Version May 2024
INTRODUCTION — The liver is an abdominal organ with multiple functions including filtering blood from the gastrointestinal (GI) tract, secreting bile into the GI tract, metabolizing drugs, and synthesizing proteins (eg, clotting factors). The liver's vascularity, location, and functions make it susceptible to several conditions that result in hepatomegaly, defined as enlargement of the liver beyond its normal size. Hepatomegaly may be suspected based on physical examination findings or imaging.
This topic provides an overview of normal liver size, causes of hepatomegaly, and an approach to evaluating hepatomegaly in adults. The diagnosis and management of hepatic injury in adults is discussed separately. (See "Management of hepatic trauma in adults".)
The approach to evaluating the adult patient with abnormal liver biochemical or function tests is discussed separately. (See "Approach to the patient with abnormal liver biochemical and function tests" and "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia".)
PROPERTIES OF THE NORMAL LIVER
Size and location — The liver is a wedge-shaped organ located in the right upper quadrant of the abdomen (figure 1). The liver typically extends from the fifth intercostal space to the right costal margin in the midclavicular line. By ultrasound, a normal liver span is usually <16 cm in the midclavicular line; however, liver size varies with sex and body size [1,2]. For example, in a study including 2080 individuals, the median liver span (as measured by transabdominal ultrasound in the midclavicular line) for males was 14.5 cm and for females was 13.4 cm [2]. Liver span >16 cm was found in 239 individuals (12 percent).
The normal liver weighs 1.4 to 1.5 kg in men and 1.2 to 1.4 kg in women [3].
Consistency — Normal liver consistency has been described as soft with a smooth contour, whereas a firm and/or nodular liver suggests underlying disease.
Anatomy — Traditionally, the liver is divided into right and left lobes (figure 2). In the normal liver, the right lobe is larger than the left lobe and occupies the right hypochondrium. The smaller left lobe is flatter and is situated in the epigastrium and left hypochondrium. (See "Overview of hepatic resection", section on 'Liver anatomy and physiology'.)
The liver can be subdivided into eight segments based on vascular supply, each containing branches of the portal vein, hepatic artery, hepatic vein, and bile ducts (figure 3). There are no surface fissures or anatomic landmarks demarcating the individual segments.
Anatomic variations — A nonenlarged liver may be palpable on physical examination or may be interpreted as hepatomegaly on imaging due to anatomic variations:
●Riedel's lobe – Riedel's lobe is a downward, tongue-like projection of the right lobe of the liver that extends below the level of the umbilicus and may give a false impression of hepatomegaly. The presence of Riedel's lobe can be confirmed on liver cross-sectional imaging (eg, computed tomography [CT], magnetic resonance imaging [MRI]), and it is regarded as a benign condition [4,5]. Riedel's lobe has been described as an accessory lobe of uncertain etiology with an incidence that varies from approximately 3 to 30 percent [5].
●Caudate lobe papillary process – Another anatomic variation that may be confused with hepatomegaly is projection of a papillary process from the caudate lobe (segment I) (figure 3). The caudate lobe papillary process may extend posteriorly, lying between the inferior vena cava (IVC) and aorta. Occasionally, the papillary process will wrap around the IVC such that its tip lies posterior to the IVC. This position of the papillary process may be mistakenly interpreted as hepatomegaly on imaging.
EXAMINING THE LIVER — Hepatomegaly may be suspected based on physical examination or liver imaging. Liver percussion and palpation are common examination methods, while imaging is used frequently to assess liver size and texture, and to look for abnormalities such as focal lesions, or portal or hepatic vein thrombosis.
Physical examination — Physical examination of the liver includes abdominal palpation and percussion [6-9]. To determine liver span, we percuss and palpate the liver in the midclavicular line with the patient in a supine position [10].
●Percussion – With the patient in a supine position and starting in the third intercostal space, the examiner uses percussion while moving inferiorly until dullness suggests the upper border of the liver (usually located in the fifth intercostal space). Next, percussion is performed from below the umbilicus in an area of tympany, and the examiner moves superiorly until dullness indicates the liver's inferior border.
