prophylaxis.
The mainstay of treatment of hepatic encephalopathy (HE) involves therapy to lower blood ammonia concentrations and includes diet modifications, lactulose, and rifaximin alone or in combination with lactulose.
Preclass Engaged Learning Activity
Create a summary table of treatment options for each complication associated with decompensated cirrhosis: ascites, SBP (acute treatment and secondary prophylaxis), HE, variceal bleeding (primary prophylaxis, acute bleeding, and secondary prophylaxis). Use the table below as a guide.
Chronic liver injury causes damage to normal liver tissue resulting in the development of regenerative nodules surrounded by dense fibrotic material, which are diagnostic hallmarks of cirrhosis.1 The distorted architecture of the cirrhotic liver impedes portal blood flow, interferes with hepatocyte perfusion, and disrupts hepatic synthetic functions such as the production of albumin. Clinical consequences of cirrhosis include increased intrahepatic resistance leading to portal hypertension, varices, and variceal bleeding; ascites; infection; encephalopathy; and hepatocellular carcinoma. Additionally, when advanced, cirrhosis can also lead to the development of both renal and pulmonary dysfunction.
While cirrhosis has many causes (Table 54-1),1–3 in more developed countries, primary etiologies include hepatitis C, excessive alcohol intake, ...