Neonatal jaundice occurs in 60% of term and 80% of preterm babies. Despite Neonatal jaundice is one of the commonest neonatal conditions, there are no national practice guidelines for its management in our country. Lack of uniform guidelines and standard practice parameters for diagnosis and management of neonatal jaundice often leads many babies to develop unnoticed hyperbilirubinemia causing kernicterus and long term poor neurological sequelae. This review after briefly discussing the epidemiology and pathophysiology of neonatal jaundice provides evidence-based pragmatic guidelines for the diagnosis and management of neonatal jaundice in resource-limited countries like Afghanistan

1. Neonatal Jaundice
Supervisor :Dr. Mohammad Zahir Safi
Prepared By Dr. Mohebullah Faqiri
E-mail: mohabfaqiri@gmail.com 2016
Ataturk National Children Hospital
Islamic Republic of Afghanistan
Ministry of Public Health

2. Neonatal jaundice
 Jaundice is one of the most common conditions requiring medical
attention in newborn babies. Approximately 60% of term and
80% of preterm babies develop jaundice in the first week of life,
and about 10% of breastfed babies are still jaundiced at 1 month
of age. In most babies with jaundice thevre is no underlying
disease, and this early jaundice (termed ‘physiological jaundice’)
is generally harmless. However, there are pathological causes of
jaundice in the newborn, which, although rare, need to be
detected. Such pathological jaundice may co-exist with
physiological jaundice

3. Neonatal jaundice
 Neonatal jaundice refers to yellow colouration of the skin
and the sclera (whites of the eyes) of newborn babies that
results from accumulation of bilirubin in the skin and
mucous membranes. This is associated with a raised level
of bilirubin in the circulation, a condition known as
hyperbilirubinaemia.
 Jaundice is yellow discoloration of skin, sclera and
mucous membrane .
 It is a common problem in the 1st week of life.

4. General consideration
 It is consequence of excess bilirubin level in the blood and
becomes visible at a level of 4-6mg/dl.
 ↑bilirubin levels may be toxic to developing CNS and may cause
neurological impairment even in term newborns.
 The majority of this jaundice is ‘physiological’( benign) and no
intervention is required.
 Approximately 5-10% of cases need phototherapy or other
therapeutic options.
 60% of fullterm & 80% preterm

5. Approach to a child with jaundice

6. Bilirubin Metabolism
 It is derived from the catabolism of heme of Hb and non
Hb heme proteins(myoglobin,cytochrome,catalase)
 Hb is converted to biliverdin which is rapidly reduced.
 Bilirubin transport in plasma: Unconjugated bilirubin
is released into the circulation by the RE cells and is
rapidly bound to albumin.
 Hepatic uptake of bilirubin: This bilirubin albumin
complex is removed from the circulation by the
hepatocyte and enters the liver cells.

7. Bilirubin Metabolism Cont...’
 Conjugation of bilirubin: In liver cells each molecule of
bilirubin conjugates with 2 molecules of glucuronic acid by a 2
step conjugation process producing water soluble bilirubin
monoglucuronide and diglucuronide.
 Bilirubin excretion: after reaching of bilirubin diglucoronide to
the intestine by baceria urobilinogen is made(stercobolin is
excerted in feces and yellow urobilinogen is excreted in urine.
 Entero hepatic bilirubin absorption: Bilirubin
monoglucuronides and diglucuronides are hydrolyzed to
unconjugated bilirubin by the enteric mucosal enzyme
(glucuronidase), unless rapidly excreted. This unconjugated
bilirubin returns to the liver via the portal circulation.

8. Bilirubin Metabolism
NJ
- 8
Hb → globin + haem
1g Hb = 34mg bilirubin
Non – heme source
1 mg / kg
Bilirubin
glucuronidase
Bilirubin
Bilirubin
Ligandin
(Y - acceptor)
Bil glucuronide
Intestine
Bil
glucuronide
Stercobilin
bacteria
Glucoronidaze enzyme

9. 1. Skin blanching (dermal zones)
2. Transcutaneous bilirubinometer
Estimation of STB levels by dermal zones:
Zone 1 = 4-6mg/dl
Zone 2 = 6-8mg/dl
Zone 3 = 8-12mg/dl
Zone 4 = 12-14mg/dl
Zone 5 = >15mg/dl
1
3
4
5
5
Clinical Methods Of Detection Of
Neonatal Jaundice:

