Cirrhosis is a chronic and usually irreversible liver disease that results from prolonged hepatocellular injury. Ultimately, regenerating hepatocytes and increased fibrosis destroy the liver architecture, and the organ’s synthetic and metabolic functions progressively decrease.

The majority of cases are due to chronic alcohol use or viral hepatitis, especially hepatitis C. However, any chronic liver disease that destroys the underlying hepatic structure (e.g., hemochromatosis, Wilson disease, sclerosing cholangitis, autoimmune hepatitis) can result in cirrhosis.

Affected individuals may initially be asymptomatic. When symptoms occur, they can be nonspecific, including weight loss, anorexia, fatigue, weakness, nausea, dull abdominal pain, muscle cramps, and constipation or diarrhea. As the disease progresses, clinical features become progressively more prominent. These include jaundice, spider angiomata, palmar erythema, gynecomastia, hypogonadism, easy bruising, and coagulopathy. Portal hypertension occurs as the liver architecture is obliterated, resulting in ascites, edema, splenomegaly, and esophageal varices.

Complications of advanced disease can be fatal. Hepatic encephalopathy (HE) can result in lethargy, confusion, slurred speech, hallucinations, asterixis, obtundation, and coma. Hemorrhage from esophageal varices is not uncommon and can result in massive hematemesis and high mortality. Other complications include spontaneous bacterial peritonitis, acute renal failure (hepatorenal syndrome), and hepatocellular carcinoma.

Risk Factors

Chronic alcohol abuse. Alcoholic liver disease results in over 19,000 deaths per year in the United States. Even moderate alcohol consumption, when continued over many years, can lead to premature death or disability.

Unprotected intercourse. Hepatitis B and, less commonly, hepatitis C infections are transmitted through unprotected sexual intercourse.

Intravenous drug use. Hepatitis B and C transmission is also common through intravenous drug use.

Inherited or acquired chronic liver disease. Hemochromatosis, Wilson disease, and autoimmune hepatitis can lead to cirrhosis.

Toxins. Exposure to chemicals such as alcohol or medications like amiodarone or methotrexate can lead to hepatic impairment and possible permanent damage.


History and physical examination should include a special focus on alcohol use, exposure to toxins, intravenous drug abuse, blood transfusion, multiple viral infections, the presence of tattoos, and the characteristic signs of cirrhosis such as spider telangiectasias, jaundice, and palmar erythema. Additional investigations are described below.

Abdominal CT scan and ultrasound can provide evidence of abnormal liver architecture to define the extent of cirrhosis. They can also identify ascites and other hepatic and abdominal pathology, such as hepatocellular carcinoma and portal hypertension.

Percutaneous liver biopsy can be diagnostic and may suggest the underlying cause of cirrhosis. Because the biopsy sample represents only about 1/10,000 of the liver tissue, the patterns of cirrhosis may be missed. Biopsy may not be necessary when portal hypertension is present and when the diagnosis is clearly established by clinical, laboratory, and radiologic findings.

Liver function tests can be normal early in the disease, but they become abnormal as the liver is destroyed. Transaminase levels reflect hepatocellular injury; alkaline phosphatase reflects cholestasis; and albumin reflects hepatic synthetic activity. These levels may normalize in the late stages of cirrhosis as the liver will no longer produce transaminases. The prothrombin time will become elevated as the liver is no longer able to produce adequate amounts of coagulation factors. Thrombocytopenia (platelet count < 160 x 10 3/μL) is a very sensitive marker of hypersplenism induced by portal hypertension.

Metabolic and electrolyte abnormalities become more pronounced as cirrhosis progresses. These can include hypoalbuminemia, hypocholesterolemia, decreased coagulation factors, decreased nitrogen, elevated ammonia, anemia, thrombocytopenia, and leukopenia.

Upper gastrointestinal (GI) endoscopy may be used to diagnose esophageal varices.


Treatment is aimed at slowing or reversing disease progression (if the underlying disease is treatable), preventing and treating complications, and, if possible, providing a cure through liver transplantation. Referral to a hepatologist is important.

