Jaundice in new babies

Infant jaundice - Symptoms and causes

Overview

Infant jaundice is yellow discoloration of a newborn baby's skin and eyes. Infant jaundice occurs because the baby's blood contains an excess of bilirubin (bil-ih-ROO-bin), a yellow pigment of red blood cells.

Infant jaundice is a common condition, particularly in babies born before 38 weeks' gestation (preterm babies) and some breast-fed babies. Infant jaundice usually occurs because a baby's liver isn't mature enough to get rid of bilirubin in the bloodstream. In some babies, an underlying disease may cause infant jaundice.

Most infants born between 35 weeks' gestation and full term need no treatment for jaundice. Rarely, an unusually high blood level of bilirubin can place a newborn at risk of brain damage, particularly in the presence of certain risk factors for severe jaundice.

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Symptoms

Yellowing of the skin and the whites of the eyes — the main sign of infant jaundice — usually appears between the second and fourth day after birth.

To check for infant jaundice, press gently on your baby's forehead or nose. If the skin looks yellow where you pressed, it's likely your baby has mild jaundice. If your baby doesn't have jaundice, the skin color should simply look slightly lighter than its normal color for a moment.

Examine your baby in good lighting conditions, preferably in natural daylight.

When to see a doctor

Most hospitals have a policy of examining babies for jaundice before discharge. The American Academy of Pediatrics recommends that newborns be examined for jaundice during routine medical checks and at least every eight to 12 hours while in the hospital.

Your baby should be examined for jaundice between the third and seventh day after birth, when bilirubin levels usually peak. If your baby is discharged earlier than 72 hours after birth, make a follow-up appointment to look for jaundice within two days of discharge.

The following signs or symptoms may indicate severe jaundice or complications from excess bilirubin. Call your doctor if:

• Your baby's skin becomes more yellow
• The skin on your baby's the abdomen, arms or legs looks yellow
• The whites of your baby's eyes look yellow
• Your baby seems listless or sick or is difficult to awaken
• Your baby isn't gaining weight or is feeding poorly
• Your baby makes high-pitched cries
• Your baby develops any other signs or symptoms that concern you

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Causes

Excess bilirubin (hyperbilirubinemia) is the main cause of jaundice. Bilirubin, which is responsible for the yellow color of jaundice, is a normal part of the pigment released from the breakdown of "used" red blood cells.

Newborns produce more bilirubin than adults do because of greater production and faster breakdown of red blood cells in the first few days of life. Normally, the liver filters bilirubin from the bloodstream and releases it into the intestinal tract. A newborn's immature liver often can't remove bilirubin quickly enough, causing an excess of bilirubin. Jaundice due to these normal newborn conditions is called physiologic jaundice, and it typically appears on the second or third day of life.

Other causes

An underlying disorder may cause infant jaundice. In these cases, jaundice often appears much earlier or much later than does the more common form of infant jaundice. Diseases or conditions that can cause jaundice include:

• Internal bleeding (hemorrhage)
• An infection in your baby's blood (sepsis)
• Other viral or bacterial infections
• An incompatibility between the mother's blood and the baby's blood
• A liver malfunction
• Biliary atresia, a condition in which the baby's bile ducts are blocked or scarred
• An enzyme deficiency
• An abnormality of your baby's red blood cells that causes them to break down rapidly

Risk factors

Major risk factors for jaundice, particularly severe jaundice that can cause complications, include:

• Premature birth. A baby born before 38 weeks of gestation may not be able to process bilirubin as quickly as full-term babies do. Premature babies also may feed less and have fewer bowel movements, resulting in less bilirubin eliminated through stool.
• Significant bruising during birth. Newborns who become bruised during delivery gets bruises from the delivery may have higher levels of bilirubin from the breakdown of more red blood cells.
• Blood type. If the mother's blood type is different from her baby's, the baby may have received antibodies through the placenta that cause abnormally rapid breakdown of red blood cells.
• Breast-feeding. Breast-fed babies, particularly those who have difficulty nursing or getting enough nutrition from breast-feeding, are at higher risk of jaundice. Dehydration or a low caloric intake may contribute to the onset of jaundice. However, because of the benefits of breast-feeding, experts still recommend it. It's important to make sure your baby gets enough to eat and is adequately hydrated.
• Race. Studies show that babies of East Asian ancestry have an increased risk of developing jaundice.

