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Two key words to think of here are histology and obstruction. The analysis of the differential diagnosis of hepatomegaly is best begun with a histologic breakdown of the liver tissue (Table 37). Thus, there are parenchymal cells that can be involved by toxic or inflammatory hepatitis. A variety of drugs (e.g., isoniazid) and toxins (e.g., carbon tetrachloride) can cause toxic hepatitis. Infectious hepatitis is most commonly caused by a virus (type A or B; which is usually transfusion-transmitted but may be transmitted by fecal–oral route) or by infectious mononucleosis.
HEPATOMEGALY
V I N D Vascular Infection Neoplasm Degenerative Parenchyma Viral hepatitis Infectious mononucleosis Amebiasis Hepatoma Metastatic carcinoma Fatty liver Supporting Tissue Sarcoma Veins Hepatic vein thrombosis Pyelophlebitis Arteries Hepatic artery ligation Lymphatics Hodgkin lymphoma Bile Ducts Cholangitis Clonorchis sinensis Papilloma Ampullary carcinoma Pancreatic carcinoma Cholangioles Bacterial cholangitis Cholangioma
HEPATOMEGALY
I C A T E Intoxication Congenital Autoimmune Trauma Endocrine Alcoholism Carbon tetrachloride Drugs Cystic disease Hamartoma Lupoid Hepatitis Contusion Laceration Hyperthyroidism Gaucher disease Hemolytic anemias Periarteritis nodosa Myeloid metaplasia Hepatic artery ligation Milk causing bile inspissation Biliary atresia Stone Stone (diabetes mellitus) Thorazine Birth control pills Dubin–Johnson syndrome Pregnancy
Beginning with the smallest organism (virus) and working up to the largest, one must consider brucellosis, TB (bacteria), syphilis, leptospirosis (spirochetal), amebiasis, amebic abscess, schistosomiasis, hydatid cysts (parasites), histoplasmosis, actinomycosis, and other systemic mycoses (fungi). When considering the supporting tissue, do not forget lupoid hepatitis, periarteritis nodosa, sarcoidosis, and cirrhosis. In addition, because the liver contains von Kupffer cells, any disease causing proliferation of the reticuloendothelial system may produce hepatomegaly. Myeloid metaplasia and Gaucher disease are good examples of this. The hepatic veins may be involved with a thrombosis and lead to hepatomegaly (Budd–Chiari syndrome). The portal veins may be obstructed by a thrombophlebitis (pyelophlebitis), usually secondary to infection elsewhere in the gut. Portal lymphatics involved in Hodgkin lymphoma may cause hepatomegaly. From the bile canaliculi down to the hepatic and common bile ducts, obstruction may occur from stones, neoplasms (pancreatic or ampullary), infection (cholangitis), or parasites (e.g., Clonorchis sinensis). Chlorpromazine and related drugs cause obstruction of the small canaliculi and present an obstructive picture. Pancreatitis may cause the pancreas to swell and produce bile duct obstruction and hepatomegaly. The parenchymal cells can respond in other ways to various etiologic agents to cause hepatomegaly. In diabetes and alcoholism, they may undergo fatty degeneration and infiltration. They may become hyperplastic in cirrhosis or neoplasm-causing hepatomas. Metastatic carcinoma is a common cause of hepatomegaly. Supporting tissue may proliferate to form a sarcoma. Edema of the liver with hepatomegaly results from chronic CHF. Infiltration with amyloid or glycogen may cause hepatomegaly; CHF and infectious hepatitis cause a tender liver, which distinguishes them from other forms of hepatomegaly. Extrinsic conditions causing apparent hepatomegaly, but which is really only displacement of the liver, are diaphragmatic abscess and pulmonary emphysema. In hemolytic anemias, the liver may be enlarged because of the increased load on the reticuloendothelial tissue (both in liver and spleen) to dispose of the damaged red cells.
The clinical picture will help to distinguish many causes of hepatomegaly. Shortness of breath, pitting edema, and hepatomegaly suggest CHF. Chronic cough, wheezing, jugular vein distention, hepatomegaly, and pitting edema suggest pulmonary emphysema and cor pulmonale. Fever, tender hepatomegaly, and jaundice suggest viral hepatitis or cholangitis. Hepatomegaly and ascites with a history of heavy alcohol intake suggest alcoholic cirrhosis. Hepatomegaly with gross or occult blood in the stool would suggest metastatic neoplasm of the GI tract. Asymptomatic hepatomegaly is probably related to congenital cystic disease, metastasis, or alcoholism. The initial workup will involve a CBC, urinalysis, sedimentation rate, chemistry panel, amylase and lipase levels, and a flat plate of the abdomen. If viral hepatitis is suspected, a hepatitis profile should be done. If CHF is suspected, a circulation time and spirometry is an inexpensive method of confirming the diagnosis. A chest x-ray and ECG need to be ordered also. If obstructive jaundice is suspected, endoscopic retrograde cholangiopancreatography may be done, but a CT scan of the abdomen should probably be done first. A CT scan of the abdomen will also identify primary and metastatic carcinoma of the liver. The many infectious diseases that are associated with hepatomegaly will need antibody titers, blood smears, or skin tests to reveal the diagnosis. Hemolytic anemias require blood smears, sickle cell prep, serum haptoglobins, and hemoglobin electrophoresis to get a definitive diagnosis. Amebic abscess can be elucidated by a CT scan, but an antibody titer will assist in the definitive diagnosis. Venography will reveal hepatic vein thrombosis.
CASE PRESENTATION #44 A 28-year-old Puerto Rican man presents with weight loss and loss of appetite. Physical examination reveals hepatosplenomegaly.
Review other book chapters online related to Hepatitis E:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Differential Diagnosis in Primary Care Authors: R. Douglas Collins MD, FACP Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-7817-6812-8 
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