It is essential to address the underlying etiology. Required measures include a voiding alcohol and hepatotoxic medications, treating viral hepatitis with appropriate antiviral regimens (such as Sofosbuvir or Tenofovir), and treating autoimmune hepatitis or severe alcoholic hepatitis with steroids or immunosuppressive agents. If not already immune, patients should be vaccinated against hepatitis A and B, as well as pneumococcus.

Also critical are prevention and treatment of cirrhosis complications. Esophageal varices can be treated with a beta blocker to decrease the risk of bleeding. Bleeding varices can be treated with endoscopic rubber banding, sclerotherapy, intravenous vasopressin or somatostatin, or balloon tamponade.

Lactulose decreases ammonia absorption from the gut, thereby decreasing the risk of HE.

Ascites can be managed with sodium restriction and diuretics. For severe or recurrent symptomatic ascites, slow removal of ascitic fluid via paracentesis is indicated. Ascites complicated by bacterial infection (spontaneous bacterial peritonitis) requires intravenous antibiotics.

Patients can be screened for the development of hepatocellular carcinoma by right-upper-quadrant ultrasound every 6 months. Model for End-stage Liver Disease (MELD) score should be monitored every 6 months in order to assess the risk for complications of cirrhosis.

Ultimately, liver transplantation is the only potential cure. Transplantation is an option for appropriate patients with advanced disease and severe complications, including variceal hemorrhage, HE, and hepatorenal syndrome. Transplantation is contraindicated in patients who continue to use alcohol or drugs. It is also contraindicated in patients who are unsuitable for surgery due to cardiopulmonary disease.

Nutritional Considerations

Malnutrition occurs in up to 80% of patients with cirrhosis and is associated with increased morbidity and mortality, as well as a reduction in post-transplant survival. The cause of malnutrition is multifactorial but occurs to a high degree due to gastrointestinal dysfunction caused by delayed gastric emptying, abdominal bloating, abdominal pain, fat malabsorption, diarrhea, and constipation, among other problems.[1]

The subjective global assessment (SGA), which uses both anthropometric and biochemical measurements, is helpful for grading patients’ nutritional status, in spite of having low sensitivity. It classifies patients with an A, B, or C grade, as well nourished (SGA-A), suspected of, or confirmed as being moderately malnourished (SGA-B), or severely malnourished (SGA-C). Common nutritional issues in cirrhotic patients include insufficient glycogen stores, sarcopenia, sarcopenic obesity, deficiencies of both fat-soluble vitamins (A, D, and E) and B-vitamins as well as minerals (e.g., zinc) and carnitine.[2]

The role of dietary protein is complex and somewhat controversial, although more in terms of quantity than quality. Although high-protein foods (particularly animal proteins) are a main source of ammonia, some authors have suggested that low-protein diets are no longer recommended due to a lack of effectiveness and the possibility of causing patients to develop a protein-malnourished state. This condition increases the risks for hepatorenal syndrome and longer hospital stays, compared with more well-nourished patients.[3] Indeed, protein malnutrition is an independent risk factor for mortality in patients with cirrhosis. In addition, HE presents chiefly in those with a diagnosis of protein malnutrition.[3] Although most patients can tolerate the fairly high protein intake (up to 1.5 g/kg/d) required for liver regeneration, roughly 35% may experience a worsening of HE on such a diet. For most (70%) of these patients, a temporary reduction to 0.5g/kg/d has been shown to reduce HE.[4]

Qualitatively, vegetable protein is preferred to animal sources. A consensus statement issued by the International Society for Hepatic Encephalopathy and Nitrogen Metabolism indicated that patients with recurrent or persistent HE should consume a diet rich in vegetable protein and low in animal protein.[5] Other benefits of a vegetarian diet are discussed below.