Complications

High levels of bilirubin that cause severe jaundice can result in serious complications if not treated.

Acute bilirubin encephalopathy

Bilirubin is toxic to cells of the brain. If a baby has severe jaundice, there's a risk of bilirubin passing into the brain, a condition called acute bilirubin encephalopathy. Prompt treatment may prevent significant lasting damage.

Signs of acute bilirubin encephalopathy in a baby with jaundice include:

• Listlessness
• Difficulty waking
• High-pitched crying
• Poor sucking or feeding
• Backward arching of the neck and body
• Fever

Kernicterus

Kernicterus is the syndrome that occurs if acute bilirubin encephalopathy causes permanent damage to the brain. Kernicterus may result in:

• Involuntary and uncontrolled movements (athetoid cerebral palsy)
• Permanent upward gaze
• Hearing loss
• Improper development of tooth enamel

Prevention

The best preventive of infant jaundice is adequate feeding. Breast-fed infants should have eight to 12 feedings a day for the first several days of life. Formula-fed infants usually should have 1 to 2 ounces (about 30 to 60 milliliters) of formula every two to three hours for the first week.

By Mayo Clinic Staff

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Newborn jaundice - NHS

Jaundice in newborn babies is common and usually harmless. It causes yellowing of the skin and the whites of the eyes. The medical term for jaundice in babies is neonatal jaundice.

Yellowing of the skin can be more difficult to see in brown or black skin. It might be easier to see on the palms of the hands or the soles of the feet.

Other symptoms of newborn jaundice can include:

• dark, yellow urine (a newborn baby's urine should be colourless)
• pale-coloured poo (it should be yellow or orange)

The symptoms of newborn jaundice usually develop 2 days after the birth and tend to get better without treatment by the time the baby is about 2 weeks old.

Find out more about the symptoms of jaundice in babies

Your baby will be examined for signs of jaundice within 72 hours of being born as part of the newborn physical examination.

If your baby develops signs of jaundice after this time, speak to your midwife, health visitor or a GP as soon as possible for advice.

While jaundice is not usually a cause for concern, it's important to determine whether your baby needs treatment.

If you're monitoring your baby's jaundice at home, it's also important to contact your midwife straight away if your baby's symptoms quickly get worse or they become very reluctant to feed.

Find out more about diagnosing jaundice in babies

Why does my baby have jaundice?

Jaundice is caused by the build-up of bilirubin in the blood. Bilirubin is a yellow substance produced when red blood cells, which carry oxygen around the body, are broken down.

Jaundice is common in newborn babies because babies have a high number of red blood cells in their blood, which are broken down and replaced frequently.

Also, a newborn baby's liver is not fully developed, so it's less effective at removing the bilirubin from the blood.

By the time a baby is about 2 weeks old, their liver is more effective at processing bilirubin, so jaundice often corrects itself by this age without causing any harm.

In a small number of cases, jaundice can be the sign of an underlying health condition. This is often the case if jaundice develops shortly after birth (within the first 24 hours).

How common is newborn jaundice?

Jaundice is one of the most common conditions that can affect newborn babies.

It's estimated 6 out of every 10 babies develop jaundice, including 8 out of 10 babies born prematurely before the 37th week of pregnancy.

But only around 1 in 20 babies has a blood bilirubin level high enough to need treatment.

For reasons that are unclear, breastfeeding increases a baby's risk of developing jaundice, which can often persist for a month or longer. 

But in most cases, the benefits of breastfeeding far outweigh any risks associated with jaundice.

Treating newborn jaundice

Treatment for newborn jaundice is not usually needed because the symptoms normally pass within 10 to 14 days, although they can occasionally last longer.

Treatment is usually only recommended if tests show very high levels of bilirubin in a baby's blood.

