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Clinical update: understanding jaundice in the breastfed infant.


Jaundice is a common condition and the National Institute for Health and Clinical Excellence (NICE) states that 60% of term and 80% of pre-term infants are jaundiced in the first week (NICE, 2010). Breastfed babies are more likely to be jaundiced than formula-fed babies. Breastfed babies are also more likely to suffer from prolonged jaundice (see Box 1) with 10% experiencing jaundice at one month (NICE, 2010). These statistics indicate that staff working in health visiting teams and children's centres (referred to in this article as community practitioners) may work with families whose breastfed infant is jaundiced.

Alex and Gallant (2008) suggest that parents can perceive a contradiction when they are provided with evidence of the overwhelming health benefits of breastfeeding, while at the same time being informed that their infant's jaundice is as a result of breastfeeding. There is a risk that a mother's decision to breastfeed may be undermined if professionals providing care and support for the family are not confident in the physiology behind jaundice and breastfeeding, and are not aware of current recommendations for management and support (Alex and Gallant, 2008). The inclusion in the NICE guidelines (2010) of the 'mother's intention to breastfeed exclusively' as an increased risk for jaundice needs to be understood so that it is not used as an argument for supplementation or for replacing breastfeeding with formula.

The aim of this article is to enable community practitioners to confidently explain to parents what jaundice is and its possible effects, the link between jaundice and breastfeeding and how this relates to feeding their infant.
Box 1. Key terms

* Prolonged jaundice. Term infant--jaundice lasting longer than 14
days. Pre-term infant--lasting longer than 21 days (NCC-WCH, 2010)

* Visible jaundice. Yellow discolouration of skin and whites of the
eye (sclera)

* Hyperbilirubinaemia. Raised levels of bilirubin

* Conjugated Bilirubin. Water soluble (needs to be in this state
for excretion)

* Unconjugated Bilirubin. Fat soluble (can be deposited in the
body's tissues)

* Physiological jaundice. Usually harmless and associated with
normal physiological processes in the newborn

* Pathological jaundice. Jaundice caused by an underlying disease
and condition

Jaundice: definition and physiology

NICE states: 'Jaundice refers to the yellow colouration of the skin and sclerae (whites of the eyes) caused by the accumulation of bilirubin in the skin and mucous membranes' (NICE, 2010: 3). This is also referred to as 'visible jaundice' (National Collaborating Centre for Women's and Children's Health (NCC-WCH), 2010).

Raised levels of bilirubin (hyperbilirubminaemia) are the cause of the yellow discolouration associated with jaundice (NICE, 2010). McIntosh and Stenson (2008) explain that bilirubin is a product of the breakdown of haemaglobin and when first produced is insoluble (also known as unconjugated). For bilirubin to be excreted from the body it must be water soluble (conjugated), as unconjugated bilirubin is fat soluble and can potentially be deposited in the body's tissues (McIntosh and Stenson, 2008).

To prevent unconjugated bilirubin being deposited in tissues it is bound to albumin (a protein) and then transported in the blood to the liver where it is converted to its conjugated form by an enzyme called glucuronyltransferase (England, 2010; McIntosh and Stenson, 2008). McIntosh and Stenson (2008) outline that conjugated bilirubin is excreted into bile and then transported to the small intestine where it is then broken down by bacteria in the intestine. A small amount is reabsorbed, to be excreted by the kidneys in the urine and a larger proportion in the stools (England, 2010; McIntosh and Stenson, 2008).

Conjugated bilirubin is gold in colour and when mixed with bile is responsible for the colouration of stools and urine (England, 2010). Preer and Phillip (2011) highlight that some conjugated bilirubin can be turned back into unconjugated bilirubin by an enzyme called beta-glucuronidase in the intestine and this unconjugated bilirubin is reabsorbed and returned to the liver via a process called 'enterohepatic circulation'.

Over half of all infants are thought to be jaundiced in the first week. This can be a result of normal physiological processes of the newborn and is termed 'physiological jaundice', which is usually harmless (NCCWCH, 2010). For example, a foetus requires more red blood cells than a newborn to supplement oxygen delivery from the placenta (England 2010). The implication of this is that excess red cells need to be broken down in the newborn and, therefore, more bilirubin is produced as a by-product.

Glucuronyltransferase, which converts unconjugated bilirubin to conjugated bilirubin, is thought to be less active in the newborn while conversely the enzyme that converts conjugated bilirubin to unconjugated bilirubin in the intestine (beta-glucuronidase) is thought to be more active (Preer and Phillip, 2011). These processes, coupled with the immaturity of the newborn's liver, result in higher levels of the fat-soluble unconjugated bilirubin (England, 2010; Preer and Phillip, 2011). This can lead to 'visible jaundice' as unconjugated bilirubin is deposited in the skin and mucous membranes.

