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Alcoholic Liver Disease 

Alcoholic Liver Disease
Chapter:
Alcoholic Liver Disease
Author(s):

Sameer D. Saini

, and Akbar K. Waljee

DOI:
10.1093/med/9780190862800.003.0034
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date: 18 September 2020

  1. A. Introduction

    1. a. The amount of alcohol required to produce liver disease in a patient is variable.

    2. b. Women in general are more susceptible than men, but men are more often affected because of relatively higher alcohol consumption rates.

    3. c. Most authorities believe that a susceptible person must drink 60–80 g of alcohol per day for at least 10 years before developing cirrhosis. Many women, however, develop cirrhosis with much lower alcohol intake. Patients with preexisting liver disease (e.g., viral hepatitis, nonalcoholic liver disease) are more susceptible to alcoholic liver injury.

    4. d. Alcohol contents of common beverages: beer: 11.5 g in 12 oz (1 can); wine: 11.5 g in 4 oz (1 glass); hard liquor: 10.3 g in 1 oz (1 shot).

    5. e. There are three commonly discussed degrees of alcoholic liver disease. These three syndromes often overlap in a given patient.

      1. i. Steatosis (fatty liver)

      2. ii. Alcoholic hepatitis

      3. iii. Micronodular (Laënnec’s) cirrhosis

        Hot Key

        Approximately all heavy drinkers (i.e., those who consume at least 60 g of alcohol per day) develop steatosis; less than one-third develop alcoholic hepatitis and cirrhosis.

  2. B. Clinical Manifestations of Alcoholic Liver Disease. Table 34.1 summarizes the clinical findings that accompany the various degrees of alcoholic liver disease.

    Table 34.1 Classic Findings in Alcoholic Liver Disease

    Syndrome

    Symptoms

    Signs

    Laboratory Findings

    Steatosis

    Usually none

    None, or possibly hepatomegaly with or without tenderness

    AST may be mildly elevated

    Alcoholic hepatitis

    Subjective fever, right upper quadrant pain, nausea, vomiting

    Common: fever, ascites, tender hepatomegaly, proximal muscle loss. The cardinal sign is a rapid onset of jaundice.

    In severe cases, splenomegaly, peripheral edema, encephalopathy may be seen.

    AST and ALT >2 times the upper limit of normal but <300 IU/L; AST/ALT ratio classically >2:1; elevated WBC, neutrophils, PT, alkaline phosphatase,* and bilirubin levels; low hematocrit, platelet count, and albumin

    Cirrhosis

    Anorexia, weight changes, jaundice, variceal bleeding, encephalopathy

    Jaundice, variable liver size (usually small), ascites, splenomegaly, palmar erythema, spider angiomas, testicular atrophy, gynecomastia, Dupuytren’s contractures, asterixis, altered mental status

    Same as alcoholic hepatitis; prerenal azotemia may also be seen and is a poor prognostic marker

    * Alkaline phosphatase may be elevated but is usually less than three times normal.

    ALT = alanine aminotransferase; AST = aspartate aminotransferase; PT = prothrombin time; WBC = serum white blood cell count.

  3. C. Approach to the Patient

    1. a. Steatosis (fatty liver) is usually diagnosed in patients with a history of alcohol consumption accompanied by mildly abnormal liver enzymes, hepatomegaly, or both. A definitive diagnosis may be made by biopsy, but this is rarely necessary. Other possible causes of steatosis include obesity, diabetes, hyperlipidemia, steroids (endogenous or exogenous), starvation, parenteral nutrition, and toxins (e.g., carbon tetrachloride).

    2. b. Alcoholic hepatitis can be mild or life-threatening. The patient often presents with the signs and symptoms after a prolonged “drinking binge.” Sometimes, the onset of symptoms coincides with cessation of drinking (as patients quit drinking because they feel so ill). Although alcoholic hepatitis is a common disease in alcoholics, other diseases (e.g., cholecystitis and cholelithiasis) may closely mimic alcoholic hepatitis. To avoid missing other pathologies, it is important to have a low threshold for obtaining an abdominal ultrasound in an alcoholic patient with right upper quadrant pain. Further, alcoholic patients who present with significantly elevated transaminase levels are likely to have an additional etiology (e.g., acetaminophen toxicity, viral infection).

      Hot Key

      Alcoholic hepatitis does not cause transaminase elevations greater than 300 U/L without an additional cause.

    3. c. Cirrhosis. Alcoholism is the most common causes of cirrhosis in the United States. The diagnosis is usually obvious clinically after the patient develops decompensated liver disease. It is important to evaluate the alcoholic patient for other common causes of liver disease. Many patients who develop chronic alcoholic liver disease also have other disease affecting the liver (e.g., hepatitis C).

  4. D. Treatment

    Hot Key

    Many patients with alcohol-related liver disease have the potential for dramatic improvement in liver function with abstinence from alcohol and supportive care. It is not uncommon for patients with alcoholic hepatitis and ascites (or even encephalopathy) to have complete clinical resolution with long-term abstinence.

    1. a. Steatosis. Abstinence is the mainstay of therapy. Most patients who achieve successful long-term sobriety do so through formal alcohol rehabilitation programs. Exercise and nutritional counseling are advisable for patients with obesity, diabetes, or hyperlipidemia.

    2. b. Alcoholic hepatitis. The long-term prognosis depends on liver function and the patient’s ability to abstain from alcohol consumption. Jaundice and fever may resolve within weeks, whereas ascites and encephalopathy may take months to years to resolve.

      1. i. Supportive therapy includes correction of fluid and electrolyte status and observation for alcohol withdrawal, seizures, and delirium tremens. Patients with alcoholic hepatitis are often significantly malnourished and need aggressive vitamin, mineral, and calorie supplementation.

      2. ii. Steroid therapy may benefit some patients with extensive liver dysfunction. However, the risk for infection outweighs the benefit of steroids in most patients. Clinical scoring systems (e.g., Maddrey’s discriminant function, Glasgow score, Model for End-Stage Liver Disease [MELD] score, and Lille score) are helpful in guiding risk versus benefit of corticosteroid treatment.

        Hot Key

        Even though alcoholic hepatitis is a treatable syndrome, 40% of patients diagnosed die within 6 months of onset.

    3. c. Cirrhosis. Abstinence is critical to prevent worsening of liver function. Management of decompensated cirrhosis is addressed in Chapter 35.

Suggested Further Readings

Carithers RL Jr., Herlong HF, Diehl AM, et al. Methylprednisolone therapy in patients with severe alcoholic hepatitis: a randomized multicenter trial. Ann Intern Med 1989;110:685–90. (Classic Article.)Find this resource:

Ge PS, Runyon BA. Treatment of patients with cirrhosis. N Engl J Med 2016;375:767–77.Find this resource:

Lucey MR, Mathurin P, Morgan TR. Alcoholic hepatitis. N Engl J Med 2009;360:2758–69.Find this resource:

Mathurin P, Louvet A, Duhamel A, et al. Prednisolone with vs without pentoxifylline and survival of patients with severe alcoholic hepatitis: a randomized clinical trial. JAMA 2013;310:1033–41.Find this resource: