Neonatal Jaundice

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Neonatal jaundiceor Neonatal hyperbilirubinemia, or Neonatal icterus(from the Greek

word ), attributive adjective: icteric, is a yellowing of theskinand other tissues of a

newborninfant.Abilirubinlevel of more than 85 mol/l (5mg/dL) manifests

clinicaljaundiceinneonateswhereas in adults a level of 34 mol/l (2mg/dL) would lookicteric.In

newborns, jaundice is detected by blanching the skin with digital pressureso that it revealsunderlying skin and subcutaneous tissue.

[1]Jaundiced newborns have an apparent ictericsclera,

and yellowing of the face, extending down onto the chest.

In neonates, the dermalicterusis first noted in the face and as the bilirubin level rises proceeds

caudal to the trunk and then to the extremities.[2]

This condition is common in newborns affecting

over half (5060%) of all babies in the first week of life.[3]

Notoriously inaccuraterules of thumbhave been applied to thephysical examof the jaundiced

infant.[citation needed]

Some include estimation of serumbilirubinbased on appearance. One such rule of

thumbincludes infants whose jaundice is restricted to the face and part of the trunk above

theumbilicus,have thebilirubinless than 204 mol/l (12mg/dL) (less dangerous level). Infants

whose palms and soles are yellow, have serum bilirubin level over 255 mol/l (15mg/dL) (more

serious level). Studies have shown that trained examiners assessment of levels of jaundice show

moderate agreement with icterometer bilirubin measurements.[2]

In infants, jaundice can be

measured usinginvasiveor non-invasive methods.
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Classification[edit]Physiological jaundice[edit]

Mostinfantsdevelop visible jaundice due to elevation of unconjugated bilirubin concentration during

their first week. This common condition is called physiological jaundice. This patternofhyperbilirubinemiahas been classified into two functionally distinct periods.

Phase one

1. Term infants - jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to

204 mol/l (12mg/dL).

2. Preterm infants - jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to

255 mol/l (15mg/dL).

Phase two - bilirubin levels decline to about 34 mol/l (2mg/dL) for two weeks, eventually

mimicking adult values.

1. Preterm infants - phase two can last more than one month.

2. Exclusively breastfed infants - phase two can last more than one month.

Causes[edit]

Mechanism involved in physiological jaundice are mainly:

Relatively low activity of the enzymeglucuronosyltransferase which normally

convertsunconjugated bilirubinto conjugated bilirubin that can be excreted into the

gastrointestinal tract.[4]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.[5]

After birth, it takes some time for this enzyme to gain function.

Shorter life span of fetal red blood cells,[4]

being approximately 80 to 90 days in a full

terminfant,[6]

compared to 100 to 120 days in adults.

Relatively low conversion of bilirubin tourobilinogenby theintestinal flora,resulting in relatively

high absorption of bilirubin back into the circulation.[4]
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Pathological Jaundice of Neonates (Unconjugated PathologicalHyperbilirubinemia)[edit]

Any of the following features characterizes pathological jaundice:

1. Clinical jaundice appearing in the first 24 hours or greater than 14 days of life.

2. Increases in the level of total bilirubin by more than 8.5 mol/l (0.5mg/dL) per hour or

(85 mol/l) 5mg/dL per 24 hours.

3. Total bilirubin more than 331.5 mol/l (19.5mg/dL) (hyperbilirubinemia).

4. Direct bilirubin more than 34 mol/l (2.0mg/dL).
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Causes of jaundice[edit]

In neonates, jaundice tends to develop because of two factors - the breakdown offetal

hemoglobinas it is replaced withadult hemoglobinand the relatively immature hepatic metabolic

pathways which are unable to conjugate and so excrete bilirubin as quickly as an adult. This causes

an accumulation of bilirubin in the blood (hyperbilirubinemia), leading to the symptoms of jaundice.

If the neonatal jaundicedoes not clear up with simplephototherapy,other causes such asbiliary

atresia,PFIC, bile duct paucity,Alagille syndrome,alpha 1-antitrypsin deficiency, and other pediatric

liver diseases should be considered. The evaluation for these will include blood work and a variety of

diagnostic tests. Prolonged neonatal jaundice is serious and should be followed up promptly.