Jaundice and the breastfed infant

Physiological jaundice occurs in exclusively breastfed and formula-fed infants; however, NICE gives 'intention to breastfeed exclusively' as one of the factors contributing to an infant developing significant hyperbilirubinaemia (NICE, 2010: 11). So why are exclusively breastfed infants particularly at risk of raised levels of bilirubin?

The first reason is often referred to as 'breastfed jaundice'. Alex and Gallant (2008) suggest that this might more accurately be termed 'not-enough-breast-milk jaundice'. UNICEF (2010) cites jaundice as one of the indications that a baby is receiving insufficient breast milk. Early onset jaundice caused by insufficient intake of breast milk usually occurs on day two or three of life (Alex and Gallant, 2008).

Preer and Phillip (2011) explain that when a newborn infant does not receive enough breast milk their meconium/stool output is decreased, which increases the reabsorption of bilirubin, resulting in higher levels of unconjugated bilirubin. In addition, an infant who is not feeding effectively may experience lethargy and this may make the baby less likely to feed, thereby perpetuating the cycle (Preer and Phillip, 2011). Preer and Phillip (2011) go on to suggest that if this process were to go unchecked there would be a risk of the levels of unconjugated bilirubin posing a severe risk to health and potentially bilirubin encephalopathy. This cycle, however, would occur in any infant who is deprived of calories in the first few days of life irrespective of the mode of feeding.

UNICEF (2010) states that there should be trained individuals available to the mother in the first few hours and days to promote skin-to-skin contact, good positioning and attachment and baby-led feeding. These are factors known to promote a good milk supply and an efficient transfer of milk from the breast to the baby, and in the early days this will help provide the baby with much-needed colostrum (UNICEF, 2010). Hockenberry and Wilson (2007) reinforce the fact that colostrum is a natural laxative, and maximising the baby's colostrum intake is the most efficient method of helping to expel meconium from the gut, preventing a build up of bilirubin (Medforth et al, 2006). If a baby is reluctant or too sleepy to feed then expressed breast milk could provide this colostrum until efficient breastfeeding is established (UNICEF, 2010).

The second reason for hyperbilirubinaemia occurring in the breastfed infant is thought to be related to the constituents of breast milk itself and is termed 'breast milk jaundice' (Paul et al, 2012). Paul et al (2012) indicate that breast milk jaundice usually reaches its peak between 14 and 21 days and is resolved by three months of age. The key aspect of this type of jaundice is that the baby is well and has a healthy weight gain (Alex and Gallant, 2008). Preer and Phillip (2011) warn that there have been many unsuccessful attempts to identify exactly the specific properties of breast milk that increase the likelihood of jaundice and NICE (2010) states that associative factors have not been fully clarified.

There have been some suggestions in the literature of what may be contributing factors. Alex and Gallant (2008) cite studies, which suggest that breastmilk is rich in beta-glucuronidase (increases uptake of unconjugated bilirubin). Preer and Phillip (2011) highlight a study suggesting that higher levels of epidermal growth factors (EGF) were present in jaundiced breastfed infants and their mother's breast milk. EGF increases intestinal absorption in the newborn infant (Preer and Phillip, 2011). Alex and Gallant (2008) reinforce that as long as the baby is thriving and other pathologies have been ruled out, breast milk jaundice is not known to result in bilirubin encephalopathy. NICE (2010) has specifically recommended research on the link between breastfeeding and jaundice so there may be developments in the evidence available in the near future.

Pathological jaundice

The physiological processes outlined above are normal and, for most infants, jaundice is harmless (NCC-WCH, 2010). England (2010) even suggests that low levels of fat-soluble bilirubin may be beneficial as it can have an antioxidant effect. However, jaundice can also occur as a result of underlying conditions this is known as 'pathological jaundice'. These conditions are rare but they can exist at the same time as physiological jaundice and need to be detected as the levels of hyperbilinaemia they can create may pose a serious risk to the infant (NCC-WCH, 2010). Please see NICE (2010: 3) and NCC-WCH, (2010: 34) for details of these conditions.

Pathological jaundice may significantly increase the amount of unconjugated bilirubin in the blood. Unconjugated bilirubin is potentially toxic to the brain and spinal chord and can cause neurological damage (NCC-WCH, 2010). England (2010) highlights that unbound unconjugated bilirubin (not attached to albumin) coupled with other risk factors, such as pre-term birth and low levels or lack of oxygen, may open up the blood-brain barrier, enabling the unconjugated bilirubin to enter the brain resulting in bilirubin encephalopathy.