10. Causes of jaundice:
1. Physiological jaundice
2. Pathological jaundice
A-causes of prolonged unconjugated hyperbilirubenemia:
Immaturiy,ABO,RH incompatibility,breast milk jaundice,
hypothyroidism,pyloric stenosis,crigler najjar syndrome, concealed
hemorrhage,malaria
B-cause of prolonged conjugated hyperbilirubenemia:
Idiopatic neonatal hepatitis,inspissated bile syndrome, infections(bacterial
sepsis, Hep.B,CMV, syphlis, toxoplasmosis etc),malformations (e.g.
biliary atresia), metabolic disorder,chromosomal disroder,TPN.

11. Physiological jaundice
 Self limiting condition, represents physiological
immaturity of the neonates to handle increased
bilirubin production.
 Appears after 48-72hrs after birth.
 Rise of bilirubin <5mg/day.
 Peak not more than 12mg/dl in full term and 15mg/dl
in preterm infants.
 Direct bilirubin <1mg/dl of total bilirubin.
 Resolves by 7-10days in full term and 15days in
preterm infants.

12. Physiological jaundice cont...’
 It is due to:
1. ↑bilirubin load on hepatocyte due to RBC breakdown
because of large hematopoietic pool at birth and
shortened RBC survival.
2. Relative immaturity of glucuronyl transferase pathway.
3. Defective bilirubin excretion.
4. ↓bilirubin clearance from plasma.
5. ↑enterohepatic circulation.
6. Physiologic polycythemia

13. Pathological jaundice
 It refers to as an elevation of STB levels to the extent where
treatment of jaundice is more likely to result into benefit than
harm.
 It appears in 1st 24 to 48hrs of life.
 Rise of bilirubin is >0.5mg/dl per hour or>5mg/dl/day
 Hemolytic anemia:
 a-RBC defect e.g. G6PDD,spherocytosis,Thalassemia,sickle cell
disease
 b-acquired RBC hemolysis e.g. ABO and Rh incompatibility
 Peak more than 15mg% in formula fed and 17mg% in breastfed
full term neonate.
 Direct bilirubin is >2mg/dl
 Do not resolve within 10days in full term and 15 days in preterm
infants.

14. Hemolytic Disease Of The Newborn Due To
Feto-maternal Blood Group Incompatibility
 1 Rh isoimmunization
Dx:
a) Baby Rh (+) , mother Rh (-)
b) Indirect bilrubin
c) Combs test direct( +), indirect (+)
d) In neonate blood reticulocytosis, nucleated RBC
e) If the condition is very sever it may cause erythroblastosis fetalis
or still birth
In hydropes fetalis :
Severe anemia , precardial effusion, pleural effusion, ascitis ,
anasarca , cardiac failure , hypoalbomenemia

15. 2 ABO incompatibility :
Feto-maternal incompatibility exists in about 25 % of
pregnancies but hemolytic disease develops in only one in ten
such offspring. The commonest materno- fetal combination are
O group mother and A or B group fetus. in some minor groups
(N, M ,Duffy cell) iso immunization may occur.
3 infections ( protozoal, congenital sephles , viral infection,
sepsis)
Hemolytic Disease Of The Newborn Due To
Feto-maternal Blood Group Incompatibility

16. 4 polycythemia
5 blood extravasation ( intra ventricular
hemorrhage ,cephalhematom, subcapsular hematom
in the liver , GI bleeding)
6 cojugation defect ( ciggler najjar syndrome)
7 glucoronyl transferase enzyme inhibition
such as novolicocin , maternal gestational hormones
Hemolytic Disease Of The Newborn Due To
Feto-maternal Blood Group Incompatibility

17. 8 Breast milk and jaundice
A-Breastfeeding jaundice
 Exclusively breastfed neonates have a tendency to develop
↑serum bilirubin levels during 1st few days of life.
 It usually disappears by 3rd week of life, but may persist into 2nd
to 3rd month of life in a few babies.
 The cause may be insufficient lactation leading to inadequate
feeding, dehydration and hemoconcentration.
 It needs no intervention, despite ensuring optimum breastfeeding
which decreases this kind of jaundice.
Hemolytic Disease Of The Newborn Due To
Feto-maternal Blood Group Incompatibility

