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Alcoholic Hepatitis Clinical Presentation

  • Author: Douglas M Heuman, MD, FACP, FACG, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Dec 27, 2015
 

History and Physical Examination

Heavy alcohol use is a prerequisite for the development of alcoholic hepatitis. The history is usually apparent; however, in some patients, alcohol use may be covert.

Clues to the presence of alcoholism include a history of multiple motor vehicle accidents, convictions for driving while intoxicated, and poor interpersonal relationships. Alcoholism exhibits a genetic predisposition, and a history of alcoholism in a close relative may also indicate that a patient is at risk.

Presentation

Patients with clinically symptomatic alcoholic hepatitis typically present with nonspecific symptoms of nausea, malaise, and low-grade fever. The clinical presentation may be precipitated by complications of impaired liver function or portal hypertension, such as upper gastrointestinal hemorrhage from esophageal varices, confusion and lethargy from hepatic encephalopathy, or increased abdominal girth from ascites.

A person who uses alcohol heavily may come to medical attention because of an intercurrent medical illness that produces altered mental status or persistent vomiting, which, in turn, triggers alcohol withdrawal symptoms. In such instances, the clinician must be alert to the presence of a precipitating illness (eg, subdural hematoma, acute pancreatitis, gastrointestinal hemorrhage) and to the likelihood of alcohol withdrawal symptoms (eg, seizures, delirium tremens) in addition to the problems associated with alcoholic hepatitis.

2010 AASLD screening and diagnostic recommendations for ALD

The 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) practice guideline includes the following recommendations for screening and diagnosis[3] :

  • After discussion of alcohol use with the patient, if abuse or excess use is suspected, screen the patient for alcohol abuse using a structured questionnaire such as the Alcohol Use Disorders Identification Test (AUDIT)
  • If the patient's history or a screening test is positive for alcohol abuse, use laboratory testing to verify the diagnosis of ALD and rule out other considerations
  • If ALD is present, examine the patient for evidence of other alcohol-related organ damage

Physical examination

Patients with alcoholic hepatitis are commonly febrile with tachycardia. Mild tachypnea with primary respiratory alkalosis may be observed. The liver is usually enlarged, often with mild hepatic tenderness. Hepatomegaly results from both steatosis and swelling of injured hepatocytes.

Manifestations of hepatic failure or portal hypertension may include scleral icterus with darkening of the urine, splenomegaly, asterixis (a flapping tremor characteristic of metabolic encephalopathies), peripheral edema, and bulging flanks with shifting abdominal dullness (indicating the presence of ascites).

Spider angiomata, proximal muscle wasting, altered hair distribution, and gynecomastia may be observed, although these findings most commonly reflect coexistent cirrhosis.

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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 (FFP) 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

Spontaneous bacterial peritonitis 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.

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Contributor Information and Disclosures
Author

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, American Gastroenterological Association

Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.

Coauthor(s)

Patrick D Hung, MD Senior Fellow, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Disclosure: Nothing to disclose.

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 Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Sigma Xi, Southern Society for Clinical Investigation, American Federation for Clinical Research, Gastroenterology Research Group

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Gilead Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership

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Liver biopsy sample shows typical findings of perivenular polymorphonuclear infiltrate and ballooning degeneration of hepatocytes (hematoxylin and eosin [H&E] stain). Courtesy of H. Robert Lippman, MD.
Ethanol (ETOH) and cytokine production. CYP = cytochrome P; IL = interleukin; NF-κB = nuclear factor-kappa B; ROS = reactive oxygen species; TNF = tumor necrosis factor.
Mechanisms of cytokine injury. IL = interleukin ; NO = nitric oxide; O2- = superoxide anion; OH- = hydroxyl radical; PMN = polymorphonuclear lymphocyte; TNF = tumor necrosis factor.
 
 
 
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