The term 'kernicticus' is often used interchangeably with 'bilirubin encephalopathy', but Hockenberry and Wilson (2007) suggest that this refers to the yellow staining of the brain caused by bilirubin encephalopathy. In its acute phase bilirubin encephalopathy may result in symptoms such as lethargy, increased tone rigidity and convulsions (England, 2010). England (2010) explains that if an infant survives into the chronic phase of the condition then effects can include partial or complete deafness and intellectual impairment.

A further condition that community practitioners need to be particularly aware of is biliary atresia as it may manifest itself a few weeks after birth when the infant is in the care of the community team (Hockenberry and Wilson, 2007). Hockenberry and Wilson (2007) describe this as a rare inflammatory condition, which results in fibrosis (hardening) of the biliary system. A child experiencing biliary atresia may display prolonged jaundice, raised conjugated bilirubin levels, dark urine and pale stools as a result of loss of bile pigment (Hockenberry and Wilson, 2007). The NCC-WCH (2010) suggests that biliary atresia requires surgical treatment preferably in the first eight weeks of life and Hockenberry and Wilson (2007) state that if untreated the condition leads to liver failure and death by the age of two.

It is not within the scope of this article to discuss the treatment of jaundice in depth--full details of this are provided by NICE (2010: 10) and NCC-WCH (2010). However, it is appropriate to highlight when an infant should be referred for further investigation and tests.

NICE (2010) recommends that any infant showing jaundice in the first 24 hours should receive an urgent medical review to exclude pathological causes of jaundice. Any infant with factors increasing the likelihood of hyperbilirubinaemia (see Box 2) should receive a visual inspection for jaundice by a health professional in the first 48 hours of life. A visual inspection is best done in bright sunlight and the professional should be aware that visual jaundice may be difficult to detect in darker skin tones (NICE, 2010).

NICE (2010: 12) states that 'examination of the sclera, gums and blanched skin is useful across all skin tones'. Visibly jaundiced infants more than 24 hours old should have bilirubin levels measured and recorded within hours of the jaundice being detected (NICE, 2010). For those infants whose bilirubin levels reach the appropriate threshold outlined by NICE (2010), phototherapy (lamp light on the blue spectrum) is the first line of treatment. This type of light converts the bilirubin in the skin to a harmless form that can be excreted by the urine (NCC-WCH, 2010). It is worth noting that natural sunlight is not recommended as a treatment for hyperbilirubinaemia (NICE, 2010). An exchange transfusion may be required for those infants exceeding the threshold for phototherapy (NICE, 2010).
Box 2. Management and support (NICE, 2010)

Infants more likely to develop significant hyperbilirubinaemia are:

* Neontates under 38 weeks gestation

* Infants with a sibling who required phototherapy for neonatal

* Infants whose mothers intend to breastfeed exclusively

* Visible jaundice in the first 24 hours of life

In infants demonstrating prolonged jaundice the colour of their stools and urine should be ascertained, as pale stools and dark urine may suggest biliary atresia (NICE, 2010). Infants should be referred to the relevant local service/clinic for a range of tests to exclude any underlying pathological conditions and to determine bilirubin levels (NICE, 2010). Paul et al (2012) argue that these tests could be seen as intrusive for healthy breastfed infants who have breast milk jaundice but concede that, at present, there is no other 'validated' way of determining whether there is any underlying pathology behind the prolonged jaundice.

Support and reassurance

What support and reassurance can the community practitioner give to a parent who has been told that their child's jaundice is either a result of insufficient intake of breast milk or breast milk jaundice? The answer can be based on the NICE (2010) guidelines on neonatal jaundice. These state that mothers of a visibly jaundiced baby should be encouraged to breastfeed their infant 'frequently' and lactation and breastfeeding support should be provided. Additional fluids, even for infants receiving phototherapy, are not recommended routinely and, where they are specified, expressed breast milk is the additional food of choice (NICE, 2010). The NCC-WCH (2010) reinforces that this recommendation emphasises the benefits of breastfeeding for the mother and child.

Once bilirubin levels indicate that treatment is not required, pathologies excluded and providing the infant remains well, the parent can be reassured that the jaundice will not harm their child and that it usually resolves on its own by three months (Paul et al, 2012). Parents should also be informed of who to contact immediately should their child's condition change.


