Newborn jaundice is a yellowing of a baby's skin and eyes. Newborn jaundice is very common and can occur when babies have a high level of bilirubin, a yellow pigment produced during normal breakdown of red blood cells. follow me on my YouTube channel :- medic o mania

1. MANAGEMENT OF CHILD
WITH NEONATAL JAUNDICE
Presented by :- Ms. Neha Malik

2. INTRODUCTION
 Jaundice comes from a word called “JAUNICE’’ that means
yellowness. Neonatal jaundice/hyperbilirubinemia refers to an
excessive level of accumulated bilirubin in the blood and is
characterised by jaundice or icterus, a yellowish discoloration of
the white part of the eyes and skin in a new born.
 Hyperbilirubinemia is a common finding in new-borns and in most
instances is relatively benign. However, in extreme cases, it can
indicate a pathologic state.
 Almost all new born experience elevated bilirubin levels, but only
about 50 -60% demonstrate observable signs of jaundice (acc. to
blackburn,2011)

3. Cont…..
 Jaundice can be caused by-
i) Increased conjugated bilirubin OR,
ii) Increased unconjugated bilirubin OR
iii) Increased conjugated and unconjugated
bilirubin(both)

4. NORMAL BILIRUBIN PATHWAY (HEME
CATABOLIZM)
RBC(120 days life span)
now old and vary RBC’S are eaten by Macrophages(part of reticuloendothelial
system, present in spleen and lymph nodes)
now, hemoglobulin found in RBC is made up of 4 subunits and each subunits is
consist of a protein called globulin and an iron element called heme
 these subunits dissociated into globulin and haem ,where globulin broken into
amino acids and got recycled and haem part further dissociate into Fe3+ and
organic ring(protoporphyrin)

5. Fe3+ got reserved for making new RBC and the organic ring got opens
up and become bilirubin or unconjugated bilirubin that is a toxic
molecule and not very water soluble
now albumin got attached to this unconjugated bilirubin and carries it
through blood to the liver
now in liver this unconjugated bilirubin converted into conjugated
bilirubin with the help of UDP enzyme
conjugated bilirubin is water soluble and from liver got stored in gall
bladder by bile duct

6. from gall bladder it goes to intestine where a bacteria acted upon this and
convert it into STERCO BILINOGEN
this sterco bilinogen got oxidized in intestine and become
STERCOBILIN which gives yellow colour to faeces.
some stercobilinogen got absorbed to blood and later filtered out by kidney
where it got converted into UROBILINOGEN and after oxidation becomes
UROBILIN

7. To understand disease conditions better one need to
understand the bilirubin metabolism in liver: -

8. JAUNDICE BECAUSE OF INCREASED
UNCONJUGATED BILIRUBIN ARE: -
Disorders like –
1. Extravascular haemolytic anaemia- breakdown of RBC early
2. Ineffective haematopoiesis – bone marrow doesn’t form RBC correctly
Because of this more breakdown and more UCB
|
Since all the sudden our body starts creating more UCB
liver cells got overwhelmed
|
As the liver cell maximize their work, there will be increased conjugated bilirubin in gall bladder
(which increases the risk of pigmented gall stones)
|
Much darker colour urine and stool

9. Genetic defects –
1.Gilbert’s syndrome: - its due to decreased activity
of the UDP GLUCURONYL TRANSFEBASE and is
mostly asymptomatic
2.Crigler Najjar syndrome: - it results from lack of
or major deficiency of UDP GLUCURONYL
TRANSFEBASE that causes the build-up of
unconjugated bilirubin

10. Physiological jaundice of the new-borns
 There are several reasons for physiological jaundice such as:
 Breakdown of RBCs due to high HB concentration at birth, RBC lifespan is 70days in new-borns,less
effective hepatic functions.
1. Immature hepatic functions – onset after 24 hours of life mostly seen in preterm infants, peak on 3rd and 4th
day , declines on 5th -7th day
New-born livers have a lower amount of the enzyme called UGT that converts UCB to conjugated bilirubin
|
After birth UCB levels can be high dur to the natural process of macrophages destroying fetal RBC’S, typically
but if this is a normal process
|
But there can be complications if UCB rises a lot, since UCB is fat soluble it gets collected in the basal ganglia
of the child’s brain and can cause damage to the brain
|
KERNICTERU

11. Breastfeeding associated jaundice (early onset)
onset on 2nd -4th day of life, peaks on 3rd - 5th day, occurs in approximately 12%- 35% of breastfed new-borns.
It mostly related to the breastfeeding process and probably results from decreased caloric and fluid intake
before the milk supply is well established
|
Decreased milk intake is associated with increased enterohepatic circulation of bilirubin or shunting :-
Relatively sterile and motile new-born bowel is initially less effective in excreting urobilinogen
|
The enzyme beta glucuronidase can convert conjugated bilirubin into unconjugated form
|
which is reabsorbed by the intestinal mucosa and transported to liver
|
Reduced fluid intake results in dehydration, which also concentrates the bilirubin in the blood

