Acute Hepatitis
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Introduction
Acute hepatitis describes a condition lasting less than 6 months, resulting in either complete resolution or rapid deterioration towards extensive necrosis and death.
Mechanisms of acute hepatitis can include direct toxin-induced necrosis (ie acetominophen, Amianita phalloides toxin) or immune-mediated damage (ie viral hepatitis).
Alcohol-induced liver injury is quite complex. Ethanol and its metabolites acetaldehyde and nicotinamide adenine dinucleotide phosphate (NADP) are directly hepatotoxic. Induction of cytochrome P-450 and TNF-alpha are also critical in initiating and perpetuating hepatic injury.
The Patient
Inform them of poteitnal risks to partners; don't share razors, etc. Public health may also become involved with contact tracing.
Health Care Team
Community Involvement
The Case of...
Causes and Risk Factors
Causes of acute hepatitis include:
viral hepatitis: HAV, HBV, HCV, HDV, HEV, CMV, EBV
drugs: acetominophen, NSAIDs (ASA, diclofenac) isonaizid, amoxicillin-calvulanic acid
alcohol, ecstacy
toxins: Amanita phalloides
Wilson's disease, hemochromatosis
herbs: comfrey, Ma huang, others
congenital: biliary atresia, Budd-Chiari syndrome
Pathophysiology
Signs and Symptoms
- history
- physical exam
History
Acute viral hepatitis typically begins with a prodromal phase lasting several days, with symptoms inculding malaise, fatigue, anorexia, nausea, vomiting, myalgia, and headache. A mild fever may be present. Arthritis and urticaria may be present due to immune complex deposition.
Taste and smell alterations can occur.
Jaundice and acholic stools soon appear, and may last days or weeks.
Alcoholic hepatitis is potentially very serious and can make people quite ill. Anorexia, nausea, vomiting, weight loss, and abdominal pain are all common. Hepatomegaly and splenomegaly are frequent. Fever is common, but may also be ude to accompanying pneumonia, UTI, or peritonitis. Jaundice may be pronounced with cholestatic features.
Cutaneous signs of liver disease may be present.
Depending on severity, disturbance of neurologic function can be present.
Physical Exam
There are often no signs on physical exam, but the liver and spleen can be enlarged and tender, and mucous membranes can become yellowed.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Liver transaminases ALT and AST are classically elevated 20-100x.
Markers of liver dysfunction can be present and variable. Elevated serum bilirubin above 2.5 mg/dL defines icteric hepatitis.
CBC most commonly shows mild lymphopenia, with anemia and thrombocytopenia also possible.
Serologic markers of viral causes of hepatitis are well-defined.
EBV and CMV can be diagnosed by the elergence of IgM.
HCV can be diagnosed through PCR.
Alcoholic hepatitis is characterized by the following triad:
- Mallory bodies (eosinophilic aggregates) seen near or around cell nuclei
- infiltration by neutrophils
- pericellular, perivenular, and perisinusoidal fibrosis
WBC count may be strikingly elevated, while aminotransferase levels only modestly so. The ratio of AST:ALT is almost always above 2:1.
Diagnostic Imaging
Differential Diagnosis
Treatments
Treatment for acute hepatitis is largely supportive, including rest, hydration, and adequate nutrient intake. Most people prefer a low-fat, high-carbohydrate diet. Alcohol should be avoided.
Nausea can be treated with small doses of metclopramide and hydroxyzine, though hospitalization should follow severe nausea and vomiting, or for people with evidence of detiorating liver function.
Consequences and Course
Acute inury can lead to chronic inflammation.
Acute hepatitis can lead to mild chronic hepatitis, to moderate/severe chronic inflammation, and then to compensated cirrhosis. Once chronic inflammation sets in, hepatocellular carcinoma or death can arise.
The Case of...
Additional Resources
Topic Development
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