APPROACH TO A CHILD
APPROACH TO A CHILD
Jaundice is the visible manifestation of
increased level of bilirubin in the body.
It is not a disease rather a symptom of
In adults sclera appears jaundiced when
serum bilirubin exceeds 2 mg/dl.
However it is difficult to see sclera in
newborn due to difficulty in opening eye.
But in new born it is very easy to see
Important problem in the 1st week of life.
Almost all neonates (60% Term and 80%
Preterm) will have bilirubin > 5 mg/dl in the
1st week of life and become visibly
jaundiced, vast majority being benign
Some of the term babies (8 to 9%) have
levels exceeding 15 mg/dl in 1st 7 days of
High bilirubin level is toxic to the developing
End product of hemoglobin metabolism
that is excreted in bile.
-75% : from catabolism of circulating
-25% :*from ineffective erythropoiesis
*from turnover of heme proteins
Conjugated Hyperbilirubinemia is present,
* >20% of total bilirubin is conjugated
* >2mg/dl is conjugated
If neither criteria is met, hyperbilirubinemia is
classified as Un-conjugated.
In new born babies bilirubin
metabolism is immature which results in the
occurrence of hyperbilirubinemia in the first
few days of life. Also there is increased
bilirubin load on the hepatic cell due to
Immaturity could be at various steps of
bilirubin metabolism like:
Defective uptake from plasma into liver
cell( deficiency of LIGANDIN)
Defective conjugation( UDP-glucoronosyl
transferase: <1% of adult activity during
the first 10 days of life)
Increased entero-hepatic circulation
Increased Bilirubin production:
Larger circulating red blood cell volume
Shortened RBC lifespan (70-90 days vs 120
days in adult)
Substantial production from other sources
First appears between
hours of age
Maximum intensity seen on 4-5th day in
term and 7th day in preterm neonates
Does not exceed 15 mg/dl
Clinically undetectable after 14 days.
No treatment is required but baby should be
observed closely for signs of worsening
Presence of any of the following signs
denotes that the jaundice is pathological.
Clinical jaundice detected before 24 hours
Rise in serum total bilirubin by more than 5
mg/dl/ day (>5mg/dl on first day , 10 mg/dl
on second day and 12- 13 mg/dl thereafter
in term babies)
Serum bilirubin more than 15 mg/dl
Clinical jaundice persisting beyond 14 days
Clay/white colored stool and/or dark urine
staining the nappy yellow
Direct bilirubin >2 mg/dl at any time.
Treatment is required in the
form of phototherapy or exchange blood
transfusion. One should investigate to find the
cause of pathological jaundice.
It can be
Blood group incompatibilities
Maternal-fetal or feto-fetal transfusions
Non Immune Hemolytic anemias
Structurally Abnormal Red cells
Blood Group Incompatibilities:
Rh negative mother & Rh positive infant
Strongly considered if there is jaundice in
the first 24 hours of life
Non-Immune Hemolytic Anemias:
1. G6PD Deficiency:
Deficiency-decreased NADPHdecreased reduced Glutathione –
decreased protection of RBCs from
2. Excess of Vitamin K given IM
Enzymatic Deficiency( Glucoronyl
Hormonal suppression (Breast milk
Inhibition of conjugation
Hepatic cell injury due to Infections
Substrate deficiency (hypoglycemia)
Mechanical obstruction (biliary atresia)
Pregnandiol present in maternal breast milk
suppresses bilirubin conjugation.
Breast feeding may be stopped and
restarted in a period of 48hours.
Thyroxine increases the activity of
Glucoronyl transferase which promotes
conjugation of bilirubin.
Inhibition of Conjugation:
Sulfonamides and Vitamin K results in
competitive conjugation inhibition of bilirubin.
Absent or deficient Galactose 1phosphoate uridyl transferase which is
needed in glucoronidaton of indirect bilirubin.
Maternal and Perinatal History:
Delivery at period of gestation, Postnatal
age in hours.
Maternal illness during pregnancy which
also includes diabetes; drug use.
Previous history of malaria.
Traumatic delivery, delayed cord
clamping, oxytocin use.
Birth asphyxia, delayed feeding, delay in
Family history of jaundice, liver disease
Previous sibling with jaundice for blood
Kernicterus: Lethargy, poor feeding, and
hypotonia. Some advanced signs are
seizures, retrocollis, paralysis of upward
gaze and shrill cry.
