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.
Granular corneal dystrophy  is a slowly progressive corneal dystrophy that most often begins in early childhood. Granular corneal dystrophy has two types:

Granular corneal dystrophy type I, also corneal dystrophy Groenouw type I, is a rare form of human corneal dystrophy. It was first described by German ophthalmologist Arthur Groenouw in 1890. Granular corneal dystrophy type II, also called Avellino corneal dystrophy or combined granular-lattice corneal dystrophy is also a rare form of corneal dystrophy. The disorder was first described by Folberg et al. in 1988. The name Avellino corneal dystrophy comes from the first four patients in the original study each tracing their family origin to the Italian province of Avellino. Presentation
Granular corneal dystrophy is diagnosed during an eye examination by an ophthalmologist or optometrist. The lesions consist of central, fine, whitish granular lesions in the cornea. Visual acuity is slightly reduced. Genetics
Granular corneal dystrophy is caused by a mutation in the TGFBI gene, located on chromosome 5q31. The disorder is inherited in an autosomal dominant manner. This indicates that the defective gene responsible for the disorder is located on an autosome (chromosome 5 is an autosome), and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. The gene TGFBI encodes the protein keratoepithelin. Diagnosis
Treatment
Corneal transplant is not needed except in very severe and late cases. Light sensitivity may be overcome by wearing tinted glasses. See also
Corneal dystrophy


== References ==