Jaundice

Jaundice: Excerpt from Field Guide to Bedside Diagnosis

Differential Overview

Conjugated

❑ Viral hepatitis

❑ Gallstone obstruction

❑ Drugs

❑ Carotinemia

❑ Alcohol-induced hepatitis

❑ Cirrhosis

❑ Pregnancy (cholestatic)

❑ Postoperative

❑ Metastatic cancer

❑ Pancreatic cancer

❑ Ampullary carcinoma

❑ Hepatoma

❑ Sclerosing cholangitis

❑ Primary biliary cirrhosis

❑ Leptospirosis

❑ Hepatic vein obstruction (Budd-Chiari)

❑ Hemochromatosis

Unconjugated

❑ Hemolysis

❑ Gilbert syndrome

❑ Sepsis

Diagnostic Approach

Jaundice becomes clinically apparent when the bilirubin level reaches 2 to 2.5 mg/dL. Scleral elastin has a high affinity for bilirubin, and with a white background, it is a sensitive indicator of jaundice. Biliary obstruction gives a greenish skin tint due to accumulation of biliverdin. Hemolysis gives a lemon-yellow tint when observed in natural light. An orange-yellow color is more consistent with hepatocellular disease. Pseudojaundice may be found in black patients with pigmented sclera, with carotinemia, with uremia (a sallow yellowish pallor), and with quinacrine (a yellow-green color).

Dark urine with green foam confirms a conjugated hyperbilirubinemia and excludes hemolysis or a conjugating defect. Unconjugated bilirubin is tightly bound to albumin, which prevents glomerular filtration.

Courvoisier law states: “In a jaundiced patient, a palpable gallbladder indicates that the jaundice is not due to stones.” Painless jaundice usually suggests a gradual process, as is found in intrahepatic cholestasis. The liver in this case is usually enlarged, smooth, and nontender. A patient with hepatocellular disease appears more ill than one with obstruction. Fluctuating jaundice occurs with gallstones, ampullary carcinoma, or toxins.

Anorexia, nausea, vomiting, or weight loss within 2 weeks of the appearance of jaundice suggests acute hepatitis or gallstones. Appearance more than 2 weeks prior suggests malignant biliary obstruction, chronic hepatitis, or toxin exposure (e.g., alcohol). Generalized pruritus suggests biliary obstruction, either extrinsic due to tumor, or canalicular due to drug-induced intrahepatic cholestasis.

Ascites with jaundice is an ominous sign, signifying decompensated cirrhosis with portal hypertension or malignancy with liver metastases. In portal hypertension, veins are engorged radially away from the umbilicus. In inferior vena cava obstruction, flow occurs upward over the abdominal wall. A harsh hepatic bruit may occur with malignancy, alcoholic hepatitis, or hemangioma. Splenomegaly without hepatomegaly occurs with hemolysis or portal vein occlusion.

Clinical Findings

Viral hepatitis  Prodromal symptoms are anorexia, nausea, abdominal pain, arthralgias, fever, and malaise. The liver is tender and slightly enlarged. There may be an exposure history (travel to endemic areas, transfusion, consumption of raw shellfish, or intravenous drug use or needlestick injury). The urine will be dark with acholic pale stools.

Gallstone obstruction  A pattern of right upper quadrant pain occurring in episodes over months to years is often seen. Pain radiates to the tip of the right scapula, shoulder, or back. Sudden onset of colicky pain, nausea, and vomiting followed by fever suggests passage of a gallstone that had obstructed the common bile duct.

Drugs  Estrogens produce canalicular cholestasis. Phenothiazines produce ductular cholestasis. Methyldopa causes autoimmune hemolytic anemia. Hepatotoxins include niacin, acetaminophen, isoniazid, phenytoin, sulfonamides, ketoconazole, erythromycin estolate, chlorpromazine, propylthiouracil, anabolic steroids, valproate, amiodarone, vitamin A and D (in high doses), carbon tetrachloride, and amanita mushrooms.

Carotinemia  An orange-yellow hue is observed, most prominently in the palms and cheeks. The urine and sclera are normal colored. It is usually due to consumption of excessive vitamins or yellow/green vegetables. Myxedema may also produce carotinemia due to altered metabolism.

Alcohol-induced hepatitis  A history of binge drinking and the odor of ethanol on the breath are found. The liver will be enlarged, as opposed to shrunken and firm in cirrhosis.

Cirrhosis  A history of alcohol abuse is discovered. The liver edge is nodular. Signs of estrogen effect such as palmar erythema, gynecomastia, testicular atrophy, and spider telangiectasias are often present. Ascites and a prominent venous pattern on the abdominal wall are late manifestations.

Pregnancy (cholestatic)  Jaundice rarely occurs in the third trimester with intrahepatic cholestasis, along with itching, pale stools, and dark urine.

Postoperative  Jaundice occurs by several mechanisms including hemolysis of transfused blood, reabsorption of a hematoma, hematoperitoneum, sepsis, hypotension, and biliary tract injury.

Metastatic cancer  The liver is nodular and firm. There is usually right upper quadrant pain, which increases with inspiration. There may be a friction rub over the liver. A primary source is usually known.

Pancreatic cancer  Deep left upper quadrant pain, dramatic involuntary weight loss preceding the appearance of jaundice, depression, and recurrent venous thromboses are clues. A palpable, nontender gallbladder (Courvoisier sign) suggests malignant obstruction of the common bile duct with gradual
distension of the gallbladder. Edema arising in a jaundiced patient without ascites or cardiorenal disease suggests pancreatic cancer with inferior vena cava obstruction.

Ampullary carcinoma  It may rarely produce the fabled “silver stools,” clay-
colored acholic stools combining with bleeding. More commonly, it is recognized when acute pancreatitis is caused by blockage of the pancreatic duct in a patient with signs of cancer (e.g., weight loss), and by fluctuating
jaundice.

Hepatoma  In a patient with a history of estrogen use, a harsh arterial murmur is heard over the liver.

Sclerosing cholangitis  It occurs with active inflammatory bowel disease. Inflammatory bowel disease is also associated with cholangiocarcinoma, cirrhosis, amyloidosis, and gallstones (with ileal Crohn disease), each of which could produce jaundice.

Primary biliary cirrhosis  Intense pruritus, splenomegaly, xanthelasmas, and tendon xanthomas are important clues.

Leptospirosis  After a person swims in contaminated water, a biphasic illness begins with fever, meningismus, prominent myalgias, and conjunctivitis. One week later, jaundice, ecchymoses, and renal insufficiency develop.

Hepatic vein obstruction (Budd-Chiari)  The presentation is acute, with severe abdominal pain, hepatomegaly, ascites, and jaundice. Oral contraceptives, paroxysmal nocturnal hemoglobinuria, and polycythemia predispose to its development.

Hemochromatosis  The patient has slate gray skin. Jaundice is a late manifestation along with diabetes and congestive heart failure.

Hemolysis  A spleen tip is usually palpable. The skin will have a lemon-yellow tint in natural light. With severe anemia, there will be paleness and an absence of a flushing reaction in the palmar creases. Urine and stool appear normal.

Gilbert syndrome  Mild jaundice is associated with fasting or viral syndromes. Prior mild hyperbilirubinemia may be found upon chart review.

Sepsis  Prolonged hypotension results in liver dysfunction.

Pictures

Book Source Details

• Book Title: Field Guide to Bedside Diagnosis
• Author(s): David S. Smith
• Year of Publication: 2007
• Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 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: Field Guide to Bedside Diagnosis Authors: David S. Smith Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-78178-165-5

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