12. Breast milk jaundice (late onset)
 onset 4th- 8th day, peaks on 10th -15th day, child may remain
jaundiced for 3 to 12 weeks or more but despite of high
bilirubin level these infants are well. It occurs in 2% -4% of
breastfed infants
The jaundice may be caused by factors in the breast milk
such as fatty acids, pregnanediol and beta glucuronidase
|
These factors either inhibit the conjugation or decrease the
excretion of bilirubin
|
Less frequent stooling by breastfed infants may allow for an
extended time of reabsorption of bilirubin from stools

13. JAUNDICE BECAUSE OF INCREASED
CONJUGATED BILIRUBIN ARE: -
Genetic disorder –
1. Dubin -Johnson syndrome: - mutation in MRP-2 protein, which means
conjugated bilirubin collects in the blood and not released in the gut and bile,
but this generally requires no treatment.
2. Rotor’s syndrome: - cause of this unknown but it is like Dubin Johnson and
results in unconjugated bilirubin in blood.
3. Glucose- 6- phosphate dehydrogenase deficiency: - its deficiency leads to
destruction of RBC’s.

14. Obstructive jaundice
blockage in common duct due to gall stones or pancreatic carcinoma or liver fluke etc
|
This cause increase pressure in the bile duct
|
That causes bile to backflow or leak through the junctions between the hepatocytes to blood
|
But with-it bile salts and acids and cholesterol also gets into the blood
|
Which leads to PRURITUS and cholesterolemia and xanthoma (fatty growths underneath the skin, mostly on
the joints)
|
Excess CB absorbs by the kidney and released through urine that will be very dark in colour
|
Also since the body is loosing a lot of bile , body is not able to absorbs fat as well which will cause increase fat
excretion and decreased vitamin absorption.

15. JAUNDICE BECAUSE OF BOTH INCREASE
IN CONJUGATED AND UNCONJUGATED
BILIRUBIN ARE: -
Viral hepatitis – hepatocytes dies off in this condition
leading to collection of unconjugated bilirubin in blood
|
Also, since the hepatocytes lines the bile duct, they shrink
and lead to leakage of bile in the blood from the bile duct
|
Which leads increase conjugated bilirubin in the blood

16. PHYSIOLOGIC JAUNDICE (non-pathologic
unconjugated hyperbilirubinemia):
Physiologic jaundice is caused by a combination of increased bilirubin production
secondary to accelerated destruction of erythrocytes, decreased excretory capacity
secondary to low levels of ligandin in hepatocytes, and low activity of the bilirubin-
conjugating enzyme uridine diphosphoglucuronyltransferase (UDPGT).
1.Term Infants:
•50-60 % of all new-borns are jaundiced in the first week of life.
•Total serum bilirubin peaks at age 3–5 d (later in Asian infants).
•Mean peak total serum bilirubin is 6 mg/dL (higher in Asian infants).
2.Preterm Infants:
•Incidence of visible jaundice is much higher than in term infants.
•Peak is later (5-7d).
•Because of ↑ risk of bilirubin encephalopathy, “physiologic” jaundice is more difficult to define and
jaundice should be followed closely.

17. NON-PHYSIOLOGIC
JAUNDICE/PATHOLOGIC JAUNDICE:
Pathologic neonatal jaundice occurs when additional factors accompany the
basic mechanisms. The following criteria are indicators of pathologic
jaundice that, when present, warrant further investigation as the cause of the
jaundice:
•Jaundice in the first 24 hours
•Serum Bilirubin rising faster than 5 mg/dL in 24 hours
•Direct bilirubin >1.5-2 mg/dL
•total serum bilirubin level
•In healthy term infants total serum bilirubin concentration >12.9mg/dL
•In preterm infants, Total serum bilirubin over 15mg/dL: and upper limit for breastfed infant is
15mg/dL

18. SIGNS AND SYMPTOMS
 Yellow discoloration of the skin, mucous membranes and the
whites of the eyes
 Light-coloured stool
 Poor feeding
 Lethargy/excessive sleepiness
 Changes in muscle tone (either listless or stiff with arching of the
back)
 High-pitched crying
 Seizures

19. DIAGNOSTIC EVALUATION
 Jaundice is not solely based on serum bilirubin levels but also on the timing of the
appearance of clinical jaundice, gestation age at birth, age in days since birth family
history, including maternal Rh factor, evidence of haemolysis , feeding method, infants
physiologic state , and the progression of serum bilirubin level
 Physical evaluation -Press the skin against bony surface for 5 seconds to blanch the
skin and observe the skin colour. Gently press over forehead or chest.
normal yellow blanching