Percussion alone may underestimate liver size because the lower border of the liver may seem resonant to percussion. However, if the distance from the upper border of the liver to the percussed liver edge is <13 cm, hepatomegaly is unlikely [11].
●Palpation – The purpose of palpation is to estimate liver span and also check for tenderness or liver lesions. With the patient in a supine position, the examining hand is placed below the level of the dullness noted on percussion in the midclavicular line, parallel to the rectus muscle. The liver is palpated during deep inspiration as it moves inferiorly to meet the examiner's finger tips. The liver edge may be tender in patients with liver inflammation (eg, acute hepatitis) or congestion (eg, congestive heart failure). Alternatively, the liver edge may feel firm and nodular in patients with cirrhosis and/or malignancy. (See 'Consistency' above.)
Comparisons of estimating liver size by physical examination or ultrasound have been limited because the techniques typically use two different axes (ie, midclavicular line for physical examination and transaxial line for ultrasound) [6,7,12]. However, some data suggested that physical examination measurements correlated well with ultrasound examination. In a study of 101 adult patients with liver disease undergoing biopsy, the mean size measured by physical examination was 9 cm, while the mean size measured by ultrasound was 14 cm [12]. Using this data, an R factor of 0.70 was calculated, indicating strong correlation between measurement techniques.
Palpable but nonenlarged liver — In addition to anatomic variants, a normal, nonenlarged liver may be palpable because it is displaced below the right costal margin. Liver displacement may occur (see 'Anatomic variations' above):
●During deep inspiration
●In patients with right pleural effusion
●In patients with chronic obstructive pulmonary disease (hyperinflation of the chest with diaphragmatic descent may result in downward displacement of the liver)
●In patients with a thin body habitus
Imaging — Imaging studies that are routinely used to assess the liver include:
●Ultrasound – Ultrasound is a common method to assess liver size and pathology, and transaxial ultrasound technique provides a quantitative measure of liver span [6,12].
●Computed tomography (CT) or magnetic resonance imaging (MRI) – Both CT and MRI can be used to determine liver size and volume [13,14]. Volumetric assessment traditionally has required manual contour tracing, segmentation of the organ in question, and application of mathematical algorithms to determine the volume. However, automated techniques have been developed that reduce the need for manual input, and thus the time needed to calculate volume [15,16]. Automated techniques appear to correlate well with manual contour tracing for volume determination [15].
CT is routinely used to measure total liver volume and segmental liver volume as part of the preoperative assessment for hepatic resection. Preoperative imaging prior to hepatic resection is discussed separately. (See "Overview of hepatic resection", section on 'Preoperative imaging'.)
CAUSES
Tender hepatomegaly
Acute hepatitis — Hepatic inflammation is a nonspecific reaction to liver damage and may result in hepatomegaly. Causes of hepatic inflammation that are commonly associated with tender hepatomegaly include infection (eg, hepatitis A virus, hepatitis E virus, bacterial, parasitic), drug-induced liver injury, and alcoholic hepatitis [17,18]:
●(See "Hepatitis A virus infection in adults: Epidemiology, clinical manifestations, and diagnosis".)
●(See "Hepatitis E virus infection".)
●(See "Pyogenic liver abscess", section on 'Clinical manifestations'.)
●(See "Liver flukes: Fascioliasis", section on 'Clinical manifestations'.)
●(See "Drug-induced liver injury", section on 'Clinical manifestations'.)
●(See "Alcoholic hepatitis: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)
For example, in a study of 59 patients with acute hepatitis A virus infection, 78 percent of patients had hepatomegaly at initial presentation [18].