Severe neonatal jaundice may indicate the presence of other conditions contributing to the elevated

bilirubin levels, of which there are a large variety of possibilities (see below). These should be

detected or excluded as part of thedifferential diagnosisto prevent the development of

complications. They can be grouped into the following categories:

Neonatal jaundice

Unconjugatedbilirubin

Conjugated

bilirubin

Pathologic Physiologicaljaundice of

Neonates

Hepatic Post-

hepatic

Hemolytic Non-hemolytic

Intrinsiccauses

Extrinsiccauses

Non Conjugated[edit]

Hemolytic[edit]
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Intrinsic causes of hemolysis[edit]

Membrane conditions

Spherocytosis

Hereditary elliptocytosis

Systemic conditions

Sepsis

Arteriovenous malformation

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[edit]

Alloimmunity(The neonatal orcord bloodgives a positivedirect Coombs testand the maternal

blood gives a positiveindirect Coombs test)

Hemolytic disease of the newborn (ABO)[1]

Rh disease[1]

Hemolytic disease of the newborn (anti-Kell)

Hemolytic disease of the newborn (anti-Rhc)

Other blood type mismatches causinghemolytic disease of the newborn

Non-hemolytic causes[edit]

Breast milk jaundice

Cephalohematoma

Polycythemia

Urinary tract infection Sepsis

Hypothyroidism

Gilbert's syndrome

Crigler-Najjar syndrome

High GI obstruction
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Conjugated[edit]

Hepatic causes[edit]

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-hepatic[edit]

Biliary atresiaorbile ductobstruction

Alagille syndrome

Choledochal cyst

Non-organic causes[edit]

Breastfeeding failure jaundice[edit]

"Breastfeeding jaundice" or "lack of breastfeeding jaundice," is caused by insufficient breast milk

intake,[7]

resulting in inadequate quantities of bowel movementsto remove bilirubin from the body.

This can usually be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate

adequate milk production.

Breast Milk jaundice[edit]

Whereas breast feedingjaundice is a mechanical problem, breast milkjaundice 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.[8]
http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=12http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=12http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=12http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=13http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=13http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=13http://en.wikipedia.org/wiki/Sepsishttp://en.wikipedia.org/wiki/Sepsishttp://en.wikipedia.org/wiki/Hepatitis_Bhttp://en.wikipedia.org/wiki/Hepatitis_Bhttp://en.wikipedia.org/wiki/TORCH_syndromehttp://en.wikipedia.org/wiki/TORCH_syndromehttp://en.wikipedia.org/wiki/Galactosemiahttp://en.wikipedia.org/wiki/Galactosemiahttp://en.wikipedia.org/wiki/Alpha-1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Alpha-1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Cystic_fibrosishttp://en.wikipedia.org/wiki/Cystic_fibrosishttp://en.wikipedia.org/wiki/Dubin-Johnson_Syndromehttp://en.wikipedia.org/wiki/Dubin-Johnson_Syndromehttp://en.wikipedia.org/wiki/Rotor_syndromehttp://en.wikipedia.org/wiki/Rotor_syndromehttp://en.wikipedia.org/wiki/Total_parenteral_nutritionhttp://en.wikipedia.org/wiki/Total_parenteral_nutritionhttp://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=14http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=14http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=14http://en.wikipedia.org/wiki/Biliary_atresiahttp://en.wikipedia.org/wiki/Biliary_atresiahttp://en.wikipedia.org/wiki/Bile_ducthttp://en.wikipedia.org/wiki/Bile_ducthttp://en.wikipedia.org/wiki/Bile_ducthttp://en.wikipedia.org/wiki/Alagille_syndromehttp://en.wikipedia.org/wiki/Alagille_syndromehttp://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=15http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=15http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=15http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=16http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=16http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=16http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-GarfunkelKaczorowski2002-7http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-GarfunkelKaczorowski2002-7http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-GarfunkelKaczorowski2002-7http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=17http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=17http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=17http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-8http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-8http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-8http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-8http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=17http://en.wikipedia.org/wiki/Neonatal_jaundice#cite_note-GarfunkelKaczorowski2002-7http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=16http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=15http://en.wikipedia.org/wiki/Alagille_syndromehttp://en.wikipedia.org/wiki/Bile_ducthttp://en.wikipedia.org/wiki/Biliary_atresiahttp://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=14http://en.wikipedia.org/wiki/Total_parenteral_nutritionhttp://en.wikipedia.org/wiki/Rotor_syndromehttp://en.wikipedia.org/wiki/Dubin-Johnson_Syndromehttp://en.wikipedia.org/wiki/Cystic_fibrosishttp://en.wikipedia.org/wiki/Alpha-1-antitrypsin_deficiencyhttp://en.wikipedia.org/wiki/Galactosemiahttp://en.wikipedia.org/wiki/TORCH_syndromehttp://en.wikipedia.org/wiki/Hepatitis_Bhttp://en.wikipedia.org/wiki/Sepsishttp://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=13http://en.wikipedia.org/w/index.php?title=Neonatal_jaundice&action=edit&section=12


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First, at birth, the gut is sterile, and normal gut flora takes time to establish. The bacteria in the

adult gut convert conjugatedbilirubintostercobilinogenwhich is then oxidized tostercobilinand

excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush

border -glucuronidase and reabsorbed. This process of re-absorption is calledenterohepatic

circulation.It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) isincreased in breast fed babies, possibly as the result of increased levels of epidermal growth

factor (EGF) in breast milk.[9]Breast milk also contains glucoronidase which will increase

deconjugation and enterohepatic recirculation of bilirubin.

Second, the breast-milk of some women contains a metabolite of progesterone called3-alpha-

20-beta pregnanediol.This substance inhibits the action of the enzyme uridine

diphosphoglucuronic acid (UDPGA)glucuronyl transferaseresponsible for conjugation and

subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at

0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin

conjugation leads to increased levels of bilirubin in the blood.[10]

However, these results have not

been supported by subsequent studies.[11]

Third, an enzyme in breast milk calledlipoprotein lipaseproduces increased concentration of

nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to

decreased conjugation and subsequent excretion of bilirubin.[12]

Despite the advantages of breast feeding, there is a strong association of breast feeding with

neonatal hyperbilirubinemia and thus risk ofkernicterus,though this is uncommon. Serum bilirubin

levels may reach as high as 30 mg/dL. Jaundice should be managed either with phototherapy or

with exchange blood transfusion as is needed. Breast feeds however need not be discontinued. The

child should be kept well hydrated and extra feeds given.
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Treatment[edit]

The bilirubin levels for initiative of phototherapy varies depends on the age and health status of the

newborn. However, any newborn with a total serum bilirubin greater than 359 mol/l ( 21mg/dL)

should receive phototherapy.[13]

Phototherapy[edit]

The use of phototherapy was first discovered, accidentally, at Rochford Hospital in Essex, England.

The ward sister (Charge Nurse) of the premature baby unit firmly believed that the infants under her

care benefited from fresh air and sunlight in the courtyard. Although this led to the first noticing of

jaundice being improved with sunlight, further studies only progressed when a vial of blood sent for

bilirubin measurement sat on a windowsill in the lab for several hours. The results indicated a much

lower level of bilirubin than expected based on the patient's visible jaundice. Further investigation

lead to the determination that blue light, wavelength of 420-448 nm, oxidized the bilirubin to

biliverdin, a soluble product that does not contribute tokernicterus.Although some pediatricians

began using phototherapy in the United Kingdom following Dr. Cremer's publishing the above facts

in the Lancetin 1958, most hospitals only began to regularly use phototherapy ten years later when

an American group independently made the same discovery.[14][15]

newborn infant undergoing (white light) phototherapy to treat neonatal jaundice

Infants with neonatal jaundice are treated with colored light called

phototherapy.Physiciansrandomly assigned 66 infants 35 weeks of gestation to receive

phototherapy. After 155 the levels of bilirubin, a yellowish bile pigment that in excessive amounts

causes jaundice, were decreased down to 0.270.25 mg/dl/h in the blue light. This suggests that

blue light therapy helps reduce high bilirubin levels that cause neonatal jaundice.[16]

Exposing infants to high levels of colored light changes trans-bilirubin to the more water soluble cis-

form which is excreted in the bile. Scientists studied 616 capillary blood samples from jaundiced

newborn infants. These samples were randomly divided into three groups. One group contained 133

samples and would receive phototherapy with blue light. Another group contained 202 samples
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would receive room light, or white light. The final group contained 215 samples, and were left in a

dark room. The total bilirubin levels were checked at 0, 2, 4, 6, 24, and 48 hours. There was a

significant decrease in bilirubin in the first group exposed to phototherapy after two hours, but no

change occurred in the white light and dark room group. After 6 hours, there was a significant

change in bilirubin level in the white light group but not the dark room group. It took 48 hours torecord a change in the dark room groups bilirubin level. Phototherapy is the most effective way of

breaking down a neonates bilirubin.[17]

Phototherapyworks through a process of isomerization that changes trans-bilirubin into the water-

soluble cis-bilirubin isomer.[18][19]

In phototherapy, blue light is typically used because it is more effective at breaking down bilirubin

(Amato, Inaebnit, 1991). Two matched groups of newborn infants with jaundice were exposed to

intensive green or blue light phototherapy. The efficiency of the treatment was measured by the rate

of decline of serum bilirubin, which in excessive amounts causes jaundice, concentration after 6, 12

and 24 hours of light exposure. A more rapid response was obtained using the blue lamps than the

green lamps. However, a shorter phototherapy recovery period was noticed in babies exposed to the

green lamps(1). Green light is not commonly used because exposure time must be longer to see

dramatic results(1).