Baby lethargic, poor feeding, temperature
instability, with apnea: Sepsis
Small for gestation: polycythemia
Cataract, rash: TORCH infections
Extra vascular bleed: Cephalhematoma
Pallor: hemolysis, blood loss
HOW DO YOU LOOK FOR
1. Dermal staining :progresses from head to
Examined in good day light skin of
forehead, chest, abdomen, thigh, legs,
palms, and soles.
Blanched with digital pressure and the
underlying color of the skin and
subcutaneous tissue should be noted.
> 12 mg/dl and infant <
24 hr old
< 12 mg/dl and infant > 24
Fraction of Bilirubin
Follow bilirubin level
Evaluate for treatable causes
1.Infections-blood, urine culture, VDRL.
2.Metabolic disorders-urine reducing substances, serum
If no abnormality ;screen for Identifiable causes
*α-1 antitrypsin deficiency
*congenital viral infections
If no abnormality; evaluate for anatomical abnormalities
Explain about benign nature of the disease
Encourage to breastfeed frequently &
Ask Mother to bring baby back if baby looks
deep yellow or palms & soles have yellow
Mainstay of treatment
Under blue-green light(460490nm), insoluble bilirubin is converted into
soluble isomers that can be excreted in
urine & feces.
To be effective, bilirubin must be present in
skin; hence nor role for prophylactic
Term & near term neonates:
The American Academy of Pediatrics (AAP)
has laid down criteria for managing babies
with elevated serum bilirubin based on
gestational age and other risk factors(
hemolysis , asphyxia, low albumin level,
Z-isomer converted to E-isomer
Reaction is instantaneous but reversible.
After exposure of 8-12 hrs, this constitutes
about 25% of the TSB which is non-toxic.
Excreted slowly from the body; hence not a
major mechanism for decrease in TSB.
Bilirubin is converted into Lumirubin.
This product forms 2-6% of TSB which is
rapidly excreted from body thus is mainly
responsible for phototherapy induced
decline in TSB.
Optimum ambient room temperature( 2528celcius) to prevent hypothermia.
Remove all clothes of baby except diaper
Cover baby’s eyes with an eye patch(to
prevent retinal degeneration) ensuring that it
does not block the baby’s nostrils.
Place the baby under the lights in a cot if
weight is more than 2kg or in an incubator if
baby is small(<2kg)
Keep the distance between the baby & the
Ensure optimum breastfeeding as
intermittent feeding sessions.
Monitor temperature of the baby every 24hrs
Measure TSB every 12-24hrs.
Discontinue, once 2 TSB values 12hr apart
fall below current age-specific cut-offs.
Monitor for rebound bilirubin rise within
Complications of Phototherapy:
Erythematous macular rash
Purpuric rash associated with transient
Bronze baby syndrome
Bronze Baby Syndrome
Intense grey-brown discoloration
of the skin, serum, and urine,
especially in premature infants;
when phototherapy was used to
reduce hyperbilirubinemia. Preexisting hepatic disease is
suspected as a cause of the
jaundice and may have
prevented the biliary excretion of
the photo oxidation products of
bilirubin; their retention resulted
in the bronze discoloration.
Double Volume Exchange Transfusion
(DVET) : 160-180ml/kg; is to be performed if
TSB levels reach age-specific cut-offs or if
the infant shows signs of bilirubin
encephalopathy, irrespective of TSB levels.
If baby shows signs of cardiac
decompensation at birth, partial exchange
transfusion with 50ml/kg of packed red cells
should be done to quickly restore oxygen
carrying capacity of blood.
Umbilical venous route.
Babies with serum bilirubin>20 mg/dl &
those who required ET should be kept under
follow-up in high-risk clinic for neurodevelopmental outcome.
Hearing assessment should be done at
3months of age.
Ante-natal screening to detect Rh isoimmunization & prompt administration of
Anti D after first obstetric event.
Ensure adequate breast feeding.
Educate parent about danger signs to
ensure immediate checkup.
Follow-up high risk babies( large cephalohematoma, family history of jaundice) for 2-3
days of discharge.
JAUNDICE IN THE CHILD &
Age at onset of symptoms. E.g.: Wilson’s
disease commonly manifests in preadolescents & adolescents.
Past/present use of any drugs
H/o of blood transfusion/ dialysis
Exposure to viral hepatitis
Any h/o of chronic illness;