Impaired venous outflow — Hepatic congestion may develop if venous outflow from the liver is obstructed. Disorders leading to hepatic congestion that result in hepatomegaly and a firm, tender liver edge include:
●Budd-Chiari syndrome – Patients with acute Budd-Chiari syndrome (ie, hepatic venous outflow tract obstruction) typically present with right upper abdominal pain, ascites, and hepatomegaly. (See "Etiology of the Budd-Chiari syndrome".)
Budd-Chiari syndrome is categorized by disease severity and duration (eg, acute fulminant, acute nonfulminant, chronic) and is more common in women during the third or fourth decade of life. However, patients with chronic disease may be asymptomatic. With complete obstruction of the hepatic veins, caudate lobe compensatory hypertrophy may develop because venous drainage of the caudate lobe is frequently spared. (See "Budd-Chiari syndrome: Epidemiology, clinical manifestations, and diagnosis".)
●Right heart failure – Patients with congestive hepatopathy and hepatomegaly from right-sided heart failure may present with dyspnea, fatigue, anorexia, chest discomfort, jaundice, jugular venous distension, and ascites. In patients with ascites, the diagnosis of right heart failure may be suggested by an elevated serum-to-ascites albumin gradient (SAAG; ≥1.1 g/dL) that can be distinguished from cirrhosis by a concomitantly elevated ascites total protein concentration (≥2.5 g/dL). (See "Right heart failure: Clinical manifestations and diagnosis" and "Evaluation of adults with ascites".)
As an example, in patients with severe tricuspid regurgitation, the liver is often enlarged and tender, and may be pulsatile on palpation. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation".)
In addition, patients with congestive hepatopathy frequently have mild elevations of serum total bilirubin (ie, bilirubin <3 mg/dL), and the diagnosis and management of congestive hepatopathy is discussed separately. (See "Congestive hepatopathy".)
●Hepatic sinusoidal obstruction syndrome (SOS) – Hepatic SOS, previously termed veno-occlusive disease, is characterized by tender hepatomegaly, right upper quadrant pain, jaundice, and ascites, most often occurring in patients undergoing hematopoietic cell transplantation and less commonly following ingestion of alkaloid toxins (usually from herbal sources), high-dose radiation therapy to the liver, or liver transplantation. Regardless of the cause, SOS is thought to begin with injury to the hepatic venous endothelium. As sinusoidal pressure increases, sinusoidal dilatation, central congestion, and hepatomegaly develop. The pathogenesis, clinical manifestations, and diagnosis of hepatic SOS are discussed separately. (See "Hepatic sinusoidal obstruction syndrome (veno-occlusive disease) in adults".)
●Peliosis hepatis – Peliosis hepatis is a rare vascular condition characterized by proliferation of the sinusoidal hepatic capillaries that results in cystic blood-filled cavities distributed randomly throughout the liver. Risk factors for peliosis hepatis include anabolic steroid use, immune deficiency, and some infections (eg, tuberculosis). Patients may present with jaundice, abdominal pain, hepatomegaly, and ascites. The pathogenesis, clinical features, and diagnosis of peliosis hepatis are discussed separately. (See "Peliosis hepatis".)
Nontender hepatomegaly
Cholestatic liver disease — Nontender hepatomegaly is a common clinical manifestation in patients with cholestatic liver disease such as primary biliary cholangitis (PBC) or primary sclerosing cholangitis (PSC) [19,20]. Other common clinical features of PBC and PSC include fatigue and pruritus, although some patients are asymptomatic at presentation. The clinical features and diagnosis of PBC and PSC are discussed separately. (See "Clinical manifestations, diagnosis, and prognosis of primary biliary cholangitis" and "Primary sclerosing cholangitis in adults: Clinical manifestations and diagnosis".)
The diagnostic approach to adults with jaundice or asymptomatic hyperbilirubinemia is discussed separately. (See "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia".)