Explaining to parents the association between breastfeeding and jaundice while stressing the overwhelming benefits of breastfeeding can be a delicate exercise in communication for the community practitioner. Linking insufficient breast milk intake with early onset jaundice and discussing the term 'breast milk jaundice' may help this explanation.

Although the community practitioner needs to be mindful of the current debate on the specific cause of jaundice in the breastfed infant, once pathologies have been ruled out and any required treatment given, they can confidently advise parents that the benefits of breastfeeding outweigh any effects of jaundice.

No potential competing interests declared
CPD questions (please visit to
submit your answers)

1. Which of the following correctly represents the incidence of
jaundice in infants?

A. 30% term, 70% pre-term

B. 80% term, 60% pre-term

C. 60% term, 80% pre-term

D. 50% term, 50% pre-term

2. For the term infant, which of the following is the correct
definition of prolonged jaundice?

A. Jaundice lasting longer than 7 days

B. Jaundice lasting longer than 14 days

C. Jaundice lasting longer than 18 days

D. Jaundice lasting longer than 21 days

3. Jaundice is caused by ...

A. Raised levels of bilirubin

B. Decreased levels of bilirubin

C. Nothing related to bilirubin

D. None of the above

4. Which of the following definition of unconjugated bilirubin is

A. It is water soluble and can be excreted

B. It is fat soluble and cannot be excreted

C. It is fat soluble and can be excreted

D. It is water soluble and cannot be excreted

5. What is the term for jaundice caused by normal healthy processes
in the body?

A. Physiological jaundice

B. Kernicticus

C. Pathological jaundice

D. None of the above

6. Which of the following processes is associated with
physiological jaundice?

A. Crossing of unconjugated bilirubin across the blood brain

B. Production of red blood cells

C. Stenosis of the biliary tract

D. Breakdown of excess red blood cells in the newborn

7. When does breast milk jaundice peak?

A. 7-14 days

B. 14-21 days

C. 28-42 days

D. 56-84 days

8. Breast milk jaundice is usually resolved by what age?

A. 3 months

B. 4 months

C. 5 months

D. 6 months

9. What is the correct treatment for hyperbilirubinaemia?

A. Acupuncture

B. Natural sunlight

C. Phototherapy

D. None of the above

10. A mother sees you in clinic. She has a healthy 2 month old who
is gaining weight well and is being exclusively breastfed. The
infant has been diagnosed by the specialist clinic as having breast
milk jaundice. Which is the correct management?

A. Advise supplementing breastfeeding with formula

B. Advise giving formula for 24 hours and then resuming

C. Advise to continue with on-demand breastfeeding

D. None of the above


Alex M, Gallant DP. (2008) Toward understanding the connections between infant jaundice and infant, feeding. J Pediatr Nurs 23(6): 429-38.

England C. (2010) Care of the jaundiced baby. In: Lumsden H, Holmes D (eds). Care of the Newborn by Ten Teachers. London: Hodder Arnold.

Hockenberry MJ, Wilson D. (2007) Wongs Nursing Care of Infants and Children, 8th edn. St. Louis: Mosby Elsevier.

Medforth J, Battersby S, Evans M, Marsh B, Walker A (eds). (2006) Oxford Handbook of Midwifery. Oxford: Oxford University Press.

Mcintosh N, Helms PJ, Smyth RL, Logan S. (2008) Forfar and ArneiVs Textbook of Paediatrics, 7th edn. London: Elsevier.

National Collaborating Centre for Women's and Children's Health (NCC-WCH) (2010). CG98 Neonatal Jaundice: Full guideline. London: Royal College of Obstetricians and Gynaecologists.

National Institute for Health and Clinical Excellence (NICE). (2010) CG98: Neonatal Jaundice. London: NICE.

Paul SP, Hall V, Taylor TM. (2012) Prolonged jaundice in neonates. Pract Midwife 15(6): 14-17.

Preer GL, Phillipp BL. (2011) Understanding and managing breast milk jaundice. Arch Dis Child Fetal Neonatal Ed 96(6): 461-6.

UNICEF. (2010) Baby Friendly Care Pathways: Breastfeeding. Available from: BabyFriendly/Health-Professionals/Care-Pathways/ Breastfeeding/ [Accessed May 2013].

Mary Clark RGN BA(Hons) PGDip HV MA PGCertHe

Senior Lecturer Child Health

Middlesex University
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Title Annotation:PRACTICE: CPD
Author:Clark, Mary
Publication:Community Practitioner
Article Type:Report
Geographic Code:4EUUK
Date:Jun 1, 2013
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