Jaundice

Jaundice: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter

James M. Brian and Cara K. Fox

The hepatobiliary system removes bilirubin, a byproduct of hemoglobin metabolism, from the blood stream. Jaundice, a yellowing of the skin and sclera, results from tissue build-up of bilirubin when the hepatobiliary system does not function properly.

Approach

The most important task in evaluating jaundice is to determine whether the jaundice is caused by the overproduction of bilirubin, by the inability of the hepatocyte and biliary drainage system to adequately clear the blood of bilirubin, or by a combination of both. Possible causes are then established based on the mechanism (1).

A. Increased bilirubin production results from hemolysis, ineffective erythropoiesis, reabsorption of hematoma, or transfusion.

 B. Impaired bilirubin elimination can be a result of either decreased hepatobiliary excretion, cholestasis, or a combination of both. Decreased hepatobiliary excretion usually results from a hereditary defect or hepatocyte damage. Poor excretion occurs because of impaired biliary uptake and transport by the liver cell, conjugation, excretion, or transport by the biliary system. Alcohol, drug toxicity, and viral hepatitis commonly cause decreased hepatobiliary excretion as well as obstruction. Cholelithiasis and malignancy often lead to obstructive cholestasis. Examples of cholestasis include viral or alcoholic hepatitis, drug-induced hepatitis, primary biliary cirrhosis, congestive heart failure, sepsis, pregnancy, neoplasm, or gallstones (2).

History

 A. Does the patient have exposure risk to alcohol, drugs, toxins, or medications? A history of nonprescription and prescription drugs and potential chemical toxins at home or work must be elicited.

 B. Recent trauma can result in hemolysis. Pruritus, dark urine, and clay-colored stools suggest cholestasis. If the patient presents with right upper quadrant pain and nausea following a fatty meal, think cholelithiasis. A fever with right upper quadrant pain suggests cholangitis or, with a history of exposure, hepatitis. Jaundice, vague epigastric discomfort, and weight loss suggest pancreatic cancer. A family history of liver disease points to a hereditary cause (e.g., Gilbert’s or Wilson’s syndromes).

C. Is the jaundice acute or chronic? Acute onset of jaundice suggests a viral hepatitis, acute liver failure, or an acute biliary tract obstruction. Gradual onset of jaundice points to chronic liver failure, alcohol toxicity, or malignancy. A lifelong history of jaundice suggests an inherited metabolic or hemolytic cause.

Physical examination

The physical examination should focus on the following: Eyes should be examined for icterus or Kayser-Fleischer rings, which are copper-colored rings suggestive of Wilson’s disease. Heart and lung examination revealing S₃ gallop or rales is suggestive of congestive heart failure, which leads to passive liver congestion. Ascites, hepatosplenomegaly, venous hum, and tenderness on abdominal examination points to portal hypertension and indicates liver cirrhosis (Chapters 9.2 and 9.9). Suspect pancreatic carcinoma when a nontender, palpable mass is found on upper abdominal examination. Signs of cirrhosis include excoriations, spider nevi, caput medusa, Dupytren’s contracture, gynecomastia, and palmar erythema. Delirium, drowsiness, asterixis, and tremor occur with liver failure.

Testing

 A. Laboratory tests. Laboratory assays measure bilirubin as indirect (unconjugated) and direct (conjugated) fractions. An elevated indirect bilirubin level is consistent with overproduction of bilirubin or decreased uptake, transport, or conjugation by the hepatocyte. Elevation of direct bilirubin points to decreased excretion or transport by the biliary system (3). Transaminase levels (aspartate aminotransferase and alanine aminotransferase) increase from hepatocellular necrosis or inflammation from the release of aspartate aminotransferase from lysed hepatocytes. Hepatocyte damage and cholestasis increase alkaline phosphatase levels. γ-Glutamyl transpeptidase levels increase in cholestasis and alcohol abuse. Pancreatitis, pancreatic carcinoma, or common bile duct stones elevate amylase levels. With hepatocellular damage, coagulation studies can be prolonged. Antimitochondrial antibodies are present in primary biliary cirrhosis. Hepatitis B serologic tests are summarized in Table 9.8. Hepatitis A IgM antibody detects acute stage hepatitis A and IgG detects chronic stage hepatitis A. Anti-hepatitis C virus indicates hepatitis C infection. Hepatitis D only occurs with hepatitis B infection and is detected by anti-hepatitis D (4).

 B. Diagnostic imaging has limited uses. Plain films of the abdomen rarely provide useful information. Cholelithiasis or pancreatic mass are best detected by ultrasound. Magnetic resonance imaging or computed tomography scans are used to examine the liver, pancreas, biliary tree, and suspected obstruction not identified by ultrasound. Hepatoiminodiacetic acid scanning is useful in a patient with suspected acute cholecystitis. Percutaneous transhepatic cholangiography and endoscopic retrograde cholangiopancreatography are used if obstructive jaundice is suspected to show the cause, location, and extent of involvement (5).

 C. Other tests. Percutaneous liver biopsy is not indicated in the routine workup of jaundice but may prove useful in diagnosing the cause of jaundice when the above-mentioned tests are inconclusive. Iron levels are increased in hemochromatosis. Copper levels are increased in Wilson’s disease.

Diagnostic assessment

The patient’s history and associated symptoms guide the initial differential diagnosis of jaundice. Physical examination further narrows the causative choices and analysis of hepatic enzyme levels and viral serologies should confirm the initial diagnosis. Imaging studies play a limited role, except in suspected cases of malignancy or biliary obstruction.

Most patients have acute viral hepatitis as the cause of jaundice. Consultation is indicated when testing is inconclusive, when a surgical cause is suspected, or as needed for treatment.

References

1. Scharschmidt BF, Goldberg HI, Schmid R. Approach to the patient with cholestatic jaundice. N Engl J Med 1983;308:1515.

2. Lucas WB, Chuttani R. Pathophysiology and current concepts in the diagnosis of obstructive jaundice. Gastroenterologist 1995;3:105–118.

3. Fevery J, Blanckaert N. What can we learn from analysis of serum bilirubin?
J Hepatol 1986;2:113–121.

4. Bakerman S. ABC’s of interpretive laboratory data, 3rd ed. Myrtle Beach, SC: Interpretive Data, Inc., 1994:279–286.

5. Barloon TJ, Bergus GR, Weissman AM. Diagnostic imaging to identify the cause of jaundice. Am Fam Physician 1996;54:556–562.

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Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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