Ultraviolet light therapy may increase the risk of skin moles, in childhood. While an increased

number of moles is related to an increased risk of skin cancer,[20][21][22]

it is not ultraviolet light that is

used for treating neonatal jaundice. Rather, it is simply a specific frequency of blue light that does

not carry these risks.

Increased feedings help move bilirubin through the neonates metabolic system.[23]

The light can be applied with overhead lamps, which means that the baby's eyes need to be

covered, or with a device called aBiliblanket,which sits under thebaby's clothingclose to its skin.
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Outlook (Prognosis)

Usually newborn jaundice is not harmful. For most babies, jaundice usually gets better without treatment

within 1 to 2 weeks.

Very high levels of bilirubin can damage the brain. This is called kernicterus.However, the condition is

almost always diagnosed before levels become high enough to cause this damage.

For babies who need treatment, the treatment is usually effective.

Possible Complications

Rare, but serious, complications from high bilirubin levels include:

Cerebral palsy

Deafness

Kernicterus -- brain damagefrom very high bilirubin levels

When to Contact a Medical Professional

All babies should be seen by a health care providerin the first 5 days of life to check for jaundice.

Those who spend less than 24 hours in a hospital should be seen by age 72 hours.

Infants sent home between 24 and 48 hours should be seen again by age 96 hours.

Infants sent home between 48 and 72 hours should be seen again by age 120 hours.

Jaundice is an emergency if the baby has a fever, has become listless, or is not feeding well. Jaundice

may be dangerous in high-risk newborns.

Jaundice is generally NOT dangerous in term, otherwise healthy newborns. Call the infant's health care

provider if:

Jaundice is severe (the skin is bright yellow)

Jaundice continues to increase after the newborn visit, lasts longer than 2 weeks, or other

symptoms develop

The feet, especially the soles, are yellow

Prevention

In newborns, some degree of jaundice is normal and probably not preventable. The risk of significant

jaundice can often be reduced by feeding babies at least 8 to 12 times a day for the first several days and

by carefully identifying infants at highest risk.

All pregnant women should be tested for blood type and unusual antibodies. If the mother is Rh negative,

follow-up testing on the infant's cord is recommended. This may also be done if the mother's blood type is

O+, but it is not needed if careful monitoring takes place.
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Careful monitoring of all babies during the first 5 days of life can prevent most complications of jaundice.

Ideally, this includes:

Considering a baby's risk for jaundice

Checking bilirubin level in the first day or so

Scheduling at least one follow-up visit the first week of life for babies sent home from the hospital

in 72 hours

Alternative Names

Jaundice of the newborn; Neonatal hyperbilirubinemia; Bili lights - jaundice


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is caused by a yellow substance called bilirubin. Infants with high blood levels of bilirubin, called

hyperbilirubinemia, develop the yellow color when bilirubin accumulates in the skin.

Jaundice is not a disease, but is a symptom of an elevated blood bilirubin level. Jaundice is not painful,

but serious complications can occur if elevated bilirubin levels are not treated in a timely manner.

Jaundice is a marker used to identify those infants who may be at risk for developing severe

hyperbilirubinemia. Severe hyperbilirubinemia can be toxic to the nervous system of infants, potentially

causing brain damage.

JAUNDICE SYMPTOMS

Jaundice initially causes the skin to become yellowed. Later, the whites of the eyes may have a yellowish

tinge. These changes may be hard to recognize in children with a dark skin coloror if a baby is unable to

open eyelids. The color change:

Is noticeable in the face first, and may progress down the chest, abdomen, arms, and then finally

thelegs .

Can be checked by pressing one finger on your baby's forehead or nose. If the skin is jaundiced, it

will appear yellow when you release pressure from the skin.

Can be tracked in some babies by pressing over the bony prominences of the chest, hips, and

knees to check if the jaundice is progressing.

Should be checked before your baby leaves the hospital. If your baby goes home sooner than 72

hours after birth, you will need to monitor the baby's skin color at home every day. In addition, your

infant should see a doctor or nurse within one to three days after going home.

Signs of worsening jaundiceCall your child's healthcare providerif you notice any of the following:

If the yellow coloring is at the knee or lower, or if the yellow color is more intense, lemon yellow to

orange yellow

If the baby has any difficulty in feeding

If it is hard to wake up your infant

If your infant is irritable and is difficult to console

If your infant arches his/her neck or body backwards

JAUNDICE CAUSES

Jaundice is caused by the accumulation of bilirubin in the blood. Bilirubin is formed when red blood cells

are broken down. Bilirubin (a yellow pigment) is naturally cleared through the liver, and then excreted in

stool and urine. Bilirubin levels become elevated when bilirubin is produced faster than it can be

eliminated.