This is because there's a small risk the bilirubin could pass into the brain and cause brain damage.

There are 2 main treatments that can be carried out in hospital to quickly reduce your baby's bilirubin levels.

These are:

• phototherapy – a special type of light shines on the skin, which alters the bilirubin into a form that can be more easily broken down by the liver
• an exchange transfusion – where your baby's blood is removed using a thin tube (catheter) placed in their blood vessels and replaced with blood from a matching donor; most babies respond well to treatment and can leave hospital after a few days

Complications

If a baby with very high levels of bilirubin is not treated, there's a risk they could develop permanent brain damage. This is known as kernicterus.

Kernicterus is very rare in the UK.

Find out more about kernicterus in babies

You can also read the National Institute for Health and Care Excellence (NICE) guidance about jaundice in newborn babies under 28 days.

Page last reviewed: 03 February 2022
Next review due: 03 February 2025

Neonatal jaundice | Ida-Tallinna Keskhaigla

The purpose of this information sheet is to provide parents with information about the causes of neonatal jaundice (jaundice of the newborn, hyperbilirubinemia) and related examinations, tests and treatment options.

Visible yellow skin tone, or jaundice, is the most common sign of jaundice in the neonatal period (days 0-28). Physiological or natural jaundice May occur from age 24 hours to 14 days after birth .

Causes

Before birth, the fetus has more red blood cells (erythrocytes) than in later periods of life, and their (erythrocytes) life expectancy in the first days is somewhat shorter than usual. After the birth of a child, red blood cells begin to break down, and a bile pigment is formed in the blood - bilirubin . The liver of a newborn has to withstand a 2-3 times greater load than in the prenatal period in order to remove bilirubin from the body, which is released during the breakdown of red blood cells. The fact that some healthy newborns develop so-called physiological jaundice and others do not is mainly due to the different ability of their liver to remove bilirubin.

Sign of physiological jaundice - yellowing of the skin. The peak of jaundice is usually observed in children on the 3-6th day of life, in premature babies - on the 6-10th day of life. To prevent physiological jaundice, it is important that the newborn is adequately fed , preferably with breast milk, which speeds up the work of the intestines and thus accelerates the excretion of bilirubin from the body.

Non-physiological jaundice can be caused by preterm birth , excessive weight loss in newborns in the first days of life, inflammation (contributes to the destruction of red blood cells), hyperemia or polycythemia , as well as some rare diseases . If jaundice occurs during the first day of life, it may be due to Rh conflict (that is, Rh incompatibility) or a conflict in the AB0 blood type. Jaundice can also be caused by breast milk, this jaundice is called breast milk jaundice .

If the child's bilirubin level is very high or rises very quickly, phototherapy alone will not be enough. In this case, 9 is used for treatment.0005 exchange transfusion , which reduces both the amount of maternal antibodies and the amount of bilirubin in the baby's blood.

The prognosis of recovery depends on the level of bilirubin. Without treatment, the level of bilirubin rises above the acceptable level, and bilirubin begins to accumulate in the tissues. Bilirubin is toxic to the brain and can cause brain damage called kernicterus or bilirubin encephalopathy .

ITK1018
The information material was approved by the Health Care Quality Committee of East-Tallinn Central Hospital on 10.02.2021 (minutes no. 3-21).

Jaundice of the newborn. What is Neonatal Jaundice?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Neonatal jaundice is a physiological or pathological condition caused by hyperbilirubinemia and manifested by icteric staining of the skin and visible mucous membranes in children in the first days of their life. Jaundice of newborns is characterized by an increase in the concentration of bilirubin in the blood, anemia, icterus of the skin, mucous membranes and sclera of the eyes, hepato- and splenomegaly, in severe cases - bilirubin encephalopathy. Diagnosis of neonatal jaundice is based on a visual assessment of the degree of jaundice on the Cramer scale; determination of the level of erythrocytes, bilirubin, liver enzymes, blood groups of mother and child, etc. Treatment of jaundice in newborns includes breastfeeding, infusion therapy, phototherapy, exchange transfusion.