18.  A small proportion of (2-4%) exclusively breastfed babies have
jaundice in excess of 10mg/dl beyond 3rd to 4th weeks of life.
 It should be considered if jaundice is unconjugated (not staining
nappies); and other causes for prolongation such as continuing
hemolysis, extravasated blood, G6PD deficiency and
hypothyroidism have been ruled out.
 It may be the result of presence of 3 alpha, 20 beta preganandiol
and free fatty acids in mother’s milk which inhibit conjugation of
bilirubin.
 It resolves on its own but some babies may require phototherapy.
 Occasionally, undue anxiety in the parents may warrant
temporary withdrawal of breastfeeding just for 2-3days.
B Breast Milk jaundice

19.  9- metabolic disorder : inborn error of metabolism ,
hypothyroidism , galactosemia, hereditary fractose intolerance
and cystic fibrosis
 10- increase interohepatic circulation(CF , pyloric stenosis,
duodenal atresia
 11- some drugs have effect on band of bilirubin and glabolin
e.g. asprine and salphonamide,ceftriaxone
 12 -some other problems may aggravate jaundice for e.g.
sepsis , acidosis, birth asphyxia and hypothermia
Hemolytic Disease Of The Newborn Due To
Feto-maternal Blood Group Incompatibility

20.  Unconjugated hyperbilirubinemia can cause
A - transient encephalopathy ( lethergic)
B - kernacterus
Predisposing factors for kernacterus :
gestational age , birth weight, neonatal age,
others (e.g. sepsis , hypoglycemia ,
hypothermia and meningitis )

21. Phases Of Kernacterus :
 Phase 1(24h-7d) : hypotonia , poor sucking, lethergy,
depressed sensorium , high pitch cry
 Phase 2 (24h-7d) : hypertonia , stiffness,
opisthotonus , seizures , paralysis of upward gaze.
 Phase 3 : stiffness is decreased in one week
 Phase 4 : sequale ( chorae attitued , SNHL , CP , MR)

22. Examination Of Jaundiced Pt
 Hx :
A . family Hx , mother Hx, child hx ,
B. S/S : jaundice , polycythemia, hepatosplenomegally , petichia ,
cephalohematom , IUGR, LGA , omphalitis , choririthenitis,
microcephaly
C. Neurologeic exam : poor sucking, hypotonia, seizure
Dx :
Lab exam : STB (direct , indirect) reticulocyte , nucleated RBC ,
screen for sepsis , peripheral blood smear for heridetary
spherocytosis , test for ABO and Rh incompatabality ,blood
albumin, urine exam , Hb electrophorisis
Radiolgic exam : CT scan and HIDA scan

24. Treatment
 Increase breast feeding more than 10 t/day
 Glucose ( if sufficient breast milk no needed )
 Extra IV fluid 30cc /kg/day
 Cause of jaundice should be treated
 If sepsis give antibiotics
 Stop drugs which cause hyperbilirubinemia
 Treat hypothyroidisum
 Treat hypoglycemia
 Specific measures ( exchange blood transfusion and
phototherapy)

25. Phototherapy
Bilrubin absorbs the rays with wave length of 400-500 nm
effectively hence the blue light can be absorbed well.
Blue light length  450-460 nm
White light length  550-600 nm
Mechanism of phototherapy :
Photochemical reaction :
1 Photo isomirization
2 Structrual isomirization
3 photo oxidation

26. Babies under phototherapy
Baby under conventional phototherapy

27. Indication Of Phototherapy
 1- unconjugated hyperbilirubenemia
 2- STB should be 5 mg lesser than EBT range
 3- after EBT
 4 - prophylactically in premature , LBW and
hymolytic disease
 5 - waiting for EBT

28. Contraindication Of Phototherapy
 1 - hypatocellular jaundice , biliary atrisia (B.baby
syndrome)
 2 - mixed hyperbilirubenemia
 3 - congenital erythropoitic porphyrine

29. Technique Of Phototherapy
 1 distance
 2 good expose
 3 eyes covering cautiously ( cornia damage ,naris open)
 4 change the baby from one side to anthor side every 2hrs
 5 Check STB

30. When To Stop Phototherapy
 1 drop STB to remove danger of toxacity
 2 age is increased that can tolerate high STB
Term STB 13±0.7 mg/dl
Preterm STB 10.7±1.2 mg/dl

31. Intensive Phototherapy
 Distance 15-20 cm
 Fibro optic blanket
 1.5 fold maintenance iv fluid
 In 4-6 hrs  1-2 mg/dl STB
 If in 4-6 hrs STB is not dropped (1-2 mg/dl ) the
condation is called phototherapy failure

