eMedicine Specialties > Gastroenterology > Liver

Alcoholic Hepatitis: Follow-up

Author: Anastasios A Mihas, MD, DMSc, FACP, FACG, Professor, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, Virginia Commonwealth University Hospitals and Clinics; Chief of GI Clinical Research, Director of GI Outpatient Service, Associate Director of Hepatology, Hunter Holmes McGuire Veterans Affairs Medical Center
Coauthor(s): Patrick D Hung, MD, Senior Fellow, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Contributor Information and Disclosures

Updated: Jun 30, 2008

Follow-up

Further Inpatient Care

  • In the absence of complications, patients generally can be discharged from acute medical inpatient care facilities once alcohol withdrawal symptoms have cleared; liver function has begun to improve; and complications of liver failure, such as encephalopathy, have resolved with appropriate treatment.
  • In patients who have a potential for rehabilitation, transferring them to an inpatient substance abuse treatment program rather than discharging them from the hospital may be appropriate.

Further Outpatient Care

  • Patients recently discharged from the hospital following an acute bout of alcoholic hepatitis should generally be observed within 2 weeks of their discharge. Subsequent periodic follow-up visits, at intervals ranging from weeks to several months, are appropriate to monitor patients' responses to treatment, including obtaining electrolyte levels and liver test results, and to encourage sobriety.
  • In patients with alcoholic hepatitis who have developed cirrhosis, especially those with coexistent chronic viral hepatitis B or C, consider periodic surveillance for hepatocellular carcinoma. A common algorithm includes determination of the serum alpha-fetoprotein level at 6-month intervals along with annual diagnostic ultrasonography. The finding of a liver nodule or an elevated alpha-fetoprotein level should lead to referral to a liver specialist and additional diagnostic studies.
  • Immunizing patients with alcoholic liver disease against common infectious pathogens, including hepatitis A virus, hepatitis B virus, pneumococci, and influenza A virus, is prudent.

Transfer

  • Patients with alcoholic hepatitis of mild-to-moderate severity can be treated in a primary care setting. In general, for patients with severe alcoholic hepatitis or cirrhosis, observation by a gastroenterologist or a hepatologist is desirable, particularly if the illness is of sufficient severity or complexity to require intensive care.
  • If patients become comatose or have complications that may require surgical intervention, the treating physician should consider emergent transfer to a tertiary care center with experience in the treatment of liver failure. In selected cases, the use of novel liver-assist devices (artificial livers) may provide transient improvement in the manifestations of liver failure.

Complications

  • Most complications of alcoholic hepatitis are identical to those of cirrhosis.

    • Variceal hemorrhage: Acute variceal bleeding constitutes one of the most devastating emergencies, not only in gastroenterology but also in medicine at large. Resuscitation of the patient and protection of the airway are the 2 most important steps in the treatment of acute variceal bleeding. Cessation of the acute bleeding is usually achieved in more than 90% of patients with the combination of interventional endoscopy (sclerotherapy or banding ligation) and the intravenous infusion of pharmaceutical agents that lower the pressure within the portal system (somatostatin or one of its long-acting analogues, eg, octreotide). Alternatively and for patients who continue to bleed in spite of interventional endoscopy and drug therapy, more invasive options, such as balloon tamponade, a transjugular intrahepatic portosystemic shunt, and an emergency portal-caval shunt, may be used.
    • Hepatic encephalopathy: The development of encephalopathy in patients with alcoholic hepatitis is invariably associated with a grave prognosis. Treatment consists of close monitoring of the patient and the administration of lactulose or nonabsorbable antibiotics. Low energy or protein intake is not indicated, except transiently in severe cases. The use of benzodiazepine receptor antagonists (ie, flumazenil [Romazicon]) is still experimental. Rarely, rapidly progressive worsening of encephalopathy leading to deep coma may be associated with cerebral edema, as observed in fulminant hepatic failure. In selected instances, aggressive treatment with intracranial pressure monitoring and liver-assist devices may be considered.
    • Coagulopathy and thrombocytopenia: Profound hypoprothrombinemia may ensue in the course of severe alcoholic hepatitis, especially in patients with variceal bleeding. Administer fresh-frozen plasma to temporarily restore the depleted hepatic prothrombin stores. The value of parenteral administration of vitamin K is dubious because the hepatocytes are incapable of synthesizing new prothrombin. Platelet transfusions are not usually necessary to correct thrombocytopenia unless the patient is actively bleeding or undergoes an invasive procedure.
    • Ascites: Acute onset of ascites may develop in patients with alcoholic hepatitis, even in the absence of overtly decompensated liver disease and portal hypertension. The ascites is typically transudative, with a very low albumin concentration (<1 g/dL). In patients who are hemodynamically stable with normal renal function, bed rest and salt restriction may be sufficient to mobilize fluid. The addition of diuretics (typically spironolactone and furosemide) permits clearing of fluid in most patients. In some individuals who do not respond to these measures, periodic large-volume paracentesis with intravenous albumin supplementation may be required. With continued abstinence, the salt-retaining tendency may improve; in many instances, the diuretics can be withdrawn safely after a period of months without any reaccumulation of ascites.
    • Spontaneous bacterial peritonitis: This condition may develop in patients with alcoholic hepatitis and ascites, especially in those with concomitant gastrointestinal bleeding. Following a confirmatory diagnostic paracentesis, broad-spectrum antibiotic therapy with a second- or third-generation cephalosporin is the treatment of choice.
    • Iron overload: Several histopathologic studies have shown that as many as 50% of patients with alcoholic liver disease have increased hepatic iron content compared with healthy controls. This excess deposition of iron may play a significant role in the progression of the alcoholic liver damage. Portosystemic shunts, especially the side-to-side variety, enormously increase the deposition of iron to the liver. Occasionally, this excessive iron deposition leads to a clinical and pathologic entity that is analogous to primary hemochromatosis. Attempts to treat alcoholic liver disease with phlebotomy to reduce iron overload have been hampered by the development of anemia, and no clear benefit has been observed.