Storage disorders — Storage disorders that may result in hepatomegaly include:
●Disorders of lipid metabolism – Disorders of lipid metabolism can result in accumulation of toxic lipids, including triglycerides, within the liver:
•Common disorders resulting in liver steatosis with nontender hepatomegaly include alcohol-associated fatty liver disease, nonalcoholic fatty liver disease, and diabetes mellitus. The accumulation of triglycerides results from excess delivery to and decreased export of free fatty acids from the liver. (See "Pathogenesis of alcohol-associated liver disease" and "Pathogenesis of nonalcoholic fatty liver disease".)
•Lysosomal acid lipase deficiency is an uncommon disorder that may be associated with fatty liver and nontender hepatomegaly. Lysosomal acid lipase deficiency disease (also referred to as cholesteryl ester storage disease) is a milder phenotype of fulminant lysosomal acid lipase deficiency (Wolman disease) and presents with hepatomegaly and fatty liver in childhood or adulthood, depending on the lysosomal acid lipase activity [21]. This disorder is characterized by hepatic accumulation of cholesteryl esters and triglycerides, elevated serum aminotransferases, and dyslipidemia [22]. (See "Metabolic dysfunction-associated steatotic liver disease in children and adolescents", section on 'Tests to exclude other liver diseases' and "Causes of primary adrenal insufficiency in children", section on 'Defects in cholesterol biochemistry'.)
The approach to the patient with hepatomegaly and a suspected inborn error of metabolism is presented separately. (See "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features", section on 'Organomegaly' and "Inborn errors of metabolism: Identifying the specific disorder", section on 'Evaluation of specific presentations'.)
●Disorders of glycogen metabolism – Glycogen accumulation within hepatocytes may be seen in patients with poorly controlled diabetes mellitus and hepatomegaly [23-25]. For example, in a study of 36 patients with type 1 diabetes mellitus and glycogenic hepatopathy, 28 patients (78 percent) had hepatomegaly [26]. Glycogenic hepatopathy is distinct from steatohepatitis, and steatosis is usually absent on liver biopsy [23].
Several inborn errors of metabolism that result in glycogen storage disorders are commonly associated with hepatomegaly, including glucose-6-phosphatase deficiency (GSD I), glycogen debrancher deficiency (GSD III), liver phosphorylase deficiency (GSD IV), and liver phosphorylase kinase deficiency (GSD IXa1). These disorders are typically diagnosed in neonates, infants, and young children, and are discussed separately. (See "Overview of inherited disorders of glucose and glycogen metabolism".)
●Gaucher disease – Gaucher disease is a lysosomal disease that affects the recycling of cellular glycolipids, resulting in their accumulation within lysosomes of macrophages (eg, liver, spleen). Type 1 Gaucher disease has a variety of presenting features that may occur at any age, while liver enlargement is common and is typically two to three times normal size for age. Splenomegaly is also common. Patients may be asymptomatic or may present with early satiety, abdominal distension, and abdominal pain. The clinical manifestations and diagnosis of Gaucher disease are presented separately. (See "Gaucher disease: Pathogenesis, clinical manifestations, and diagnosis".)
●Alpha-1 antitrypsin deficiency (AAT) – Liver disease in AAT deficiency is caused by pathologic polymerization of the variant AAT, resulting in intrahepatocyte accumulation of AAT molecules. Patients with liver manifestations of AAT deficiency may present with hepatomegaly, elevated aminotransferases, and ascites, and liver disease may progress to cirrhosis. Patients with AAT deficiency typically have respiratory symptoms (eg, dyspnea, cough). The clinical manifestation and diagnosis of AAT deficiency are discussed separately. (See "Clinical manifestations, diagnosis, and natural history of alpha-1 antitrypsin deficiency" and "Extrapulmonary manifestations of alpha-1 antitrypsin deficiency".)
●Hereditary hemochromatosis – Hereditary hemochromatosis is an autosomal recessive disorder in which mutations in the HFE gene cause increased intestinal iron absorption. Progressive iron deposition in the liver is associated with hepatomegaly, elevated transaminases, and hepatic fibrosis that may progress to cirrhosis. However, with identification of the HFE gene, a laboratory diagnosis of hereditary hemochromatosis is often made in asymptomatic individuals before iron deposition results in symptoms such as lethargy, skin hyperpigmentation, diabetes mellitus, and arthralgias. (See "Clinical manifestations and diagnosis of hereditary hemochromatosis".)