Jaundice is common in newborns, since two to three times more bilirubin is produced during this period

as compared with during adulthood. "Physiologic jaundice" or benign jaundice, which affects nearly all

newborns, is caused by a mild elevation of bilirubin and is not usually harmful to infants. It developsbetween 72 and 96 hours after birth, and usually goes away by one to two weeks after birth. In infants

who are born at 35 to 37 weeks of gestation and those who are severely jaundiced, the jaundice may

require more time to resolve.

Newborns with higher levels of bilirubin in the blood have "severe hyperbilirubinemia", a more serious

condition than physiologic jaundice. Infants may develop severe hyperbilirubinemia within the first 24

hours of life. If this happens, you must consult your doctor urgently.
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One reason that bilirubin levels are higher in infants is that more red blood cells are broken down (and as

a result, more bilirubin is produced). This can be related to:

Bruising and mild injuries from the birth process.

If the mother and infant's blood types are incompatible; the mother's immune system may attack

the infant's red blood cells.

Inherited causes of red blood cell breakdown (such as deficiency of an enzyme called glucose-6-

phosphate dehydrogenase [G6PD], which may occur more frequently among African-American,

Mediterranean, and Asian races).

Asian race or ancestry.

Bilirubin is also more slowly eliminated in the newborn compared with in adults because a newborns liver

and intestines are not fully mature.

BreastfeedingJaundice is common in infants who are breastfed because of two different reasons:

Breastfeeding failure occurs in infants with inadequate intake of breast milkbecause of difficulty in

feeding or if the mother does not have an adequate milk supply. These infants lose a large amount

ofweight ,thereby increasing bilirubin concentration. Increasing the mother's milk supply, frequent

feeding, and ensuring good sucking (latch) are the best treatments for inadequate intake jaundice.

(See"Patient information: Common breastfeeding problems (Beyond the Basics)" .)

Breast milk jaundice is thought to be due to the infants immature liver and intestines. It typically

begins the first week after birth, peaks within two weeks after birth, and declines over the next few

weeks. Breast milk jaundice is not a reason to stop breastfeedingas long as the baby is feeding

well, gaining weight, and otherwise thriving. Infants with breast milk jaundice rarely need treatment

unless severe hyperbilirubinemia develops. All infants with jaundice should be monitored by a doctor

or nurse. (See"Patient information: Common breastfeeding problems (Beyond the Basics)" .)

In either setting, the mother should be encouraged to continue breastfeeding because of the overall

benefits of human milk.

JAUNDICE DIAGNOSIS

Newborn jaundice can be diagnosed by examining the infant and testing blood levels of bilirubin. A blood

test involves collecting a small amount (less than one-half teaspoon or 2.5 mL) of blood. Results of blood

testing are available in most hospitals within a few hours.

JAUNDICE COMPLICATIONS

In babies whose bilirubin blood levels reach harmful levels, bilirubin may get into the brain and cause

reversible damage (called acute bilirubin encephalopathy) or permanent damage (called kernicterus).

Frequent monitoring and early treatment of infants athigh riskfor jaundice can help to prevent severe

hyperbilirubinemia.

JAUNDICE TREATMENT

The goal of jaundice treatment is to quickly and safely reduce the level of bilirubin. Infants with mild

jaundice may need no treatment. Infants with higher bilirubin levels or hyperbilirubinemia will require

treatment, which is described below. (See"Treatment of unconjugated hyperbilirubinemia in term and late

preterm infants".)
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Jaundice is common in premature infants(those born before 38 weeks of gestation). Premature infants

are at greater risk for hyperbilirubinemia because brain toxicity occurs at lower levels of bilirubin than in

term infants. As a result, premature infants are treated at lower levels of bilirubin, but with the same

treatments discussed here.

Encourage feedingProviding adequate breast milk or formula is an important part of preventing and

treating jaundice because it promotes elimination of the yellow pigment in stools and urine. You will knowthat your child is getting enough milk or formula if s/he has at least six wet diapers per day, the color of

the bowel movements changes from dark green to yellow, and s/he seems satisfied after feeding.

PhototherapyPhototherapy (light therapy) is the most common medical treatment for jaundice in

newborns. In most cases, phototherapy is the only treatment required. It consists of exposing an infant's

skin to a special blue light, which breaks bilirubin down into parts that are easier to eliminate in the stool

and urine. Treatment with phototherapy is successful for almost all infants.

Phototherapy is usually done in the hospital, but in select cases, it can be done in the home if the baby

ishealthy and at low risk for complications.