Sodium restriction. A sodium-restricted diet is standard treatment for patients with ascites.[6] A 2 g sodium-restricted diet, when combined with diuretic therapy, is effective for controlling fluid overload in 90% of patients with cirrhosis and ascites.[7] Patients should begin by avoiding processed foods, then restrict the adding of salt to meals. However, overly restricting salt can further reduce food intake due to changes in perceived palatability and can combine with diuretic treatment to produce hyponatremia. This is an independent risk factor for mortality in patients with cirrhosis.[8]

Vegetarian diets. Plant-based diets provide several advantages over omnivorous diets for patients with cirrhosis. Vegetable proteins are lower than animal proteins in sulfur-containing amino acids that upon digestion yield indole compounds and mercaptans that are implicated in HE.[3], [9] The high fiber content of plant-based diets helps to clear nitrogen waste products from the GI tract.[10] Clinical trials have not yet established effectiveness of such diets either in the prevention or treatment of cirrhosis.

Micronutrient status. Plasma selenium concentrations are depressed in patients with cirrhosis,[11] as are magnesium and zinc.[12] Other studies have documented vitamin A deficiency in patients with cirrhosis, with one noting over 50% of patients were affected.,[13] ,[9] In spite of these findings, a dearth of information exists regarding any impact of micronutrient supplementation, with few exceptions (see below).

Zinc supplementation. Poor zinc status, common in patients with cirrhosis due to losses from both muscle breakdown and diuretic treatment, impairs the liver’s ability to regenerate. Zinc is needed for conversion of ammonia to urea and glutamic acid,[14] and blood concentrations of this mineral are inversely associated with ammonia levels.[15] High-dose supplementation (150-175 mg/d) has been found to effectively lower ammonia levels when used as monotherapy[16] or when combined with antioxidant supplements.[17]

Vitamin D deficiency. Roughly one-third of patients with cirrhosis are low in vitamin D.[18] Levels ≤ 6 ng/mL are predictive of mortality in these patients; however, the role of vitamin D supplementation is unclear.[19]

Branched-chain amino acids (BCAAs). A Cochrane review concluded that BCAA treatment reduced the risk for HE by roughly 25% when compared with placebo treatment.[20] Other actions of BCAA supplements include improvement of hypoalbuminemia, fatty acid metabolism, esophageal varices, and ascites; reduction of insulin resistance and oxidative stress; and inhibition of angiogenesis, among others.[2] However, the American Society for Parenteral and Enteral Nutrition (ASPEN) and it’s European counterpart recommend that BCAAs be used only in patients with chronic HE when pharmacotherapy is ineffective.[2]

Oral and enteral nutritional supplementation for malnourished patients. A comparison of oral and enteral supplementation regimens with neither treatment concluded that while oral supplementation was associated with a 60% reduction in mortality, no such benefit was found for enteral nutrition.[21]

Probiotic treatment. Intestinal dysbiosis is present in persons with cirrhosis, more so in decompensated than compensated disease, and the resulting endotoxemia is a cause of liver injury. Several studies have revealed a benefit of probiotic treatments in patients with cirrhosis, including one that demonstrated a significant reduction in the risk for hospitalization for HE.[22]

Coffee consumption. Several studies have found dose-dependent relationships between increases in coffee intake and a decrease in liver enzymes (ALT, AST, GGT) in both regular alcohol consumers and non-consumers. A multi-ethnic, US-based cohort study found the risk of cirrhosis decreased with increasing coffee intake, but this was only among individuals whose liver disease was caused by alcohol rather than hepatitis viruses. Explanations for these benefits include the ability of phytochemicals in coffee to induce phase II detoxification enzymes with antioxidant effects and the downregulation of proinflammatory, fibrogenic cytokines and hepatic stellate cells.[23]


See Basic Diet Orders Chapter

Provide small, frequent meals with adequate energy, protein, and fluid.

Sodium less than 2 g daily.

Nutrition assessment by a registered dietitian.

Daily multivitamin with minerals.

What to Tell the Family

Cirrhosis of the liver is a life-threatening chronic illness, which is ultimately terminal without transplantation. However, the management of some cirrhosis cases may be improved with diet, thorough compliance with prescribed medications, and abstinence from alcohol.


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Last updated: November 15, 2017