CONFIRMING DIAGNOSIS Liver biopsy, the definitive test for cirrhosis, detects destruction and fibrosis of hepatic tissue.
Liver scan shows abnormal thickening and a liver mass. Cholecystography and cholangiography visualize the gallbladder and the biliary duct system, respectively; splenoportal venography visualizes the portal venous system. Percutaneous trans-hepatic cholangiography differentiates extrahepatic from intrahepatic obstructive jaundice and discloses hepatic pathology and the presence of gallstones.
Laboratory findings that are characteristic of cirrhosis include:
❑ decreased white blood cell count, hemoglobin level and hematocrit, albumin, serum electrolyte levels (sodium, potassium, chloride, and magnesium), and cholinesterase
❑ elevated levels of globulin, serum ammonia, total bilirubin, alkaline phosphatase, serum aspartate aminotransferase, serum alanine aminotransferase, and lactate dehydrogenase and increased thymol turbidity
❑ anemia, neutropenia, and thrombocytopenia, characterized by prolonged prothrombin and partial thromboplastin times
❑ deficiencies of folic acid, iron, and vitamins A, B12, C, and K.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hepatitis:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Patients may complain of anorexia, fever, arthralgia, malaise, vomiting, diarrhea, or chills. Complaints of dark urine or jaundice are highly suggestive of hepatitis. As these symptoms are seen in many types of hepatitis, specific questions help categorize the cause.
A. Viral hepatitis. Does the patient have exposure to blood (transfusions before 1990, tattoos, body piercing, shared razor, needlestick, sharing needles, intranasal cocaine use)? Hepatitis B is most commonly transmitted via contaminated blood or sexually via risky sexual behaviors (anal intercourse, prostitution, multiple sexual partners). Hepatitis A and E are transmitted via the fecal-oral route. Does the patient have a history of travel to developing countries, raw shellfish ingestion, or work in an institution or daycare?
B. Drug-induced hepatitis. Does the patient use prescription or over-the-counter medication? The drugs most often associated with hepatitis are anesthetics (halothane), neuropsychotropics (chlorpromazine, haloperidol, tricyclics), anticonvulsants (phenytoin), analgesics (acetaminophen, ibuprofen), antigout (allopurinol), hormonal derivatives and drugs used in endocrine disease (glipizide, tamoxifen, anabolic steroids, oral contraceptives), antimicrobials (tetracyclines), cardiovascular drugs (amiodarone, procainamide), antineoplastic (cisplatin), vitamin A, propoxyphene, cimetidine, and ferrous sulfate.
C. Alcoholic hepatitis. Could the patient be an alcoholic? Inquire about quantitative alcohol intake and obtain a history from both patient and family members. Use the CAGE questionnaire to help identify individuals at high risk. Inquire about alcohol-associated illnesses (pancreatitis) and motor vehicle citations.
D. Chronic hepatitis. Has the patient ever been jaundiced or diagnosed with hepatitis before (Chapter 9.10)? Has the patient had elevated liver enzymes for at least 6 months? The most common cause of chronic hepatitis and cirrhosis is alcohol. Viral hepatitis B and C often cause chronic hepatitis, cirrhosis, or hepatocellular carcinoma. Other causes of chronic hepatitis are drug-induced, Wilson’s disease, and α1-antitrypsin deficiency.
E. Autoimmune hepatitis. Is there a history of arthritis, amenorrhea, or rash? Mediated by the deposition of circulating immune complexes, this disease is also referred to as “chronic active hepatitis.” It is more common in female patients and adolescents; prior hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is a triggering factor.
Physical examination
A. General examination. Common findings in viral, alcoholic, or drug-induced hepatitis include fever, jaundice, scleral icterus, weight loss, muscle tenderness or weakness, and a palpable tender liver. Ecchymosis or petechiae indicates significant clotting factor abnormalities and, coupled with a small liver which diminishes in size, is suggestive of severe hepatitis or impending hepatic failure.
B. Chronic liver disease results in progressive liver dysfunction, fluid retention, and portal hypertension. The liver plays a key role in the detoxification of endogenous hormones, drugs, and ingested substances. Abnormalities in estrogen metabolism have often been considered the cause of peripheral stigmata such as spider angiomata, palmar erythema, gynecomastia, parotid enlargement, and testicular atrophy.