Infants undergoing phototherapy should have as much skin exposed to the light as possible. Infants areusually naked (or wearing only a diaper) in an open bassinet or warmer, but wear eye patches to protect

the eyes (picture 1). It is important to ensure that the lamps do not generate excessive heat, which could

injure an infant's skin. In some institutions, phototherapy blankets are used (picture 2). Phototherapy

should be continuous, with breaks only for feeding.

Exposure to sunlight was previously thought to be helpful, but is not currently recommended due to the

risk of sunburn. Sunburn does not occur with the lights used in phototherapy when used properly.

Phototherapy is stopped when bilirubin levels decline to a safe level. It is not unusual for infants to still

appear jaundiced after phototherapy is completed. Bilirubin levels may rebound 18 to 24 hours after

stopping phototherapy, although this rarely requires further treatment.

Side effectsPhototherapy is very safe, but it can have temporary side effects, including a skin

rash and loose bowel movements. Overheating and dehydration can occur if the infant does not get

enough breast milk or formula. Therefore, the infant's skin color, body temperature, and number of

wet diapers are closely monitored.

Rarely, some infants will develop "bronze baby" syndrome, a dark, grayish-brown discoloration of

the skin and urine. Bronze baby syndrome is not harmful and gradually resolves without treatment

after several weeks.

HydrationIt is important for infants receiving phototherapy to drink adequate fluids (breast milk or

a supplement) since bilirubin is excreted in urine and bowel movements. Breast- or bottle-feeding

should continue during phototherapy. Use of oral glucose water is not necessary. In some babies

with severe dehydration, intravenous fluids may be necessary.BreastfeedingBreastfed infants who are not able to consume enough breast milk, whose weight

loss is excessive, or who are dehydrated may need extra expressed breast milk or other milk

supplements. Mothers who supplement should continue to breastfeed and/or pump to maintain

their milk supply.
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There is some controversy about the practice of using cow milk or soy formula to exclusively breastfed

infants. Parents should discuss these issues with the child's doctor. (See "Patient information:

Breastfeeding guide (Beyond the Basics)".)

Exchange transfusionExchange transfusion is a procedure that is done urgently to prevent or

minimize bilirubin-related brain damage. The transfusion replaces an infant's blood with donated blood in

an attempt to quickly lower bilirubin levels. Exchange transfusion may be performed in infants who have

not responded to other treatments and who have signs of or are at significant neurologic risk of bilirubin

toxicity.

PREVENTION OF SEVERE HYPERBILIRUBINEMIA

Prevention of severe hyperbilirubinemia is important in avoiding serious complications. Infants who are at

risk for hyperbilirubinemia need close surveillance and follow-up. The following information applies to

infants who arehealthy and late preterm or older (greater than or equal to 35 weeks of gestation).

ScreenLeading experts recommend that all infants have bilirubin blood testing before going home.

This is especially true for infants who are jaundiced before 24 hours of age.

MonitorParents and healthcare providers should monitor the infant closely if jaundice develops.

Hyperbilirubinemia is usually easy to prevent and treat initially, but the complications can be serious and

irreversible if treatment is delayed. You should contact your child's healthcare provider immediately if you

are concerned about worsening jaundice.

Treat promptlyInfants with elevated bilirubin levels should be treated by a qualified doctor or nurse to

safely reduce bilirubin levels and prevent the risk of brain damage. Parents and healthcare providers

should not delay treatment for any reason.
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Fort Belvoir, Virginia

Am Fam Physician.2002 Feb 15;65(4):599-607.

Patient Information Handout

Hyperbilirubinemia is one of the most common problems encountered in term newborns.Historically, management guidelines were derived from studies on bilirubin toxicity in infants

with hemolytic disease. More recent recommendations support the use of less intensive

therapy inhealthy term newborns with jaundice. Phototherapy should be instituted when

the total serum bilirubin level is at or above 15 mg per dL (257 mol per L) in infants 25 to 48

hours old, 18 mg per dL (308 mol per L) in infants 49 to 72 hours old, and 20 mg per dL (342

mol per L) in infants older than 72 hours. Few term newborns with hyperbilirubinemia have

serious underlying pathology. Jaundice is considered pathologic if it presents within the first

24 hours after birth, the total serum bilirubin level rises by more than 5 mg per dL (86 mol per

L) per day or is higher than 17 mg per dL (290 mol per L), or an infant has signs and

symptoms suggestive of serious illness. The management goals are to exclude pathologiccauses of hyperbilirubinemia and initiate treatment to prevent bilirubin neurotoxicity.

Neonatal hyperbilirubinemia, defined as a total serum bilirubin level above 5 mg per dL (86 molper

L), is a frequently encountered problem. Although up to 60 percent of term newborns have clinical

jaundice in the first week of life, few have significant underlying disease.1,2However,

hyperbilirubinemia in the newborn period can be associated with severe illnesses such as hemolytic

disease, metabolic and endocrine disorders, anatomic abnormalities of the liver, and infections.