●Wilson disease – Liver is the initial site of copper accumulation in patients with Wilson disease, and hepatomegaly is among the clinical manifestations that also include abdominal pain and jaundice. (See "Wilson disease: Clinical manifestations, diagnosis, and natural history".)
Infiltrative diseases — Infiltrative disease that may result in hepatomegaly include:
●Granulomatous disease – Granulomas are found in the liver in several disorders, such as infection (eg, tuberculosis), autoimmune conditions (eg, sarcoidosis), and drug-induced liver injury [27]. Patients with granulomatous liver disease may have hepatomegaly in addition to fever, anorexia, or malaise, while symptoms may vary, depending on the underlying disease. The causes and evaluation of granulomatous liver disease is discussed separately. (See "Evaluation of the adult patient with hepatic granuloma", section on 'Causes'.)
●Hepatic amyloidosis – Hepatomegaly is common in patients with hepatic amyloidosis (primary or secondary). For example, in a study including 98 patients with hepatic amyloidosis, hepatomegaly was seen in over 80 percent of patients [28]. Associated signs and symptoms may include weight loss, abdominal pain, and elevated alkaline phosphatase. The clinical manifestations and diagnosis of hepatic amyloidosis are discussed separately. (See "Gastrointestinal amyloidosis: Clinical manifestations, diagnosis, and management", section on 'Hepatic amyloidosis'.)
●Hepatosplenic T cell lymphoma – Hepatomegaly is a common clinical manifestation of hepatosplenic T cell lymphoma (HSTCL), a rare form of non-Hodgkin lymphoma. In addition to hepatomegaly, common signs and symptoms include splenomegaly, thrombocytopenia, pancytopenia, mildly abnormal aminotransferases and alkaline phosphatase.
The liver is diffusely enlarged as liver sinusoids are markedly expanded by the lymphoma, and the clinical manifestations and diagnosis of HSTCL are discussed separately. (See "Clinical manifestations, pathologic features, and diagnosis of hepatosplenic T cell lymphoma".)
●Malignant tumors – Hepatomegaly may be seen in patients with hepatic infiltration by solid tumors. Common primary liver malignancies associated with nontender hepatomegaly include hepatocellular carcinoma and cholangiocarcinoma. In addition, patients with extensive liver metastases may also have hepatomegaly. (See "Clinical features and diagnosis of hepatocellular carcinoma", section on 'Clinical features' and "Clinical manifestations and diagnosis of cholangiocarcinoma", section on 'Clinical presentation'.)
●Benign lesions – Benign liver lesions that may cause hepatomegaly include hepatic hemangiomas, hepatocellular adenomas, and focal nodular hyperplasia. These lesions typically appear as noncystic lesions on hepatic imaging:
•(See "Hepatic hemangioma".)
•(See "Hepatocellular adenoma".)
•(See "Focal nodular hyperplasia".)
Other conditions — Hepatomegaly may be found in patients with cystic liver lesions:
●Caroli disease – Hepatomegaly is a common clinical manifestation of Caroli disease, a congenital disorder characterized by multifocal, segmental dilatation of large intrahepatic bile ducts. The condition is usually associated with renal cystic disease of varying severity. Patients with Caroli disease may develop abdominal pain, pruritus, bacterial cholangitis, ascites, and variceal bleeding. (See "Caroli disease".)
●Polycystic liver disease – Polycystic liver disease predominantly occurs in patients with autosomal dominant polycystic kidney disease (ADPKD), with an increasing burden of liver cysts occurring with age and in patients with more advanced renal disease. Women tend to develop cysts earlier in life, and massive cysts are more commonly seen in women. (See "Autosomal dominant polycystic kidney disease (ADPKD): Extrarenal manifestations".)
