Nonviral hepatitis is an inflammation of the liver that usually results from exposure to certain chemicals or drugs. Most patients recover from this illness, although a few develop fulminating hepatitis, hepatic failure, or cirrhosis.
Viral hepatitis is a common infection, resulting in hepatic cell destruction, necrosis, and autolysis. In most patients, hepatic cells eventually regenerate with little or no residual damage. However, old age and serious underlying disorders make complications more likely. The prognosis is poor if edema and hepatic encephalopathy develop.
· Hepatotoxic chemicals, such as carbon tetrachloride, trichloroethylene, vinyl chloride
· Hepatotoxic drugs, such as acetaminophen
· Poisonous mushrooms
· Vinyl chloride
· Infection by hepatitis virus A, B, C, D, E, G, or transfusion transmissible virus
After exposure to a hepatotoxin, hepatic cellular necrosis, scarring, Kupffer cell hyperplasia, and infiltration by mononuclear phagocytes occur with varying severity. Alcohol, anoxia, and preexisting liver disease exacerbate the effects of some toxins.
Drug-induced hepatitis may begin with a hypersensitivity reaction unique to the individual, unlike toxic hepatitis, which appears to affect all exposed people indiscriminately. Symptoms usually manifest after 2 to 5 weeks of therapy.
Hepatic damage is usually similar in all types of viral hepatitis, but extent of cell injury or necrosis varies.
The virus causes hepatocyte injury and death, either by directly killing the cells or by activating inflammatory and immune reactions. The inflammatory and immune reactions, in turn, injure or destroy hepatocytes by lysing the infected or neighboring cells. Later, direct antibody attack against the viral antigens causes further destruction of the infected cells. Edema and swelling of the interstitium lead to collapse of capillaries, decreased blood flow, tissue hypoxia, scarring, and fibrosis. Complications include chronic persistent hepatitis (which may prolong recovery up to 8 months), chronic active hepatitis, cirrhosis, hepatic failure and death, and primary hepatocellular carcinoma.
Signs and symptoms
· Anorexia, nausea, vomiting
· Jaundice, dark urine, clay-colored stool
· Possible abdominal pain
Viral, prodromal phase
· Easy fatigue, generalized malaise, anorexia, mild weight loss
· Arthralgia, myalgia
· Nausea, vomiting, changes in senses of taste and smell
· Right upper quadrant tenderness
· Dark-colored urine, clay-colored stools
Viral, icteric phase
· Worsening of prodromal symptoms
· Abdominal pain or tenderness
Viral, recovery phase
· Symptoms subside and appetite returns
Diagnostic test results
· Hepatitis profile study identifies antibodies specific to the causative virus, establishing the type of hepatitis.
· Blood chemistry reveals elevated serum aspartate aminotransferase and serum alanine aminotransferase levels in the prodromal stage.
· Serum alkaline phosphatase level is slightly increased.
· Serum bilirubin level may remain high into late disease, especially in severe cases.
· Prothrombin time is prolonged (greater than 3 seconds longer than normal indicates severe liver damage).
· White blood cell counts reveal transient neutropenia and lymphopenia followed by lymphocytosis.
· Liver biopsy identifies underlying disease.
· Lavage, catharsis, or hyperventilation, depending on the route of exposure—as soon as possible after exposure
· Acetylcysteine as antidote for acetaminophen poisoning
· Rest to minimize energy demands
· Avoidance of alcohol or other hepatotoxic drugs
· Small, high-calorie meals
· Parenteral nutrition if patient can't eat
· Standard immunoglobulin
· Alfa-2B interferon
· Liver transplantation
Vaccination against hepatitis A and B provides immunity to these viruses before transmission occurs.
UNDERSTANDING LIVER BIOPSY RESULTS