32. Baby under triple unit intense
phototherapy

33. Side Effect Of Phototherapy
 Insensible water loss
 Watery diarrhea
 Rittinal damage
 Hypocalcamia
 Erythematose macular skin rash
 Bronze baby syndrome
 DNA mutation
 Dicreased child mother interaction
 Hypothermia in winter
 Nasal block

34. Exchange Blood Transfusion
 Indication of BET
 In newborn
1 cord Hb less than 12 mg/dl
2 commbs test (+)
3 reticulocytes more than 15 %
4 TSB 5mg/dl higher than phototherapy level
 In 1st week of life :
1TSB : term 20 mg/dl , prterm 15 mg/dl
2 rise 1mg/dl/h or 10 mg/dl /d
3 p hx of EBT, death 4 coombs test(+)

35. Technique Of Exchange Blood
Transfusion
 General measures :
 1 sepsis : give antibiotic
 2 take care of feeding
 3 prevantion of Rh immunization in mother
 Equipment
1 Sterile towels 2 artery forceps
3 Sponge forceps 4 tooth forceps
5 Scalp blade 6 sterile gas
Sites of application
1 Umblical vein 2 jugular vein
3 Saphenous vein

36. Types Of Blood Group In EBT
 Rh incompatibility : Rh of the mother /ABO of the baby
 ABO incompatibility : ABO of the mother /Rh of the baby
Double volume blood should be transfused
How to prepare the baby for exchange :
1 Pass NG tube and suction the stomach
2 NPO
3 Check vital sign
4 Cut the cord near stump, insert NG tube 5-6 cm in umblical vein
5 Heparenise the equipments
6 Perform EBT in first phase of kernicterus

37. Taking Care After EBT
 NPO for 24 hrs
 Give sufficient iv fluid
 Control of vital sign
 Warm room
 Check STB after 6-8 hr of EBT ( if STB high
repeat the procedure )
 F up after 3w and 3 months
 EBT drops the bilirubin at range of 6-7 mg /dl

38. Complication Of EBT
 1 sepsis ( hepatitis , cholangitis )
 2 Hypothermia in winter
 3 blood reaction
 4 hypervolamia
 5 hypoglycemia
 6 CCF
 7 hypocalcemia
 8 vomiting and aspiration
 9 Hyperkalemia
 10 cardiac arrythmia and arrist
 11 Air emboly
 12 thrombos
 13 NEC
 14 anemia

39. Persistent Neonatal Jaundice
 definition: jaundice whether unconjugated or conjugated with
duration of more than 2wk is called per.neo.jaundice.
Persistent unconjugated hyperbilirubenemia:
Some causes of this jaundice could be:breast milk
jaundice,Down’s syn,cri.naj.syn,cretinism
Persistent conjugated hyperbilirubenemia:
This is very rare in first wk of life.some causes are as below:
Idiopatic neonatal hepatitis
Inspissated bile syndrome
Infections(sepsis,hep.B,CMV,toxoplasmosis,TB,malaria,

40. Management:
 Idiopatic neonatal hepatitis recover spontaneously by the age of one year
 Corticosterion have no role
 If mother is Hbs Ag positive:for neonat give HBIG 0.5ml in 12hrs, hep.B
vaccinge is also given
 Biliary atresia:operation (casai procedure)
 For cholestatic hepatitis:
a) Low fat diet
b) High protein diet
c) Vitmines A,D,E,K
d) Ca,zn
e) Cholestramine(0.25g/kg/d)lower bilirubin and relieve itching
f) If ascitis:give spironolactone,salt restriction
g) End stage liver disease:liver transplantaion

41. Guidelines To Start Phototherapy
Birth weight Serum bilirubin at which
phototherapy is indicated
<1500g 5-8mg/dl
1500-1999g 8-12mg/dl
2000-2499g 11-14mg/dl
>2500g ( no hemolysis) 17-22mg/dl
>2500g( with hemolysis) 13-15mg/dl

42. Guide Lines For Exchange Transfusion
Birth weight (gm.) Bilirubin level mg%
<1500 13-16
1500-1999 16-18
2000-2499 18-20
>2500 (no hemolysis) 25-29
>2500 (with hemolysis) 17-22

43. Thanks For Your Kind
Attention