Palpability of liver does not always indicate enlargement.It only reflects the relation of the liver to adjacent structures.In normal children,liver is palpable 1 cm below the costal margin and in Infants it may be felt up to 2 cm below the rib margin.

Besides the size and shape of the liver, consistency and character of the surface and palpable margin should be evaluated for the assessment of hepatomegaly. Liver should be examined for tenderness and also auscultated for any murmurs. The upper border of the liver should be defined by percussion. Abdomen should be palpated for other masses or enlargement of the spleen.
Pathogenesis of liver enlargement. The liver may be enlarged due to any of the following causes:
(a) Inflammation
(b) Fatty infiltration
(c) Kupffer’s cell hyperplasia
(d) Congestion
(e) Cellular infiltration and
(f) Storage of metabolites

CAUSES OF LARGE LIVER

Newborn
Infections, (a) Intrauterine infection e.g., toxoplasmosis, cytomegalic inclusion disease, congenital syphilis., (b) septicemia, and (c) neonatal hepatitis including viral hepatitis.
Cellular infiltration. Erythroblastosis fetalis.
Hepatobiliary obstruction.   Biliary atresia.
Congestive cardiac failure.
Alpha-1-anti trypsin deficiency.
Infants and children
1.  Benign hypertrophy. Periportal round cell infiltration following viral infections of upper respiratory tract. The liver regresses in 6 to 8 weeks.
2.  Fatty infiltration. Kwashiorkor, Reye’s syndrome, tetracycline toxicity, tuberculosis, diabetes mellitus, cystic fibrosis and galactosemia.
3.   Inflammatory processes. (i) Intrauterine and intrapartum infection, (ii) hepatitis, (iii) infectious mononucleosis, (iv) parasitic infestations (visceral larva migrans, amebic hepatitis), (v) pyogenic or amebic abscess of liver, cholangitis (vi) toxins and (vii) drugs.
4.   Cellular infiltration. (i) Leukemia and lymphomas (ii) neoplasms-primary (hepatoblastoma, hemangioendothelioma), (iii) secondaries to Wilms’ tumor and neuroblastoma and (iv) histiocytosis (Letterer-Siwe disease).
5.   Storage disorders (Metabolic). (i) Glycogen storage disease, (ii) galactosemia, (iii) mucopolysaccharidoses, (iv) lipidosis (Gaucher, Niemann Pick, gangliosidosis M). (v) amyloidosis, (vi) alpha-1-anritrypsin deficiency, (vii) hepatic porphyria, (viii) cystinosis and (ix) hemosiderosis, Wilson disease, cystinosis and tyrosinosis.
6.    Congestion. (i) Congestive cardiac failure, (ii) pericarditis, (iii) Budd Chiari syndrome (thrombosis of hepatic vein) and (iv) veno-occlusive disease of the liver.
7.   Kupffer’s cell hyperplasia. Granulomatous hepatitis as in tuberculosis and sarcoidosis.
8.  Miscellaneous. Cirrhosis of liver—Indian Childhood cirrhosis, congenital cysts and hydatid cyst.

EVALUATION OF THE HEPATIC ENLARGEMENT

Assess if the liver is just palpable or is actually enlarged. Determine if the enlargement is due to organic causes and also the nature and severity of the illness responsible for it.
A good medical history, intelligent interpretation of the associated clinical manifestation and judicious use of laboratory investigations and ultrasonography are helpful in arriving at a correct diagnosis in most cases of hepatic enlargement. The following points may help in diagnosis.
Age of the patient. Age of onset of the illness limits the etiological possibilities.
Geographic factors. Indian childhood cirrhosis is common in children of Indian extraction. Thalassemia is more frequent in North West India, Bengal, Indochina, Sri Lanka and persons of Mediterranean extraction. Veno-occlusive disease is observed in Jamaica and West Indies. It has been recently reported from Afghanistan and some parts of central India.
Associated clinical manifestations which aid in diagnosis of hepatomegaly
Protein-energy malnutrition. There is fatty infiltration of the liver.
Jaundice. Intrauterine infections, septicemia, neonatal hepatitis, viral hepatitis, biliary atresia and Indian childhood cirrhosis in terminal stages present with jaundice.
Engorged neck veins and raised jugular venous pressure.

Constrictive Pericarditis
Skin rash. Histiocytosis.
Microcephaly or hydrocephaly. Intrauterine infections like toxoplasmosis and cytomegalic inclusion disease.
Eyes. Cataract and mental retardation with hepatosplenomegaly suggest galactosemia.
Presence of Kayser-Fleischer ring over the cornea indicates Wilson     disease.         Hazy     cornea     is     seen     in
Mucopolysaccharidosis type 1.
Neurological manifestations. Wilson disease may present with neurological manifestations.
Skeletal changes of rickets may be observed in cystinosis and tyrosinosis.
Mental retardation. Patients with galactosemia may show gross mental retardation.