Source: Sease JM. Portal
Hypertension and Cirrhosis. In: DiPiro JT, Talbert RL, Yee GR, Wells
BG, Posey LM. Pharmacotherapy: A Pathophysiologic Approach. 8th edition. http://accesspharmacy.com/content.aspx?aid=7979093.
Accessed April 27, 2012.
- Diffuse injury to liver characterized by destruction of
hepatocytes and their replacement by fibrous tissue.
- Most common causes are excessive alcohol intake and chronic
viral hepatitis (types B and C, Table 1).
Table 1. Etiology of Cirrhosis |Favorite Table|Download (.pdf)
Table 1. Etiology of Cirrhosis
Chronic alcohol consumption
Chronic viral hepatitis (types
B, C, and D)
Metabolic liver disease
Nonalcoholic steatohepatitis (“fatty liver”)
Primary biliary cirrhosis
Primary sclerosing cholangitis (90% associated
with ulcerative colitis)
Isoniazid, methyldopa, amiodarone, methotrexate, tamoxifen,
retinol (vitamin A), propylthiouracil, and didanosine
- Elevation of portal blood pressure because of fibrotic
changes within hepatic sinusoids, changes in levels of vasodilatory
and vasoconstrictor mediators, and increase in blood flow to splanchnic vasculature.
- Resistance to blood flow contributes to portal hypertension
and the development of varices, ascites, hepatic encephalopathy
(HE), and coagulopathy.
- Portal hypertension characterized by:
- Increased cardiac index
- Decreased systemic vascular resistance
- Ranges from asymptomatic, with abnormal laboratory or
radiographic tests, to decompensated with ascites, spontaneous bacterial
peritonitis, HE, or variceal bleeding.
- Weight loss
- Palmar erythema
- Spider angiomata
- Pleural effusion
- Respiratory difficulties
- Mental status changes
Means of Confirmation and Diagnosis
- No laboratory or radiographic tests of hepatic function
can accurately diagnose cirrhosis.
- Routine liver function tests include alkaline phosphatase,
bilirubin, aspartate transaminase (AST), alanine aminotransferase
(ALT), and γ-glutamyl transpeptidase (GGT).
- Albumin and prothrombin time (PT)
- Complete blood count (CBC): Thrombocytopenia relatively common
feature in chronic liver disease; found in 15–70% of
- Clinical improvement or resolution of acute complications
- Resolution of hemodynamic instability
- Prevention of complications
- Adequate lowering
of portal pressure with medical therapy
- Support of abstinence from alcohol
- Identify and eliminate causes of cirrhosis (e.g., alcohol
- Assess risk for variceal bleeding and begin pharmacologic
prophylaxis where indicated, reserving endoscopic therapy for high-risk
patients or acute bleeding episodes.
- Evaluate for clinical signs of ascites and manage with pharmacologic
treatment (e.g., diuretics) and paracentesis. Careful monitoring
for spontaneous bacterial peritonitis (SBP) in patients with ascites
who undergo acute deterioration.
- HE is common complication of cirrhosis and requires clinical
vigilance and treatment with dietary ...