• Classification and causes of neonatal jaundice
• Symptoms of jaundice in newborns
  • Physiological neonatal jaundice
  • Hereditary jaundices
  • Jaundice in endocrine pathology
  • Jaundice in neonates with asphyxia and birth trauma
  • Pregnane jaundice
  • Kernic jaundice and bilirubin encephalopathy
• Diagnosis of neonatal jaundice
• Treatment of neonatal jaundice
• Prognosis of neonatal jaundice
• Prices for treatment

General

Neonatal jaundice is a neonatal syndrome characterized by a visible icteric coloration of the skin, sclera and mucous membranes due to an increase in the level of bilirubin in the child's blood. According to observations, in the first week of life, neonatal jaundice develops in 60% of full-term and 80% of premature babies. In pediatrics, physiological neonatal jaundice is the most common, accounting for 60–70% of all cases of the syndrome. Newborn jaundice develops when the level of bilirubin rises above 80-90 µmol/l in term infants and more than 120 µmol/l in preterm infants. Prolonged or severe hyperbilirubinemia has a neurotoxic effect, i.e. causes brain damage. The degree of toxic effects of bilirubin depends mainly on its concentration in the blood and the duration of hyperbilirubinemia.

Newborn jaundice

Classification and causes of neonatal jaundice

First of all, neonatal jaundice can be physiological and pathological. By origin, jaundice in newborns is divided into hereditary and acquired. Based on laboratory criteria, i.e., an increase in one or another fraction of bilirubin, hyperbilirubinemia is distinguished with a predominance of direct (bound) bilirubin and hyperbilirubinemia with a predominance of indirect (unbound) bilirubin.

Conjugational jaundice in newborns includes cases of hyperbilirubinemia resulting from reduced clearance of bilirubin by hepatocytes:

• Physiological (transient) jaundice of term newborns
• Jaundice of premature newborns
• Hereditary jaundice associated with Gilbert syndrome, Crigler-Najjar type I and II, etc.
• Jaundice due to endocrine pathology (hypothyroidism in children, diabetes mellitus in the mother)
• Jaundice in newborns with asphyxia and birth trauma
• Pregnane jaundice in breastfed children
• Drug-induced jaundice of newborns due to the prescription of chloramphenicol, salicylates, sulfonamides, quinine, large doses of vitamin K, etc.

Hemolytic jaundice of newborns is characterized by an increase in the level of bilirubin due to increased destruction (hemolysis) of the child's red blood cells. These types of hyperbilirubinemia include:

• Hemolytic disease of the fetus and newborn
• Erythrocyte enzyme and membranopathies
• Hemoglobinopathy (sickle cell anemia, thalassemia)
• Polycythemia

Obstructive jaundice in newborns is caused by a violation of the removal of bilirubin with bile through the biliary tract and intestines. They can occur with defects (atresia, hypoplasia) of the intrahepatic and extrahepatic ducts, intrauterine cholelithiasis, compression of the bile ducts from the outside by an infiltrate or tumor, blockage of the bile ducts from the inside, bile thickening syndrome, pyloric stenosis, intestinal obstruction, etc.

Jaundice of mixed origin (parenchymal) occurs in newborns with fetal hepatitis caused by intrauterine infections (toxoplasmosis, cytomegaly, listeriosis, herpes, viral hepatitis A, B, D), toxic-septic liver damage with sepsis, hereditary metabolic diseases (cystic fibrosis, galactosemia ).

Symptoms of neonatal jaundice

Physiological neonatal jaundice

Transient jaundice is a borderline condition of the neonatal period. Immediately after the birth of a child, excess red blood cells, in which fetal hemoglobin is present, is destroyed with the formation of free bilirubin. Due to the temporary immaturity of the liver enzyme glucuronyltransferase and intestinal sterility, the binding of free bilirubin and its excretion from the body of the newborn with feces and urine is reduced. This leads to the accumulation of excess bilirubin in the subcutaneous fat and staining of the skin and mucous membranes in yellow.

