Jaundice is one of the most common conditions needing medical attention in newborn babies. Jaundice refers to the yellow colouration of the skin and the sclerae (whites of the eyes) caused by the accumulation of bilirubin in the skin and mucous membranes. It is caused by a raised level of bilirubin in the body, a condition known as hyperbilirubinaemia.

Approximately 60% of term and 80% of preterm babies develop jaundice in the first week of life, and about 10% of breastfed babies are still jaundiced at 1 month. For most babies, jaundice is not an indication of an underlying disease, and this early jaundice (termed 'physiological jaundice') is usually harmless.

Breastfed babies are more likely than bottle‑fed babies to develop physiological jaundice within the first week of life. Prolonged jaundice – that is, jaundice persisting beyond the first 14 days – is also seen more commonly in breastfed babies. Prolonged jaundice is usually harmless, but can sometimes be an indication of serious liver disease.

Jaundice has many possible causes, including blood group incompatibility (most commonly rhesus or ABO incompatibility), other causes of haemolysis (breaking down of red blood cells), sepsis (infection), liver disease, bruising and metabolic disorders. Deficiency of a particular enzyme, glucose‑6‑phosphate‑dehydrogenase, can cause severe neonatal jaundice. Glucose‑6‑phosphate‑dehydrogenase deficiency is more common in certain ethnic groups and runs in families.

Bilirubin is mainly produced from the breakdown of red blood cells. Red cell breakdown produces unconjugated (or 'indirect') bilirubin, which circulates mostly bound to albumin although some is 'free' and hence able to enter the brain. Unconjugated bilirubin is metabolised in the liver to produce conjugated (or 'direct') bilirubin which then passes into the gut and is largely excreted in stool. The terms direct and indirect refer to the way the laboratory tests measure the different forms. Some tests measure total bilirubin and do not distinguish between the two forms.

In young babies, unconjugated bilirubin can penetrate the membrane that lies between the brain and the blood (the blood–brain barrier). Unconjugated bilirubin is potentially toxic to neural tissue (brain and spinal cord). Entry of unconjugated bilirubin into the brain can cause both short‑term and long‑term neurological dysfunction (bilirubin encephalopathy). The term kernicterus is used to denote the clinical features of acute or chronic bilirubin encephalopathy, as well as the yellow staining in the brain associated with the former. The risk of kernicterus is increased in babies with extremely high bilirubin levels. Kernicterus is also known to occur at lower levels of bilirubin in term babies who have risk factors, and in preterm babies.

Clinical recognition and assessment of jaundice can be difficult, particularly in babies with darker skin tones. Once jaundice is recognised, there is uncertainty about when to treat, and there is widespread variation in the use of phototherapy and exchange transfusion. There is a need for more uniform, evidence‑based practice and for consensus‑based practice where such evidence is lacking. This guideline provides guidance regarding the recognition, assessment and treatment of neonatal jaundice. The advice is based on evidence where this is available and on consensus‑based practice where it is not.

In 2016, we reviewed the evidence on tests for recognising neonatal jaundice, bilirubin thresholds for retesting, and the type and procedure for phototherapy. New and updated recommendations have been added on bilirubin thresholds for retesting and the type of phototherapy to use.