Hepatomegaly refers to an abnormal enlargement of the liver and often indicates reversible or progressive primary or secondary liver disease. It may result from diverse pathophysiologic mechanisms, including:

• Dilated hepatic sinusoids (e.g., in right-sided heart failure)

• Persistently elevated venous pressure causing congestion (e.g., chronic constrictive pericarditis)

• Hepatocyte dysfunction and engorgement (e.g., hepatitis)

• Fatty infiltration of parenchymal cells leading to fibrosis (e.g., nonalcoholic fatty liver disease, cirrhosis)

• Glycogen accumulation in hepatocytes (e.g., diabetes mellitus)

• Infiltration of abnormal substances (e.g., amyloidosis)

Hepatomegaly may be detected by palpation, percussion, or imaging but can be confounded by displacement of the liver due to respiratory movements, abdominal tumors, spinal deformities, gallbladder enlargement, or colonic content.

Pathophysiology

Enlargement of the liver occurs through mechanisms that affect hepatic architecture and blood flow:

• Congestive hepatopathy: Chronic venous congestion causes sinusoidal dilation and hepatocyte atrophy.

• Inflammatory enlargement: Hepatocyte swelling and infiltration by immune cells during viral, bacterial, or autoimmune hepatitis.

• Infiltrative diseases: Deposition of amyloid, glycogen, or fat increases liver volume.

• Neoplastic growth: Tumor proliferation (primary or metastatic) enlarges the organ and may distort normal architecture.

• Obstructive processes: Biliary obstruction or hepatic vein thrombosis can lead to liver congestion and enlargement.

History and physical examination

Hepatomegaly is rarely a primary complaint and is usually discovered on routine abdominal examination. Important aspects include:

History

• Alcohol consumption, viral hepatitis exposure, or medication use

• Presence of abdominal pain, jaundice, or systemic symptoms (fever, malaise, weight loss)

• History of metabolic, cardiac, or hematologic disorders

Physical Examination

• Inspect for jaundice, spider angiomas, abdominal contour, distension, ascites, or dilated veins

• Measure abdominal girth and assess nutritional status for muscle wasting or edema

• Percuss liver borders along midclavicular and sternal lines to estimate span (normal right lobe: 6–12 cm; left lobe: 4–8 cm)

• Palpate the liver edge: tender and rounded in hepatitis, firm in cirrhosis, rocklike in carcinoma

• Assess level of consciousness for signs of hepatic encephalopathy (personality changes, confusion, asterixis, or coma)

Medical causes

Special considerations

• Evaluate liver function via enzymes, bilirubin, albumin, globulin, and alkaline phosphatase

• Confirm size and morphology using ultrasound, CT, liver scan, or celiac arteriography

• Bed rest, stress reduction, and adequate nutrition support hepatic regeneration

• Protein intake may need monitoring to prevent worsening hepatic encephalopathy

• Avoid hepatotoxic medications or adjust doses carefully

Patient counseling

• Explain the underlying cause and treatment plan

• Avoid alcohol and exposure to infectious agents

• Encourage gradual activity pacing and sufficient rest

Pediatric considerations

• Causes include Reye’s syndrome, biliary atresia, Wilson’s disease, Gaucher’s disease, Niemann-Pick disease, or poorly controlled type 1 diabetes

• Examination is similar to adults; monitor for associated systemic symptoms

References

• Musso, G., Gambino, R., & Cassader, M. (2011). Need for a three-focused approach to nonalcoholic fatty liver disease. Hepatology, 53(5), 1773.

• Stepanova, M., & Younossi, Z. M. (2012). Independent association between nonalcoholic fatty liver disease and cardiovascular disease in the US population. Clinical Gastroenterology and Hepatology, 10(6), 646–650.