Physiological jaundice of newborns develops 2-3 days after birth, reaches its maximum at 4-5 days. The peak concentration of indirect bilirubin averages 77-120 µmol/l; urine and feces are of normal color; the liver and spleen are not enlarged.

With transient jaundice of newborns, a mild degree of yellowness of the skin does not extend below the umbilical line and is detected only with sufficient natural light. With physiological jaundice, the health of the newborn is usually not disturbed, however, with significant hyperbilirubinemia, sluggish sucking, lethargy, drowsiness, and vomiting may be noted.

In healthy newborns, the occurrence of physiological jaundice is associated with a temporary immaturity of the liver enzyme systems, therefore it is not considered a pathological condition. When observing the child, organizing proper feeding and care, the manifestations of jaundice subside on their own by the age of 2 weeks.

Jaundice in premature newborns is characterized by an earlier onset (1–2 days), reaching a peak of manifestations by 7 days and subsiding by three weeks of a child's life. The concentration of indirect bilirubin in the blood of premature babies is higher (137-171 µmol/l), its increase and decrease is slower. Due to the longer maturation of liver enzyme systems in premature babies, there is a threat of developing nuclear jaundice and bilirubin intoxication.

Hereditary jaundice

The most common form of hereditary conjugative jaundice in newborns is constitutional hyperbilirubinemia (Gilbert's syndrome). This syndrome occurs in the population with a frequency of 2-6%; inherited in an autosomal dominant manner. Gilbert's syndrome is based on a defect in the activity of liver enzyme systems (glucuronyl transferase) and, as a result, a violation of the uptake of bilirubin by hepatocytes. Jaundice of newborns with constitutional hyperbilirubinemia proceeds without anemia and splenomegaly, with a slight rise in indirect bilirubin.

Hereditary neonatal jaundice in Crigler-Najjar syndrome is associated with very low activity of glucuronyl transferase (type II) or its absence (type I). In type I syndrome, neonatal jaundice develops already in the first days of life and steadily increases; hyperbilirubinemia reaches 428 µmol/l and above. The development of nuclear jaundice is typical, a fatal outcome is possible. Type II syndrome, as a rule, has a benign course: neonatal hyperbilirubinemia is 257-376 µmol/l; nuclear jaundice rarely develops.

Jaundice due to endocrine pathology

It usually occurs in children with congenital hypothyroidism due to a deficiency of thyroid hormones that disrupts the maturation of the glucuronosyltransferase enzyme, the processes of conjugation and excretion of bilirubin. Jaundice with hypothyroidism is detected in 50-70% of newborns; manifests itself on the 2-3rd day of life and lasts up to 3-5 months. In addition to jaundice, newborns have lethargy, pastosity, arterial hypotension, bradycardia, a rough voice, and constipation.

Early jaundice can occur in newborns whose mothers have diabetes mellitus due to hypoglycemia and acidosis. It is manifested by a protracted icteric syndrome and indirect hyperbilirubinemia.

Jaundice in newborns with asphyxia and birth trauma

Fetal hypoxia and neonatal asphyxia delay the formation of enzyme systems, resulting in hyperbilirubinemia and kernicterus. Various birth injuries (cephalohematomas, intraventricular hemorrhages) can be sources of formation of indirect bilirubin and its increased penetration into the bloodstream with the development of icteric staining of the skin and mucous membranes. The severity of neonatal jaundice depends on the severity of the hypoxic-asphyxic syndrome and the level of hyperbilirubinemia.

Pregnane jaundice

Aries syndrome, or jaundice in breastfed babies, develops in 1-2% of newborns. It can occur in the first week of a child's life (early jaundice) or on days 7-14 (late neonatal jaundice) and persist for 4-6 weeks. Among the possible causes of pregnane jaundice in newborns are the presence in the milk of maternal estrogens that prevent the binding of bilirubin; unsteady lactation in the mother and relative malnutrition of the child, causing reabsorption of bilirubin in the intestine and its entry into the bloodstream, etc. It is believed that the risk factors for jaundice in newborns who are breastfed are later (after 12 hours of life) meconium discharge, delayed clamping umbilical cord, labor induction. The course of this type of neonatal jaundice is always benign.

