Clinical Features

A careful history and physical examination coupled with judicious use of the clinical laboratory enables the emergency physician to determine whether jaundice is produced by a hemolytic process, hepatocellular disease, or a potentially surgically correctable obstructive process. Often, more extensive diagnostic procedures are needed before the precise etiology of jaundice can be determined.

The sudden appearance of jaundice in a previously healthy young person, especially if preceded by a brief prodrome of fever, malaise, and myalgias, is likely to be caused by a viral hepatitis. Inquire about body fluid exposure over the previous few months, including transfusion of blood products, intimate contact with someone with hepatitis or jaundice, promiscuous sexual activity, intravenous drug use, accidental needle-stick injuries or mucosal contact with body fluids, travel to countries where hepatitis is prevalent, raw shellfish ingestion, and recent tattoos or body piercing. Many times, however, no history of exposure can be elicited. Right upper quadrant pain and tenderness and hepatomegaly may be present, but pruritis is usually absent. Examine for needle tracks, since patients may not volunteer a history of drug use.

Jaundice that develops gradually and is accompanied by weakness, peripheral muscle wasting, ascites, spider angiomata, pruritus, and symptoms of portal hypertension is frequently caused by alcoholic liver disease and cirrhosis. A history of sustained, significant alcohol intake should be elicited from the patient or from family and friends. A history of any previous episodes of jaundice, pancreatitis, or hematemesis should be obtained. Fever, vomiting, and right upper quadrant tenderness accompany episodes of alcoholic hepatitis. The presence of asterixis, fetor hepaticus, or encephalopathy indicates advanced disease.

Toxic hepatitis should be suspected if a history of ingestion or exposure to a known hepatotoxin is obtained. Signs of hepatocellular damage may be present with toxicity from agents such as acetaminophen, halothane, methyldopa, isoniazid, or phenytoin. Cholestatic changes predominate in toxicity from anabolic steroids, oral contraceptives, and chlorpromazine. Mushroom poisoning, carbon tetrachloride, and phosphorus can produce massive hepatic necrosis.

A family history of jaundice or a history of recurrent mild jaundice that resolves spontaneously is most consistent with a familial cause, such as Gilbert's syndrome. Most patients with sickle cell disease develop chronic jaundice, but in the presence of abdominal pain, vomiting, and fever, acute cholecystitis or biliary obstruction must be strongly suspected. The patient should also be asked about other hemoglobinopathies or prior episodes of hemolysis.

Jaundice that develops acutely with abdominal pain, vomiting, fever, and right upper quadrant tenderness is strongly suggestive of acute biliary obstruction from choledocholithiasis. A history of fatty food intolerance and typical biliary colic is supportive. Cholecystitis alone does not produce jaundice. Painless jaundice in an older patient, especially if accompanied by an epigastric mass and weight loss, strongly suggests biliary obstruction from a malignancy. A history of known gastrointestinal malignancy accompanied by a hard, nodular liver indicates metastatic disease as the cause of jaundice. A history of prior biliary tract surgery, pancreatitis, cholangitis, or inflammatory bowel disease should be elicited, since they may be associated with the development of biliary obstruction.

Hepatomegaly with pedal edema, jugular venous distention, and a gallop rhythm makes congestive cardiac failure the likely cause of jaundice.

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