20. Kramer’s rule:
Kramer recognised the cephalocaudal progression of jaundice
with increasing total serum bilirubin levels and divided the
baby into 5 zones, with an estimated total serum bilirubin level
measurement associated with each zone.
 Grade 1 (Face and neck only): 10 mg/dl
 Grade 2 (Upper trunk upto umbilicus): 15 mg/dl
 Grade 3 (Lower trunk below umbilicus to knee): 20 mg/dl
 Grade 4 (Arms and lower legs below knee): 25 mg/dl
 Grade 5 (Palms and soles): >25 mg/dl

21. SHADES/COLOURS OF JAUNDICE
Reddish shade (Rubin jaundice): Hepatitis
Lemon yellow with a reddish hue (Flavin
jaundice): Hemolysis
Greenish yellow (Verdin jaundice): Obstructive
jaundice
Grayish or blackish green (Melas
jaundice): Prolonged obstructive jaundice

22. TIMELINE :-

23. NON-INVASIVE MONITORING OF
BILIRUBIN: -
Transcutaneous bilirubinometer
TcB:-It measures bilirubin via cutaneous
reflectance, it allows for repetitive
estimation of bilirubin and ,when used
correctly ,may decrease the need for invasive
monitoring. TcB provide
Accurate measurements within 2mg/dL in
most neonatal at serum level below
15mg/dL.
*after phototherapy has been initiated,
TcB is no longer useful as a screening tool

24. NANOGRAM: -
 The use of hour specific serum bilirubin levels to predict new-borns at risk
for rapidly rising level has now become the standard of care as well as an
official recommendation American academy of paediatrics.
 The monitoring with the help of nanogram should be done for healthy
neonates of 35 weeks of gestation or more

25. BLOOD INVESTIGATIONS TO BE DONE ARE: -
 Serum bilirubin, total, direct, indirect
 Mother blood group
 Baby blood group
 If the child is male, then screening for G6PD

26. COMPLICATIONS: -
BILIRUBIN ENCEPHALOPATHY: it is a syndrome of severe brain
damage resulting from the deposition of unconjugated bilirubin in brain
cells.
 The mildest form of bilirubin encephalopathy: -is sensorineural
hearing loss due to damage to the cochlear nuclei.
 THE PREDROMINAL SYMPTOMS of bilirubin encephalopathy
consists of decreased activity, lethargic, irritability, hypotonia, and
seizures
 Severe encephalopathy causes KERNICTERUS: - yellow staining of
the brain cells

27. NEUROTOXICITY:
Factors predisposing to neurotoxicity of unconjugated hyperbilirubinemia include:
 When bilirubin concentration exceeds the binding capacity of serum albumin
 Displacement of bilirubin from albumin by acidosis or certain drugs (e.g.,
sulfonamides, ceftriaxone)
 Sepsis
 Preterm infants due to↑ risk due lower serum albumin concentrations and ↑ risk
for acidosis and sepsis.
 Abrupt fluctuation in bp
 Any condition that increases the metabolic demand for oxygen or glucose such
as fetal distress, hypoxia, hypothermia, hypoglycaemia also increases the risk of
brain damage at lower serum levels of bilirubin

28. THERAPEUTIC MANAGEMENT OF
JAUNDICE: -
 The primary goal in the treatment of hyper bilirubinaemia are to identify
the infants at high risk; monitor serum bilirubin levels; prevent
encephalopathy and, in any blood group incompatibility, to reverse the
haemolytic process
 FREQUENT BREASTFEEDING
 Healthy near term and full-term infants with jaundice may also benefit
from early initiation of feeding and frequent breastfeeding.it promotes
increased intestinal motility and decreasing enterohepatic shunting and
establish normal bacterial flora in the bowel to effectively enhance the
excretion of unconjugated bilirubin.

29. IVIG (INTRAVENOUS IMMUNOGLOBULINE)
It is effective in reducing bilirubin levels
in infants with Rh incompatibility and
ABO incompatibility but the evidence
supporting IVIG is limited, and further
research is recommended.

30. MANAGEMENT of UNCONJUGATED
HYPERBILIRUBINEMIA:
1. Healthy Term Newborns
2. Sick Term Newborns: Start above therapies at lower total serum bilirubin levels.
3. Preterm Infants: Because of ↑ risk of bilirubin encephalopathy, therapy should be
started at lower bilirubin concentrations. In general, bilirubin should not be
allowed to exceed the infant’s weight in kg x 10 (e.g., for 1.0 kg infant, keep
bilirubin

31. PHOTOTHERAY
1. Phototherapy is treatment with a special type of light (not
sunlight). It's used to treat new-born jaundice by lowering the
bilirubin levels in your baby's blood through a process called
photo-oxidation/ photoisomerization. Photo-oxidation adds
oxygen to the bilirubin (LUMIRUBIN) so it dissolves easily in
water.
2. Studies indicate that blue fluorescent light is more effective than
the white fluorescent light in reducing bilirubin levels. However,
because blue light alters the infant’s coloration, the normal light
of fluorescent bulbs in the spectrum of 420-460nm is often
preferred so the infant’s skin can be observed for better colour.

