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#Scleral icterus skin#

Often requested for better assessment of cholestasis.

Second-line imaging if ultrasound is inconclusive.

Modalities: CT abdomen with IV contrast, MRCP.

Visualization of cause of obstruction (e.g., gallstones, malignancy, or cysts).

Intrahepatic cholestasis: dilated intrahepatic bile ducts, double-barrel shotgun sign.

Cirrhosis: surface nodularity, portal hypertension, ascites.

Possible hepatomegaly in conditions causing hemolysis (e.g., malaria, thalassemia).

DiagnosticsĮxamples of findings in abdominal ultrasound Depending on the clinical scenario, jaundice and cholestasis may occur separately or concurrently.

Features associated with acute liver failure: anorexia, fatigue, nausea, abdominal pain (see “ Clinical features of acute liver failure”)Ĭholestasis may be seen in the absence of jaundice, particularly during the early stages of cholestasis.

Features associated with hemolysis: pallor, fatigue, exertional dyspnea (see “ Clinical features of hemolytic anemia”).

Chronic biliary obstruction leading to backflow of bile may result in inflammation and hepatomegaly.

Fat malabsorption ( steatorrhea, weight loss).

Accompanying features: vary depending on the underlying etiology.

#Scleral icterus skin#

Skin discoloration becomes apparent at serum bilirubin levels > 4–5 mg/dL.

Scleral icterus (yellow discoloration of the sclerae) develops at serum bilirubin levels > 2–3 mg/dL.Posthepatic jaundice is characterized by conjugated hyperbilirubinemia caused by extrahepatic cholestasis from biliary obstruction. Hepatitis and cirrhosiscan cause both conjugated and unconjugated hyperbilirubinemia. Infectious diseases: e.g., malaria, icteric leptospirosis.Progressive familial intrahepatic cholestasis.Infiltrative disease: e.g., tuberculosis, sarcoidosis, amyloidosis, lymphoma.Intrahepatic biliary tract disorders: e.g., primary biliary cholangitis, primary sclerosing cholangitis, vanishing bile duct syndrome, postoperative cholestasis.Drug toxicity: e.g., acetaminophen, estrogens, macrolides, arsenic.Liver disease e.g., alcoholic hepatitis, nonalcoholic steatohepatitis, cirrhosis, congestive hepatopathy, Wilson disease, autoimmune hepatitis.Viral hepatitis: e.g., hepatitis A–E, EBV, CMV, yellow fever.Mixed unconjugated and conjugated hyperbilirubinemia The treatment of jaundice is determined by the underlying disease process and can often be complemented with symptomatic treatment (e.g., for pruritus) or ursodeoxycholic acid. Diagnosis is based on laboratory studies (e.g., liver function tests) and, in most cases, a transabdominal right upper quadrant ( RUQ) ultrasound. In jaundice that arises from cholestasis, patients may present with pruritus, dark urine, and pale stools. Posthepatic jaundice is caused by the accumulation of conjugated hyperbilirubinemia usually due to extrahepatic cholestasis from biliary obstruction. Intrahepatic jaundice may be caused by intrahepatic cholestasis, impaired bilirubin conjugation, or impaired excretion of bilirubin by the liver. Prehepatic jaundice is caused by the accumulation of unconjugated bilirubin, which is due to either increased hemoglobin breakdown or impaired hepatic uptake. Jaundice can be divided into prehepatic, intrahepatic, and posthepatic etiologies. Bilirubin deposition most commonly occurs in the skin and the sclerae and becomes apparent when bilirubin levels reach > 2 mg/dL. Jaundice, or icterus, is a yellowish discoloration of tissue caused by the accumulation of bilirubin deposits.