1. APPROACH TO A CHILD
WITH JAUNDICE
APPROACH TO A CHILD
WITH JAUNDICE
S.BALASANKAR
S.BALASANKAR
2009 MBBS
2009 MBBS
2. JAUNDICE
Jaundice is the visible manifestation of
increased level of bilirubin in the body.
It is not a disease rather a symptom of
diseases.
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
3. BURDEN
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
life.
High bilirubin level is toxic to the developing
CNS.(KERNICTERUS; Bilirubin≥25mg/dl)
4. BILIRUBIN
End product of hemoglobin metabolism
that is excreted in bile.
In neonates
-75% : from catabolism of circulating
RBCs
-25% :*from ineffective erythropoiesis
(bone marrow)
*from turnover of heme proteins
&
12. PHYSIOLOGICAL JAUNDICE:
•
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
physiological polycythemia.
13. 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)
Decreased excretion
Increased entero-hepatic circulation
14. 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
15. Characteristics:
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
jaundice.
16. PATHOLOGICAL JAUNDICE
Presence of any of the following signs
denotes that the jaundice is pathological.
Clinical jaundice detected before 24 hours
of age
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)
17. Serum bilirubin more than 15 mg/dl
Clinical jaundice persisting beyond 14 days
of life
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.
19. Overproduction Hyperbilirubinemia:
Blood group incompatibilities
Maternal-fetal or feto-fetal transfusions
Non Immune Hemolytic anemias
Structurally Abnormal Red cells
Extra-vascular Hemolysis
20. Blood Group Incompatibilities:
Rh negative mother & Rh positive infant
ABO incompatibilities
Strongly considered if there is jaundice in
the first 24 hours of life
21. Non-Immune Hemolytic Anemias:
1. G6PD Deficiency:
Deficiency-decreased NADPHdecreased reduced Glutathione –
decreased protection of RBCs from
oxidants-hemolysis.
2. Excess of Vitamin K given IM
23. Under-secretion Hyperbilirubinemia:
Enzymatic Deficiency( Glucoronyl
transferase)
Hormonal suppression (Breast milk
jaundice)
Inhibition of conjugation
Hepatic cell injury due to Infections
Substrate deficiency (hypoglycemia)
Mechanical obstruction (biliary atresia)
24. Hormonal Suppression:
Pregnandiol present in maternal breast milk
suppresses bilirubin conjugation.
Breast feeding may be stopped and
restarted in a period of 48hours.
27. Inhibition of Conjugation:
Sulfonamides and Vitamin K results in
competitive conjugation inhibition of bilirubin.
GALACTOSEMIA:
Absent or deficient Galactose 1phosphoate uridyl transferase which is
needed in glucoronidaton of indirect bilirubin.
29. HISTORY
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
meconium passage.
30. Family history of jaundice, liver disease
Previous sibling with jaundice for blood
group incompatibility.
Kernicterus: Lethargy, poor feeding, and
hypotonia. Some advanced signs are
seizures, retrocollis, paralysis of upward
gaze and shrill cry.
Breast feeding.
31. ON EXAMINATION:
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
33. HOW DO YOU LOOK FOR
ICTERUS?
1. Dermal staining :progresses from head to
toe
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.
34.
35.
36. Clinical Jaundice
Measure Bilirubin
> 12 mg/dl and infant <
24 hr old
< 12 mg/dl and infant > 24
hr old
Fraction of Bilirubin
Follow bilirubin level
Indirect
Direct
37. Direct bilirubin
Evaluate for treatable causes
1.Infections-blood, urine culture, VDRL.
2.Metabolic disorders-urine reducing substances, serum
amino acids,T4,TSH.
If no abnormality ;screen for Identifiable causes
*α-1 antitrypsin deficiency
*cystic fibrosis
*congenital viral infections
If no abnormality; evaluate for anatomical abnormalities
*Stool color
*USG
*Hepato-biliary scintigraphy
*Liver biopsy
41. PHYSIOLOGICAL JAUNDICE
Explain about benign nature of the disease
Encourage to breastfeed frequently &
exclusively
Ask Mother to bring baby back if baby looks
deep yellow or palms & soles have yellow
staining.
43. PHOTOTHERAPY
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
phototherapy
44.
45. 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,
hypothermia)
48. Configurational Isomerization
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.
51. Administering Phototherapy:
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)
52. Keep the distance between the baby & the
light 30-45cm.
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
24hrs.
53. Complications of Phototherapy:
Loose stools
Erythematous macular rash
Purpuric rash associated with transient
porphyrinemia
Over-heating
Dehydration
Bronze baby syndrome
54. 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.
55. EXCHANGE TRANSFUSION
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.
56.
57. FOLLOWUP
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.
58. PREVENTION
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.
59. JAUNDICE IN THE CHILD &
ADOLESCENT
HISTORY:
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;
hemoglobinopathies.