A less common disorder, autosomal dominant polycystic liver disease is distinct from ADPKD, since it is not associated with kidney involvement. Most patients with autosomal dominant polycystic liver disease are initially asymptomatic; however, with progressive enlargement and an increasing number of cysts, patients may present with abdominal distension, abdominal pain, nausea, and early satiety. (See "Diagnosis and management of cystic lesions of the liver", section on 'Polycystic liver disease'.)
INITIAL EVALUATION — The initial evaluation of a patient with hepatomegaly includes obtaining a history to identify symptoms suggestive of underlying systemic disease and risk factors for liver disease, performing a physical examination to look for clues to the etiology and for signs of liver disease, and obtaining liver biochemical and function tests and Doppler ultrasound. Subsequent testing is determined based on the information gathered from the history and physical examination as well as the pattern of laboratory test abnormalities, if they are present. (See 'Subsequent evaluation' below.)
History — The initial evaluation includes obtaining a history to identify symptoms of systemic disease (eg, fever, weight loss) and risk factors for liver disease, including exposure to potential hepatotoxins (eg, alcohol, medications). While some patients with hepatomegaly are asymptomatic, other patients may report right upper quadrant pain or symptoms related to the underlying disorder. (See 'Causes' above.)
Physical examination — In addition to evaluating liver size and consistency, physical examination includes assessment for (see 'Examining the liver' above):
●Stigmata of chronic liver disease (eg, spider nevi, palmar erythema, gynecomastia) (see "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis", section on 'Physical examination')
●Increased jugular venous pressure, a sign of right-sided heart failure (see 'Impaired venous outflow' above)
●Spleen size (a palpable spleen is two to threefold enlarged) (see "Splenomegaly and other splenic disorders in adults", section on 'How to examine the spleen')
●Ascites (typically detected by flank dullness to percussion) (see "Evaluation of adults with ascites", section on 'Physical examination')
Diagnostic testing — Initial laboratory testing is performed to look for abnormalities in liver biochemistries or function, while initial imaging evaluates liver size, consistency, and blood flow:
●Serum aminotransferases: alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
●Alkaline phosphatase
●Total bilirubin
●Serum albumin
●Prothrombin time/international normalized ratio
●Doppler ultrasound
SUBSEQUENT EVALUATION — Subsequent evaluation is based on results of the initial evaluation (laboratory tests and imaging in addition to signs and symptoms):
Abnormal liver biochemical tests — For patients with hepatomegaly and abnormal liver biochemical and/or function tests, additional diagnostic testing is performed based on the pattern of the laboratory findings, and the approach is discussed in detail separately:
●Hepatocellular (predominantly elevated transaminases) (see "Approach to the patient with abnormal liver biochemical and function tests", section on 'Elevated serum aminotransferases')
●Cholestatic (predominantly elevated alkaline phosphatase) (see "Approach to the patient with abnormal liver biochemical and function tests", section on 'Elevated alkaline phosphatase')
●Isolated hyperbilirubinemia (see "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia")
Normal liver tests with imaging-confirmed hepatomegaly — For patients with hepatomegaly but without liver biochemical or function test abnormalities, additional testing is typically based on signs or symptoms suggestive of systemic disease. As an example, for patients with fatigue, weight loss, hepatomegaly confirmed by ultrasound, and normal liver biochemical tests, subsequent evaluation includes serum and urine protein electrophoresis to evaluate for amyloidosis with hepatic involvement. (See "Gastrointestinal amyloidosis: Clinical manifestations, diagnosis, and management" and "Clinical presentation, laboratory manifestations, and diagnosis of immunoglobulin light chain (AL) amyloidosis".)
Normal liver tests and ultrasound — For patients with hepatomegaly suspected by physical examination but without liver biochemical/function test or ultrasound abnormalities, additional testing is generally not required.
