In the axial plane, the caudate lobe should normally have a cross-section of less than 0.55 of the rest of the liver.Other ultrasound studies have suggested hepatomegaly as being defined as a longitudinal axis > 15.5 cm at the hepatic midline, or > 16.0 cm at the midclavicular line. Workup
Blood tests should be done, importantly liver-function series, which will give a good impression of the patients broad metabolic picture.A complete blood test can help distinguish intrinsic liver disease from extrahepatic bile-duct obstruction. An ultrasound of the liver can reliably detect a dilated biliary-duct system,
it can also detect the characteristics of a cirrhotic liver.Computerized tomography (CT) can help to obtain accurate anatomical information, in individuals with hepatomegaly for the purpose of a complete diagnosis. Treatment
Treatment of hepatomegaly will vary depending on the cause of the liver enlargement and hence accurate diagnosis is the primary concern. In the case of auto-immune liver disease, prednisone and azathioprine may be used for treatment.In the case of lymphoma the treatment options include single-agent (or multi-agent) chemotherapy and regional radiotherapy, also surgery may be an option in specific situations. Meningococcal group C conjugate vaccine are also used in some cases.In primary biliary cirrhosis ursodeoxycholic acid helps the bloodstream remove bile which may increase survival in some affected individuals. See also
Hepatosplenomegaly
Liver function tests

References
Further reading
Hoffmann, Georg F.; Zschocke, Johannes; Nyhan, William L. (2009-11-21). Inherited Metabolic Diseases: A Clinical Approach. Springer Science & Business Media. ISBN 9783540747239.
Skeletal abnormalities occur by about age 6 months, but may not be clinically obvious until 10–14 months. Patients may experience debilitating spine and hip deformities, carpal tunnel syndrome, and joint stiffness. Patients may be normal height in infancy, but stop growing by the age of 2 years. They may not reach a height of greater than 4 feet.Other early symptoms may include inguinal and umbilical hernias. These may be present at birth, or they may develop within the first months of life. Clouding of the cornea and retinal degeneration may occur within the first year of life, leading to blindness. Enlarged liver and spleen are common. There is no organ dysfunction, but GAG deposition in these organs may lead to a massive increase in size. Patients may also have diarrhea. Aortic valve disease may occur.Airway obstruction is frequent, usually secondary to abnormal cervical vertebrae. Upper and lower respiratory tract infections can be frequent.Developmental delay may become apparent by age 1–2 years, with a maximum functional age of 2–4 years. Progressive deterioration follows. Most children develop limited language capabilities. Death usually occurs by age 10. Genetics
Children with Hurler Syndrome carry two defective copies of the IDUA gene, which has been mapped to the 4p16.3 site on chromosome 4. This is the gene which encodes for the protein iduronidase. As of 2018, more than 201 different mutations in the IDUA gene have been shown to cause MPS I.Because Hurler syndrome is an autosomal recessive disorder, affected persons have two nonworking copies of the gene.