Phase oneTerm infants - jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to 204 μmol/L (12 mg/dL). Preterm infants - jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to 255 μmol/L (15 mg/dL).Phase two - bilirubin levels decline to about 34 μmol/L (2 mg/dL) for two weeks, eventually mimicking adult values.Preterm infants - phase two can last more than one month. Exclusively breastfed infants - phase two can last more than one month.Mechanisms involved in physiological jaundice include:

Relatively low activity of the enzyme glucuronosyltransferase which normally converts unconjugated bilirubin to conjugated bilirubin that can be excreted into the gastrointestinal tract. Before birth, this enzyme is actively down-regulated, since bilirubin needs to remain unconjugated in order to cross the placenta to avoid being accumulated in the fetus. After birth, it takes some time for this enzyme to gain function. Shorter life span of fetal red blood cells, being approximately 80 to 90 days in a full term infant, compared to 100 to 120 days in adults. Relatively low conversion of bilirubin to urobilinogen by the intestinal flora, resulting in relatively high absorption of bilirubin back into the circulation. Diagnosis
Diagnosis is often by measuring the serum bilirubin level in the blood. In those who are born after 35 weeks and are more than a day old transcutaneous bilirubinometer may also be used. The use of an icterometer, a piece of transparent plastic painted in five transverse strips of graded yellow lines, is not recommended.
They can be grouped into the following categories:

Unconjugated
Hemolytic
Intrinsic causes of hemolysis
Membrane conditions
Spherocytosis
Hereditary elliptocytosis
Enzyme conditions
Glucose-6-phosphate dehydrogenase deficiency (also called G6PD deficiency)
Pyruvate kinase deficiency
Globin synthesis defect
sickle cell disease
Alpha-thalassemia, e.g. HbH disease

Extrinsic causes of hemolysis
Systemic conditions
Sepsis
Arteriovenous malformation
Alloimmunity (The neonatal or cord blood gives a positive direct Coombs test and the maternal blood gives a positive indirect Coombs test)
Hemolytic disease of the newborn (ABO)
Rh disease
Hemolytic disease of the newborn (anti-Kell)
Hemolytic disease of the newborn (anti-Rhc)
Other blood type mismatches causing hemolytic disease of the newborn

Non-hemolytic causes
Breastfeeding jaundice
Breast milk jaundice
Cephalohematoma
Polycythemia
Urinary tract infection
Sepsis
Hypothyroidism
Gilberts syndrome
Crigler–Najjar syndrome
High GI obstruction (Pyloric stenosis, Bowel obstruction)

Conjugated (Direct)
Liver causes
Infections
Sepsis
Hepatitis A
Hepatitis B
TORCH infections
Metabolic
Galactosemia
Alpha 1-antitrypsin deficiency, which is commonly missed, and must be considered in DDx
Cystic fibrosis
Dubin–Johnson syndrome
Rotor syndrome
Drugs
Total parenteral nutrition
Idiopathic

Post-liver
Biliary atresia or bile duct obstruction
Alagille syndrome
Choledochal cyst

Non-organic causes
Breastfeeding jaundice
"Breastfeeding jaundice" (or "lack of breastfeeding jaundice") is caused by insufficient breast milk intake, resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines. Usually occurring in the first week of life, most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production. Breast milk jaundice
Whereas breastfeeding jaundice is a mechanical problem, breast milk jaundice is a biochemical occurrence and the higher bilirubin possibly acts as an antioxidant. Breast milk jaundice occurs later in the newborn period, with the bilirubin level usually peaking in the sixth to 14th days of life. This late-onset jaundice may develop in up to one third of healthy breastfed infants.