Kernic jaundice and bilirubin encephalopathy

With a progressive increase in the concentration of indirect bilirubin in the blood, it can penetrate the blood-brain barrier and deposit in the basal nuclei of the brain (kernicterus of the newborn), causing the development of a dangerous condition - bilirubin encephalopathy.

At the first stage, the clinic is dominated by signs of bilirubin intoxication: lethargy, apathy, drowsiness of the child, monotonous cry, wandering eyes, regurgitation, vomiting. Soon, newborns develop classic signs of nuclear jaundice, accompanied by stiff neck, spasticity of the muscles of the body, periodic excitation, bulging of the large fontanel, extinction of sucking and other reflexes, nystagmus, bradycardia, convulsions. During this period, which lasts from several days to several weeks, irreversible damage to the central nervous system occurs. Over the next 2-3 months of life, a deceptive improvement is observed in the condition of children, however, already at 3-5 months of life, neurological complications are diagnosed: cerebral palsy, mental retardation, deafness, etc.

Diagnosis of neonatal jaundice

Jaundice is detected even at the stage of the child's stay in the maternity hospital by a neonatologist or pediatrician when visiting a newborn shortly after discharge.

The Kramer scale is used to visually assess the degree of neonatal jaundice.

• I degree - jaundice of the face and neck (bilirubin 80 µmol/l)
• II degree - jaundice extends to the level of the navel (bilirubin 150 µmol/l)
• III degree - jaundice extends to the level of the knees (bilirubin 200 µmol/l)
• IV degree - jaundice extends to the face, trunk, limbs, except for the palms and soles (bilirubin 300 µmol/l)
• V - total jaundice (bilirubin 400 µmol/l)

The necessary laboratory tests for the primary diagnosis of neonatal jaundice are: bilirubin and its fractions, complete blood count, blood group of the child and mother, Coombs test, PTI, urinalysis, liver tests. If hypothyroidism is suspected, it is necessary to determine the thyroid hormones T3, T4, TSH in the blood. Identification of intrauterine infections is carried out by ELISA and PCR.

As part of the diagnosis of mechanical jaundice, newborns undergo ultrasound of the liver and bile ducts, MR cholangiography, FGDS, plain radiography of the abdominal cavity, consultation of a pediatric surgeon and a pediatric gastroenterologist.

Treatment of neonatal jaundice

To prevent jaundice and reduce the degree of hyperbilirubinemia, all newborns need early onset (from the first hour of life) and regular breastfeeding. In newborns with neonatal jaundice, the frequency of recommended breastfeeding is 8–12 times a day without a night break. It is necessary to increase the daily volume of fluid by 10-20% compared with the physiological need of the child, the intake of enterosorbents. If oral hydration is impossible, infusion therapy is performed: glucose drip, physical. solution, ascorbic acid, cocarboxylase, vitamins of group B. In order to increase the conjugation of bilirubin, a newborn with jaundice may be prescribed phenobarbital.

The most effective treatment for indirect hyperbilirubinemia is continuous or intermittent phototherapy, which converts indirect bilirubin into a water-soluble form. Complications of phototherapy can be hyperthermia, dehydration, burns, allergic reactions.

With hemolytic jaundice of newborns, exchange transfusion, hemosorption, and plasmapheresis are indicated. All pathological neonatal jaundices require immediate treatment of the underlying disease.

Prognosis of neonatal jaundice

Transient jaundice in newborns in the vast majority of cases resolves without complications. However, a violation of the mechanisms of adaptation can lead to the transition of physiological jaundice of newborns into a pathological state. Observations and evidence base indicate that there is no relationship between hepatitis B vaccination and neonatal jaundice. Critical hyperbilirubinemia can lead to the development of kernicterus and its complications.

Children with pathological forms of neonatal jaundice are subject to dispensary observation of a district pediatrician and a pediatric neurologist.

Sources

1. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests.

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