Jaundice typically results from the deposition of unconjugated bilirubin pigment in the skin and

mucus membranes. Depending on the underlying etiology, this condition may present throughout the

neonatal period. Unconjugated hyperbilirubinemia, the primary focus of this article, is the most

common form of jaundice encountered by family physicians. The separate topic of conjugated

hyperbilirubinemia is beyond the scope of this article.

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Risk Factors for Hyperbilirubinemia

Infants without identified risk factors rarely have total serum bilirubin levels above 12 mg per dL (205

mol per L). As the number of risk factors increases, the potential to develop markedly elevated

bilirubin levels also increases.2

Common risk factors for hyperbilirubinemia include fetal-maternal blood group incompatibility,

prematurity, and a previously affected sibling (Table 1).24Cephalohematomas, bruising, and trauma

from instrumented delivery may increase the risk for serum bilirubin elevation. Delayed meconium

passage also increases the risk. Infants with risk factors should be monitored closely during the first

days to weeks of life.

TABLE 1 Risk Factors for Hyperbilirubinemia in Newborns
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View Table

Bilirubin Production and Newborns

Bilirubin is the final product of heme degradation. At physiologic pH, bilirubin is insoluble in plasma

and requires protein binding with albumin. After conjugation in the liver, it is excreted in bile.3,57

Newborns produce bilirubin at a rate of approximately 6 to 8 mg per kg per day. This is more than

twice the production rate in adults, primarily because of relative polycythemia and increased red

blood cell turnover in neonates.7Bilirubin production typically declines to the adult level within 10 to

14 days after birth.2

Bilirubin Toxicity

Kernicterus refers to the neurologic consequences of the deposition of unconjugated bilirubin in

brain tissue. Subsequent damage and scarring of the basal ganglia and brainstem nuclei may

occur.5

The precise role of bilirubin in the development of kernicterus is not completely understood. If the

serum unconjugated bilirubin level exceeds the binding capacity of albumin, unbound lipid-soluble

bilirubin crosses the blood-brain barrier. Albumin-bound bilirubin may also cross the blood-brain

barrier if damage has occurred because of asphyxia, acidosis, hypoxia, hypoperfusion,

hyperosmolality, or sepsis in the newborn.3,8

The exact bilirubin concentration associated with kernicterus in thehealthy term infant is

unpredictable.1Toxicity levels may vary among ethnic groups, with maturation of an infant, and in the

presence of hemolytic disease. Although the risk of bilirubin toxicity is probably negligible in a

healthy term newborn without hemolysis,9the physician should become concerned if the bilirubin

level is above 25 mg per dL (428 mol per L).1,3,10In the term newborn with hemolysis, a bilirubinlevel above 20 mg per dL (342 mol per L) is a concern.1,3

The effects of bilirubin toxicity are often devastating and irreversible (Table 2).3,9Early signs of

kernicterus are subtle and nonspecific, typically appearing three to four days after birth. However,

hyperbilirubinemia may lead to kernicterus at any time during the neonatal period.2After the first

week of life, the affected newborn begins to demonstrate late effects of bilirubin toxicity. If the infant

survives the initial severe neurologic insult, chronic bilirubin encephalopathy (evident by three years

of age) leads to developmental and motor delays, sensorineural deafness, and mild mental

retardation.

TABLE 2 Effects of Bilirubin Toxicity in Newborns

View Table

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Classification of Neonatal Hyperbilirubinemia
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The causes of neonatal hyperbilirubinemia can be classified into three groups based on mechanism

of accumulation: bilirubin overproduction, decreased bilirubin conjugation, and impaired bilirubin

excretion (Table 3).11

TABLE 3 Classification of Neonatal Hyperbilirubinemia Based on

Mechanism of Accumulation

View Table

PHYSIOLOGIC JAUNDICE

Physiologic jaundice inhealthy term newborns follows a typical pattern. The average total serum

bilirubin level usually peaks at 5 to 6 mg per dL (86 to 103 mol per L) on the third to fourth day of

life and then declines over the first week after birth.2Bilirubin elevations of up to 12 mg per dL, with

less than 2 mg per dL (34 mol per L) of the conjugated form, can sometimes occur. Infants with

multiple risk factors may develop an exaggerated form of physiologic jaundice in which the total

serum bilirubin level may rise as high as 17 mg per dL (291 mol per L) .3

Factors that contribute to the development of physiologic hyperbilirubinemia in the neonate include

an increased bilirubin load because of relative polycythemia, a shortened erythrocyte life span (80

days compared with the adult 120 days), immature hepatic uptake and conjugation processes, and