Specialist referral — Consultation with a hepatologist is obtained for patients with any of the following:
●Acute hepatitis with symptoms or signs of liver failure (eg, hepatic encephalopathy, coagulopathy) (see "Acute liver failure in adults: Etiology, clinical manifestations, and diagnosis")
●Suspected chronic liver disease (eg, signs of portal hypertension such as ascites)
●Acute or chronic liver disease requiring a specialized approach (eg, suspected Budd-Chiari syndrome)
●Symptoms such as right upper quadrant or abdominal pain in the setting of hepatomegaly of uncertain etiology
SPECIAL POPULATIONS
Pregnant women — In late pregnancy, physical examination of the liver is difficult because of the expanding uterus. The liver is forced up further into the chest, and a palpable liver is an abnormal finding. In addition, spider angiomas and palmar erythema, which are associated with chronic liver disease, are common during pregnancy and usually disappear after delivery. The approach to liver disease occurring during pregnancy is presented separately. (See "Approach to evaluating pregnant patients with elevated liver biochemical and function tests".)
SUMMARY AND RECOMMENDATIONS
●Properties of the normal liver – The liver is a wedge-shaped organ located in the right upper quadrant of the abdomen (figure 1). The liver typically extends from the fifth intercostal space to the right costal margin in the midclavicular line. By ultrasound, a normal liver span is usually <16 cm in the midclavicular line. (See 'Properties of the normal liver' above.)
●Examining the liver – Hepatomegaly may be suspected based on physical examination or liver imaging. Liver percussion and palpation are common examination methods, while imaging is used frequently to assess liver size and texture, and to look for abnormalities such as focal lesions, or portal or hepatic vein thrombosis. (See 'Examining the liver' above.)
For patients with hepatomegaly, ultrasound is a common method to assess liver size and pathology, and transaxial ultrasound technique provides a quantitative measure of liver span. (See 'Imaging' above.)
●Causes of hepatomegaly – Causes of tender hepatomegaly include acute hepatitis (eg, viral hepatitis, drug-induced liver disease) and disorders of impaired venous outflow (eg, Budd-Chiari syndrome, right-sided heart failure). (See 'Tender hepatomegaly' above.)
Causes of nontender hepatomegaly include cholestatic liver diseases (eg, primary biliary cholangitis [PBC] or primary sclerosing cholangitis [PSC]), storage disorders (eg, lipids, glycogen), and infiltrative disorders (eg, hepatic amyloidosis). (See 'Nontender hepatomegaly' above.)
●Initial evaluation – For patients with hepatomegaly, the initial evaluation includes obtaining a history to identify symptoms suggestive of underlying systemic disease and risk factors for liver disease, performing a physical examination to look for clues to the etiology and for signs of liver disease, and obtaining liver biochemical and function tests and Doppler ultrasound. (See 'Initial evaluation' above.)
●Subsequent evaluation – For patients with hepatomegaly and abnormal liver biochemical and/or function tests, additional diagnostic testing is performed based on the pattern of the laboratory findings, and the approach is discussed in detail separately (see 'Abnormal liver biochemical tests' above):
•Hepatocellular (predominantly elevated aminotransferases) (see "Approach to the patient with abnormal liver biochemical and function tests", section on 'Elevated serum aminotransferases')
•Cholestatic (predominantly elevated alkaline phosphatase) (see "Approach to the patient with abnormal liver biochemical and function tests", section on 'Elevated alkaline phosphatase')
•Isolated hyperbilirubinemia (see "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia")
Consultation with a hepatologist is obtained for patients with any of the following (see 'Specialist referral' above):
•Acute hepatitis with symptoms or signs of liver failure (eg, hepatic encephalopathy, coagulopathy)
•Suspected chronic liver disease (eg, ascites)
•Acute or chronic liver disease requiring a specialized approach (eg, suspected Budd-Chiari syndrome)
•Symptoms such as right upper quadrant or abdominal pain in the setting of hepatomegaly of uncertain etiology
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