If you’ve ever had a bruise, you may have noticed that the skin went through a series of color changes as it healed. When you saw yellow in the bruise, you were seeing bilirubin.

Normally, about 1% of our red blood cells retire every day, to be replaced by fresh red blood cells. The old ones are processed in the liver and disposed of. Much of the resulting bilirubin leaves the body in the stool.

If there are too many red blood cells retiring for the liver to handle, yellow pigment builds up in the body. When there is enough to be visible, jaundice results.

Jaundice can be caused by too many red blood cells retiring, by the liver being overloaded or damaged, or by the inability to move processed bilirubin from the liver through the biliary tract to the gut.

Most babies have some jaundice during the first week of life. The ordeal of birth can send many red blood cells to an early retirement (especially if a vacuum is used!), and babies’ livers are often unprepared for the load. Before Mom’s milk comes in and stooling begins in earnest, bilirubin accumulates more easily. Jaundice is even more common in premature babies.

Physiologic jaundice is the name for normal jaundice commonly seen in healthy babies.

Pathologic jaundice is the name given when jaundice presents a health risk, either because of its degree or its cause. Pathologic jaundice can occur in children or adults. It arises for many reasons, including blood incompatibilities, blood diseases, genetic syndromes, hepatitis, cirrhosis, bile duct blockage, other liver diseases, infections, or medications. The term also applies to physiologic jaundice exaggerated by dehydration, prematurity, difficult delivery, or other reason.

Another condition called Gilbert's syndrome is a benign, hereditary condition in which mild jaundice develops. It is caused by low levels of some bilirubin-processing enzymes in the liver. This condition, once recognized, requires no further treatment or evaluation. There are other more rare hereditary causes of elevated bilirubin levels.

A yellow-to-orange color may be imparted to the skin by consuming too much beta carotene, the orange pigment seen in carrots. In this condition, the whites of the eyes remain white, while people with true jaundice often have a yellowish tinge to the eyes.

This condition is called hypercarotenemia or just carotenemia.

Jaundice is a symptom of liver and gallbladder disorders. The skin and the eyes become yellow due to the accumulation of bilirubin in the skin.

Jaundice-associated conditions include:
Viral hepatitis (Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E)
Obstruction of the bile ducts (by infection, tumor, biliary stricture or gallstones)
Pancreatic carcinoma (cancer of the pancreas)
Cirrhosis (all causes)
Primary biliary cirrhosis
Autoimmune hepatitis
Drug-induced cholestasis (bile pools in the liver because of the effects of drugs)
Drug-induced hepatitis (hepatitis triggered by medications)
Ischemic hepatitis (jaundice caused by inadequate oxygen and/or inadequate blood flow to the liver)
Gilbert's syndrome
Dubin-Johnson syndrome
Biliary atresia
Newborn jaundice
Congenital disorders of bilirubin metabolism
Intrahepatic cholestasis of pregnancy (bile pools in the liver)
Hemolytic anemia
Malaria.

At birth, babies have a relatively immature liver function. Therefore, jaundice is present to some degree in almost all newborns. Even the normal destruction of red blood cells by the liver in the newborn infant can cause jaundice. This form of jaundice usually appears between the 2nd and 5th days of life and clears by 2 weeks. It usually causes no problems.

Jaundice in a newborn is rarely caused by a serious illness. Disorders which can cause jaundice in a baby include:
biliary atresia
ABO incompatibility (similar to a transfusion reaction, caused when fetal and maternal blood mingle before birth)
Rh incompatibility (Anti-Rh antibodies)
galactosemia (see galactosemia screen)
cephalohematoma
polycythemia
glucose-6-phosphate dehydrogenase deficiency
neonatal sepsis
congenital cytomegalovirus infection (CMV)
congenital toxoplasmosis
congenital syphilis
congenital herpes
congenital rubella
vcongenital hypothyroidism
late pregnancy administration of sulfa drugs to the mother
Crigler-Najjar syndrome
spherocytosis (congenital hemolytic anemia)
cystic fibrosis
pyruvate kinase deficiency
thalassemia
Gilbert's syndrome
Lucey-Driscol syndrome
Gaucher's disease
Niemann-Pick disease.