increased enterohepatic circulation.7

JAUNDICE AND BREASTFEEDINGEarly-Onset Breastfeeding Jaundice

Breast-fed newborns may be at increased risk for early-onset exaggerated physiologic jaundice

because of relative caloric deprivation in the first few days of life.12Decreased volume and frequency

of feedings may result in mild dehydration and the delayed passage of meconium. Compared withformula-fed newborns, breastfed infants are three to six times more likely to experience moderate

jaundice (total serum bilirubin level above 12 mg per dL) or severe jaundice (total serum bilirubin

level above 15 mg per dL [257 mol per L]).12,13

In a breastfed newborn with early-onset hyperbilirubinemia, the frequency of feedings needs to be

increased to more than 10 per day. If the infant has a decline in weight gain, delayed stooling, and

continued poor caloric intake, formula supplementation may be necessary, but breastfeeding should

be continued to maintain breast milk production. Supplemental water or dextrose-water

administration should be avoided, as it decreases breast milk production and places the newborn at

risk for iatrogenic hyponatremia.3,5,11

Late-Onset Breast Milk Jaundice

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 ofhealthy

breastfed infants.1Total serum bilirubin levels vary from 12 to 20 mg per dL (340 mol per L) and

are nonpathologic.
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The underlying cause of breast milk jaundice is not entirely understood. Substances in maternal

milk, such as -glucuronidases, and nonesterified fatty acids, may inhibit normal bilirubinmetabolism

.5,7,14,15The bilirubin level usually falls continually after the infant is two weeks old, but it may remain

persistently elevated for one to three months.

If the diagnosis of breast milk jaundice is in doubt or the total serum bilirubin level becomesmarkedly elevated, breastfeeding may be temporarily interrupted, although the mother should

continue to express breast milk to maintain production. With formula substitution, the total serum

bilirubin level should decline rapidly over 48 hours (at a rate of 3 mg per dL [51 mol per L] per

day),1confirming the diagnosis. Breastfeeding may then be resumed.

PATHOLOGIC JAUNDICE

All etiologies of jaundice beyond physiologic and breastfeeding or breast milk jaundice are

considered pathologic. Features of pathologic jaundice include the appearance of jaundice within 24

hours after birth, a rapidly rising total serum bilirubin concentration (increase of more than 5 mg per

dL per day), and a total serum bilirubin level higher than 17 mg per dL in a full-term newborn.3,5

Otherfeatures of concern include prolonged jaundice, evidence of underlying illness, and elevation of the

serum conjugated bilirubin level to greater than 2 mg per dL or more than 20 percent of the total

serum bilirubin concentration. Pathologic causes include disorders such as sepsis, rubella,

toxoplasmosis, occult hemorrhage, and erythroblastosis fetalis.

Diagnosis

PHYSICAL EXAMINATION

The presence of jaundice can be determined by examining the infant in a well-lit room and blanching

the skin with digital pressure to reveal the color of the skin and subcutaneous tissue. Neonatal

dermal icterus is not noticeable at total serum bilirubin levels below 4 mg per dL (68 mol per L).16

Increasing total serum bilirubin levels are accompanied by the cephalocaudal progression of dermal

icterus, predictably from the face to the trunk and extremities, and finally to the palms and

soles.16,17The total serum bilirubin level can be estimated clinically by the degree of caudal extension:

face, 5 mg per dL; upper chest, 10 mg per dL (171 mol per L); abdomen, 12 mg per dL; palms and

soles, greater than 15 mg per dL.

The only consistently reliable estimation of total serum bilirubin occurs when dermal icterus is

confined to above the nipple line. In this situation, the bilirubin level is invariably below 12 mg per dL.

As jaundice extends below the middle of the chest, the correlation between physical signs and

measured bilirubin levels becomes increasingly unreliable. Differences in skin color among races,

delays in dermal deposition with rapidly rising bilirubin levels, interobserver variability, and other

factors contribute to the difficulty of accurately predicting the total serum bilirubin concentration

based on caudal progression alone.18
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The physical examination should focus on identifying one of the known causes of pathologic

jaundice. The infant should be assessed for pallor, petechiae, extravasated blood, excessive

bruising, hepatosplenomegaly,weight loss, and evidence of dehydration.

LABORATORY EVALUATION

The initial evaluation of jaundice depends on the age of the newborn (Figure 1).2If the serum

conjugated bilirubin level is above 2 mg per dL, the infant should be evaluated for possible

hepatocellular disease or biliary obstruction.

Laboratory Evaluation of Term Newborn with Jaundice

FIGURE 1.

Algorithm for the suggested evaluation of a term newborn with hyperbilirubinemia.
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Neonatal Jaundice