Alcoholic Hepatitis Clinical Presentation
- Author: Douglas M Heuman, MD, FACP, FACG, AGAF; Chief Editor: BS Anand, MD more...
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.
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 :
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
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.
Most complications of alcoholic hepatitis are identical to those of cirrhosis.
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.
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.
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.
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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