Quick Medical Diagnosis & Treatment 2024

Jaundice

For further information, see CMDT Part 18-01: Jaundice & Evaluation of Abnormal Liver Biochemical Tests

KEY FEATURES

Essentials of Diagnosis

Jaundice results from accumulation of bilirubin—a product of heme metabolism—in body tissues; the cause may be hepatic or nonhepatic (Table 18–1)
Hyperbilirubinemia may be due to abnormalities in the formation, transport, metabolism, or excretion of bilirubin (Table 18–2)
Persistent mild elevations of the aminotransferase levels are common in clinical practice and caused most often by nonalcoholic fatty liver disease (NAFLD)
Evaluation of obstructive jaundice begins with ultrasonography and is usually followed by cholangiography

Table 18–1.Classification of jaundice.

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Table 18–1. Classification of jaundice.

Type of Hyperbilirubinemia

Location and Cause

Unconjugated hyperbilirubinemia (predominantly indirect bilirubin)

Increased bilirubin production (eg, hemolytic anemias, hemolytic reactions, hematoma, pulmonary infarction)

Impaired bilirubin uptake and storage (eg, posthepatitis hyperbilirubinemia, Gilbert syndrome, Crigler-Najjar syndrome, drug reactions)

Conjugated hyperbilirubinemia (predominantly direct bilirubin)

Hereditary Cholestatic Syndromes (see also Table 18–2)

Faulty excretion of bilirubin conjugates (eg, Dubin-Johnson syndrome, Rotor syndrome) or pathogenic variant in genes coding for bile salt transport proteins (eg, progressive familial intrahepatic cholestasis syndromes, benign recurrent intrahepatic cholestasis, and some cases of intrahepatic cholestasis of pregnancy)

Hepatocellular Dysfunction

Biliary epithelial and hepatocyte damage (eg, hepatitis, hepatic cirrhosis)

Intrahepatic cholestasis (eg, certain drugs, biliary cirrhosis, sepsis, postoperative jaundice)

Hepatocellular damage or intrahepatic cholestasis resulting from miscellaneous causes (eg, spirochetal infections, infectious mononucleosis, cholangitis, sarcoidosis, lymphomas, hyperthyroidism, industrial toxins)

Biliary Obstruction

Choledocholithiasis, biliary atresia, carcinoma of biliary duct, sclerosing cholangitis, IgG₄-related cholangitis, ischemic cholangiopathy, COVID cholangiopathy, choledochal cyst, external pressure on bile duct, pancreatitis, pancreatic neoplasms

Ig, immunoglobulin.

Table 18–2.Hyperbilirubinemic disorders.

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Table 18–2. Hyperbilirubinemic disorders.

Nature of Defect

Type of Hyperbilirubinemia

Clinical and Pathologic Characteristics

Gilbert syndrome¹

Reduced activity of uridine diphosphate glucuronyl transferase

Unconjugated (indirect) bilirubin

Benign, asymptomatic hereditary jaundice. Hyperbilirubinemia increased by 24- to 36-hour fast. No treatment required. Associated with reduced mortality from CVD.

Dubin-Johnson syndrome²

Reduced excretory function of hepatocytes

Conjugated (direct) bilirubin

Benign, asymptomatic hereditary jaundice. Gallbladder does not visualize on oral cholecystography. Liver darkly pigmented on gross examination. Biopsy shows centrilobular brown pigment. Prognosis excellent.

Rotor syndrome³

Reduced hepatic reuptake of bilirubin conjugates

Conjugated (direct) bilirubin

Similar to Dubin-Johnson syndrome, but the liver is not pigmented, and the gallbladder is visualized on oral cholecystography. Prognosis excellent.

Recurrent or progressive intrahepatic cholestasis⁴

Cholestasis, often on a familial basis

Predominantly conjugated (direct) bilirubin

Episodic attacks or progressive jaundice, itching, and malaise. Onset in early life; may persist for a lifetime. Alkaline phosphatase increased. Cholestasis found on liver biopsy. (Biopsy may be normal during remission.) Prognosis is generally excellent for “benign” recurrent intrahepatic cholestasis but may not be for familial forms.

Intrahepatic cholestasis of pregnancy⁵

Cholestasis

Predominantly conjugated (direct) bilirubin

Benign ...

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Jaundice

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KEY FEATURES

Essentials of Diagnosis

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