C. Does the abdominal examination reveal hepatosplenomegaly? Modest enlargement of the liver occurs in acute viral and chronic hepatitis, whereas marked enlargement (>10 cm below the costal margin) is seen in alcoholic hepatitis. Ascites, prominent abdominal collateral veins, bruits, rubs, abdominal masses, or a palpable gallbladder can also indicate hepatitis, whereas a small liver can indicate cirrhosis.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hepatitis, viral:
Diagnosis
(Handbook of Diseases)
In suspected viral hepatitis, a hepatitis profile is routinely performed. This study identifies antibodies specific to the causative virus, establishing the type of hepatitis as follows:
❑ Type A: Detection of an antibody to hepatitis A confirms the diagnosis.
❑ Type B: The presence of HBsAg and hepatitis B antibodies confirms the diagnosis.
❑ Type C: The diagnosis depends on serologic testing for the specific antibody 1 or more months after the onset of acute hepatitis. Until then, the diagnosis is established primarily by obtaining negative test results for hepatitis A, B, and D.
❑ Type D: Detection of intrahepatic delta antigens or immunoglobulin (Ig) M antidelta antigens in acute disease (or IgM and IgG in chronic disease) establishes the diagnosis.
❑ Type E: Detection of hepatitis E antigens supports the diagnosis; the diagnosis may also be determined by ruling out hepatitis C.
❑ Type G: Detection of hepatitis G antigen supports diagnosis; the patient may be otherwise symptomless.
Additional findings from liver function studies support the diagnosis:
❑ Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the prodromal stage of acute viral hepatitis.
❑ Serum alkaline phosphatase levels are slightly increased.
❑ Serum bilirubin levels are elevated. Levels may continue to be high late in the disease, especially in severe cases.
❑ Prothrombin time (PT) is prolonged (more than 3 seconds longer than normal indicates severe liver damage).
❑ White blood cell counts commonly reveal transient neutropenia and lymphopenia followed by lymphocytosis.
❑ Liver biopsy is performed if chronic hepatitis is suspected. (It’s performed for acute hepatitis only if the diagnosis is questionable.)
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Source: Handbook of Diseases, 2003
Hepatic encephalopathy:
Diagnosis
(Handbook of Diseases)
Clinical features, a positive history of liver disease, and elevated serum ammonia levels in venous and arterial samples confirm hepatic encephalopathy. Other supportive test results include an EEG that slows as the disease progresses, an elevated bilirubin level, and prolonged prothrombin time.
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Source: Handbook of Diseases, 2003
Hepatitis, nonviral:
Diagnosis
(Handbook of Diseases)
Diagnostic findings include elevations in serum aspartate aminotransferase, alanine aminotransferase, both total and direct bilirubin (with cholestasis), and alkaline phosphatase levels; white blood cell (WBC) count; and eosinophil count (possible in the drug-induced type).
A liver biopsy may help identify the underlying pathology, especially infiltration with WBCs and eosinophils. Liver function tests have limited value in distinguishing between nonviral and viral hepatitis.
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Source: Handbook of Diseases, 2003
Cirrhosis:
Diagnosis
(Handbook of Diseases)
A liver biopsy, the definitive test for cirrhosis, detects destruction and fibrosis of hepatic tissue. A liver scan shows abnormal thickening and, possibly, a liver mass.
Plain films of the abdomen may reveal hepatic or splenic enlargement. Ultrasonography can aid in the assessment of liver size and the detection of ascites or hepatic enlargement. Doppler ultrasonography is used to evaluate patency of the splenic, portal, and hepatic veins. Computed tomography with I.V. contrast or magnetic resonance imaging with serum alpha-fetoprotein levels can help with further assessment of liver nodules. A biopsy of suspicious liver nodules or masses can be performed to check for cancer. Esophagogastroscopy can be used to detect causes of bleeding in the esophagus, stomach, and proximal duodenum and confirm the presence of varices.
The following laboratory findings are characteristic of cirrhosis:
❑ decreased platelet count, decreased hematocrit, and decreased levels of hemoglobin, albumin, electrolytes (sodium, potassium, chloride, and magnesium), and folate
❑ elevated levels of globulin, serum ammonia, total bilirubin, alkaline phosphatase, serum aspartate aminotransferase, serum alanine aminotransferase, and lactate dehydrogenase
❑ increased thymol turbidity
❑ coagulation abnormalities characterized by prolonged prothrombin and partial thromboplastin times.
Clinical tip The best indications of hepatic function are prothrombin time and cholesterol and albumin levels.
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Source: Handbook of Diseases, 2003
Hepatitis:
Diagnosis
(Pediatric Infectious Disease)
The diagnosis of hepatitis A is made by serology. Serum immunoglobulin M (IgM)
to hepatitis A is usually present at the onset of illness. The presence of
hepatitis A IgG without IgM indicates past infection and immunity.
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Source: Pediatric Infectious Disease, 2004
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