Prognosis

  • During the past several decades, various formulas and algorithms have been proposed for predicting the outcome of severe alcoholic hepatitis. The single most reliable indicator of severity is the presence of hepatic encephalopathy.
  • The discriminant function (DF) of Maddrey and coworkers is based on PT and bilirubin, and it is calculated as follows:
    DF = (4.6 X PT prolongation) + total serum bilirubin in mg/dL
    • Values greater than 32 indicate severe disease and predict a 30-day mortality rate of approximately 50%, assuming only supportive treatment is given.
    • Subsequent studies have found the DF to be an inexact predictor of mortality in patients with alcoholic hepatitis, especially in those who receive glucocorticoids.
  • Other formulas have been proposed for the assessment of prognosis of alcoholic hepatitis, but none has become popular among clinicians. The Combined Clinical and Laboratory Index of the University of Toronto permits a linear estimate of acute mortality in persons with alcoholic hepatitis. Its major disadvantages are the large number (14) of variables that must be scored and the complexity of the calculation itself.
  • In contrast to the Combined Clinical and Laboratory Index, a much simpler formula for assessing mortality was proposed in a large series of 142 patients with histologically proven alcoholic hepatitis based on PT, serum bilirubin level, and serum albumin level.36

    • According to this study, the mortality rate in patients with a serum bilirubin level greater than 2 mg/dL, a serum albumin level less than 2.5 g/dL, and a PT greater than 5 seconds was 75%.
    • Conversely, patients who did not meet all 3 criteria had a much lower mortality rate (approximately 25%).
  • Model for end-stage liver disease (MELD) score: In recent years, several retrospective studies have shown that the MELD score is useful in predicting 30- and 90-day mortality in patients with alcoholic hepatitis. Moreover, the MELD score seems to contain some practical and statistical advantages over Maddrey's DF in predicting mortality among these patients. In a cohort of 73 patients with alcoholic hepatitis at the Mayo Clinic, the MELD score was the only independent predictor of mortality.10 Likewise, in another much larger retrospective study of 202 patients with alcoholic hepatitis, the MELD score was found superior to not only Maddrey's DF but also the classical Child-Turcotte-Pugh (CTP) score.50
  • Glasgow alcoholic hepatitis score (GAHS): GAHS is one of the most recently described predictors of outcome in patients with alcoholic hepatitis. GAHS uses 5 different variables, including age, bilirubin, BUN, PT, and white blood cell count. The overall accuracy of GAHS, which was validated in 195 patients with alcoholic hepatitis, was 81%, when predicting 28-day outcome. In contrast, the modified DF had an overall accuracy of only 50%.12
  • Asymmetric dimethylarginine (ADMA) score: The ADMA score is the most recently proposed predictor of adverse clinical outcome in patients with severe alcoholic hepatitis. In a small prospective study of 27 patients with alcoholic hepatitis, the ADMA score was a better predictor of outcome than the CTP score, the DF, or the MELD score.38  
  • Other factors that correlate with poor prognosis include older age, impaired renal function, encephalopathy, and a rise in the white blood cell count in the first 2 weeks of hospitalization.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Tort claims regarding steroid-induced aseptic necrosis of the hip are very common. Physicians treating patients with alcoholic hepatitis for longer than the recommended period should discuss the issue with the patient and the patient's family and obtain consent. Patients with mild forms of alcoholic hepatitis should not be treated with steroids.
  • Changes in the mental status of patients with alcoholic hepatitis do not always imply the presence of hepatic encephalopathy. Entities (eg, subdural hematomas) should be excluded by obtaining a CT scan of the brain.
 


More on Alcoholic Hepatitis

Overview: Alcoholic Hepatitis
Differential Diagnoses & Workup: Alcoholic Hepatitis
Treatment & Medication: Alcoholic Hepatitis
Follow-up: Alcoholic Hepatitis
Multimedia: Alcoholic Hepatitis
References
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Further Reading

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Keywords

alcoholic steatohepatitis, alcoholic steatonecrosis, sclerosing hyaline necrosis, subacute alcoholic cirrhosis, florid alcoholic cirrhosis, fatty liver with hepatic failure, acute hepatic insufficiency of patients with chronic alcoholism, steatosis, cirrhosis, alcoholism, alcoholic cirrhosis, alcoholic liver disease, chronic alcoholism, alcohol-induced cirrhosis, alcohol-induced hepatitis, hepatomegaly, portal hypertension, ascites, variceal hemorrhage, hepatic encephalopathy, Mallory hyaline inclusions, protein-energy malnutrition, PEM, giant mitochondria, megamitochondria, hepatitis C infection, acetaminophen-alcohol interactions, jaundice, coagulopathy, delirium tremens, respiratory alkalosis, scleral icterus, splenomegaly, flapping tremor, spider angiomata, gynecomastia, heavy intake of ethanol

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Contributor Information and Disclosures

Author

Anastasios A Mihas, MD, DMSc, FACP, FACG, Professor, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, Virginia Commonwealth University Hospitals and Clinics; Chief of GI Clinical Research, Director of GI Outpatient Service, Associate Director of Hepatology, Hunter Holmes McGuire Veterans Affairs Medical Center
Anastasios A Mihas, MD, DMSc, FACP, FACG is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Federation for Clinical Research, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Gastroenterology Research Group, Sigma Xi, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Coauthor(s)

Patrick D Hung, MD, Senior Fellow, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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