33. Cont…..
1. Mechanism of phototherapy are
 Configurational isomerization
 Structural isomerization
 Photo oxidation
When serum bilirubin levels are rapidly increasing or
approaching critical levels, intensive phototherapy is
recommended., it is more effective than standard
phototherapy for rapid reduction of serum bilirubin
Best result occurs within the first 4-6 hours of treatment.

34. The recommendation to start phototherapy for
infants are (WATCHKO AND MAISELS, 2010)
Infants weighing less than 1500grams is 5-8mgldL
Infants weighing 1500-1999grams is 8-12mg/dL
Infants weighing 2000-2499grams is 11-14mg/Dl
Prophylactic phototherapy may be used in pre term infants
to prevent a significant increase in serum bilirubin levels
(stokowaki , 2011)

35. ADMINISTRING PHOTOTHERAPY
 Make sure ambient room temperature is optimum 25degree to
28degree Celsius
 Remove all clothes of the baby except diaper to project the
genitals of the child
 Cover the eyes of the infant with eye patch
 Place the child under the lights in a cot if >2kg and in an
incubator if <2kg
 Keep baby at the distance of 30-45cms from the light source
 Ensure optimum breast feeding

36. MONITORING AND STOPPING
PHOTOTHERAPY
 Monitor temp at every 2-4 hours
 Measure TSB level every 12-24hrs
 Discontinue once two TSB values falls below age specific cut-offs
,12 hours apart
 Monitor for rebound bilirubin rise with 24hrs after stopping
phototherapy, although it usually resolves without any intervention.

38. SIDE EFFECTS OF PHOTOTHERAPY: -
Phototherapy has not been found to cause long
term adverse effects, but it can mask signs of
sepsis, haemolytic disease or hepatitis.
Causes parent infant separation
Breast feeding disturbances

39. EXCHANGE TRANSFUSION: -
 it is a potentially life-saving procedure that is done to counteract the effects of serious
jaundice or changes in the blood due to diseases such as sickle cell anaemia.The
procedure involves slowly removing the person's blood and replacing it with fresh donor
blood or plasma.
1. SBR approaching 20mh/dl or increasing at rate of 1mg/dl/hour or 10mg/dl/day, then
exchange transfusion is needed.

40. Selection of blood for exchange transfusion
 Fresh blood not older than 72hours
 Ideally it is o-ve
 Blood transfusion in ABO incompatibility: - select
blood group of mother and RH of the baby
 Blood transfusion in RH incompatibility: - select
blood group of baby and RH of the mother

41. Procedure for exchange transfusion: -
 Prerequisites: -
 Counsel the parents
 Keep NPO for 4 hours
 Clean umbilicus with aseptic technique
 Identify umbilical vein and insert catheter 5cm under aseptic condition
 Arrange for fresh blood
 Arrange for inj. Ca. gluconate (4cc in 20 cc syringe)
 Arrange for inj. Na. bicarbonate (4cc in 20 cc syringe)
 Fill one syringe with normal

42. Procedure: -
 Connect one end of the three-way cannula with
 Infusion chamber
 Another end with catheter
 And 3rd end with 20cc syringe
 Fill the infusion chamber with 100ml blood
 Draw 10ml of blood and inject 1o ml of blood, till 100ml of blood.
 Then inject 5ml of Na. bicarbonate and 5ml of Ca. Gluconate at the end of
the cycle
 Now repeat 2nd cycle of 100ml blood but now with 20ml of blood each
time infused and extracted.
 Keep the child NPO for 3 hours after the blood transfusion.

43. Possible complications: -
 Blood clots.
 Changes in blood chemistry (high or low potassium, low
calcium, low glucose, change in acid-base balance in the
blood)
 Heart and lung problems.
 Infection (very low risk due to careful screening of blood)
 Shock if not enough blood is replaced.

44. PREVENTIVE MEASURES OF NEONATAL
JAUNDICE
Encourage frequent breastfeeding, preferably every 2
hours
Avoid glucose water, formula, water supplementation
Monitoring for early stooling
The infant’s weight, voiding, stooling should be
evaluated along with the breastfeeding pattern

45. Reference: -
 Marilyn j. Hockenberry, Wong’s essentials of paediatric
nursing, second south Asia edition, page no: - 386-394
 Intensive Care Nursery House Staff Manual, UCSF
medical centre
 https://medlineplus.gov/ency/article/002923.htm
 https://en.wikipedia.org/wiki/Neonatal_jaundice