NEONATAL

JAUNDICE
BY
DR OKONYE HILARY
 OBJECTIVES OF THE STUDY

1. Definition
2. Bilirubin metabolism/
pathophysiology
3. Aetiology of neonatal
jaundice
4. Age at onset
OBJECTIVES OF THE STUDY contd.

5) Clinical assessment
6) Types
7) Risk factors for Hyperbilirubinaemia
8. Complication of Bilirubin toxicity.
9. Management
10. Indications for management
11. Complications
12. Techniques
13. Conclusion
 INTRODUCTIO
N
 Jaune= Yellow
 97% healthy term infants have biochemical
hyperbilirubinaemia
 65% clinical jaundiced physiologically
 Jaundice in newborn might signal a serious treatable illness
which may cause neurological damage if bilirubin is high.
 DEFINITION

Jaundice is yellow discoloration of

the skin noted on the Face, tip of
nose and nasolabial folds.
 BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY

 Jaundice occurs when liver cannot clear the required amount of

bilirubin.
Mechanisms
 Excessive bilirubin production
 Limited uptake and conjugation
 The unconjugated bilirubin appearing in the blood
 Normal destruction of circulating erythrocytes accounts for 75%
of the daily bilirubin production.
 BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY CONTED
 In neonates non- haemoglobin heme protein contributes about 25%
of bilirubin production.
 Bilirubinproduction also derived from free heme and ineffective
erythropoiesis
 The catabolism of heme results in equimolar production of bilirubin
and carbon monoxide
 Carbon monoxide gets firmly bound to haemoglobin to form
carboxyhaemoglobin.
 Normal newborn produces 8-10mg/kg of bilirubin per day twice the
rate in adults.
 BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY CONTED
 Neonate has larger circulating erythrocyte volume, a shorter
mean erythrocyte life span, larger early- labelled bilirubin
peak from non- heme sources.
 Bilirubin is bound to albumin in the plasma transported to
the liver
 One high affinity site exists for albumin which binds
bilirubin in the molar ratio of 1:1
 Binding also occurs at low affinity sites bringing bilirubin:
albumin molar ratio to 3:1
 BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY CONTED
 In normal conditions, toxic unbound free bilirubin circulating
in newborn is extremely low
 At plasma membrane of hepatocytes, a proportion of bilirubin
is transferred across the cell and bound to ligandin
 Ligandintransports bilirubin from the plasma membrane to the
endoplasmic reticulum where conjugation of bilirubin occurs
 Conversion from nonpolar and insoluble form to a water
soluble conjugate to facilitate excretion into the bile occurs
here.
 BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY CONTD
 Bilirubin combined enzymatically with a sugar glucuronic acid
producing bilirubin monoglucuronide and diglucuronide pigments that
are more water soluble and sufficiently polar to be excreted into the
bile or filtered through the kidney

 Bilirubinconjugate in the intestines acted upon by intestinal flora to

produce urobilirubin and stercrobilin

 Urobilin re-absorbed and excreted in urine as urobilin

BILIRUBIN METABOLISM/
PATHOPHYSIOLOGY CONTD
 As a result of fewer bacteria in infants, greater
activity of the deconjugating, enzyme β-
glucuronidase in the intestine, hence conjugated
bilirubin is not converted to urobilinogen but
hydrolyzed to unconjugated bilirubin which is
reasbsorbed and increases bilirubin load in the liver
.
 CAUSES OF JAUNDICE

1. G6PD deficiency 17.7%

2. ABO incompatibility 6.1%
3. Rh incompatibility 2.9%
4. Sepsis 7.4%
5. Polycythemia 2.1%
6. Extravasations 4.9%
7. Idiopathic 57.8%
8. Oxytocin 0.8%
 AGE AT ONSET OF JAUNDICE

Less than 24nrs of birth

 Rh isomunization
 ABO and minor blood groups
 Intrauterine infants (TORCH+ HIV),Malaria, Bacteria
 G6PD deficiency
24-72hrs of age
 Physiological
 sepsis
 AGE AT ONSET OF JAUNDICE
CONTED
 Polycythemia
 Extravasations
 Increased enterohepatic circulation

After 72hrs of age

 Sepsis
 Neonatal hepatitis
 Extrahepatic biliary atresia.
 AGE AT ONSET OF JAUNDICE
CONTED
 Breastmilk jaundice
 Metabolic (eg. galactosaemia, tyrosaemia,
fructoseamia, alpha-1-antitrypsin deficiency, cystic
fibrosis, hypertrophic pyloric stenosis and
intestinal obstruction
 TYPES

 Physiologic
 Pathologic

PHYSIOLOGIC
 Bilirubin rises to over 2mg/dl in the first week of life
 It peaks in full term infants with 6-8mg/dl by day 3-4 and then
gradually falls
 In premature infants peak may be 10-12mg/dl by the 5th-6th day of
life.
 RISK FACTORS FOR
HYPERBILIRUBINAEMIA IN NEONATES

A. Increased bilirubin production

 Increased red blood cell volume (RBC) per kg body weight
 Decreased RBC survival (90 versus 120 days)
 Increased ineffective erythropoiesis and increased turnover of
non-haemoglobin heme protein
B. Increased enterohepatic circulation
 High level of intestinal β-glucuronidase
 Preponderance of bilirubin monoglucuronide over diglucuronide
 FACTORS FOR RISK OF
HYPERBILIRUBINAEMIA
IN NEONATES CONTED
 Decreased intestinal bacteria
 Decreased gut motility with poor evacuation of bilirubin-laden meconium

C. Defective uptake of bilirubin from plasma

 Decreased ligandin
 Binding of ligandin by other anions
D. Defective conjugation due to decreased Uridine
diphosphoglucuronide transferase(UDPGT)
E. Decreased hepatic excretion of bilirubin
 DANGERS OF HYPERBILIRUBINAEMIA

 Free bilirubin damages brain cells

 It’s low solubility allows it aggregates in tissues
 By binding to nerve terminals, causes a reversible
lowering of membrane potentials and decrease in
nerve conductions.
 Higher concentrations injures nerve terminals and
bilirubin penetrates the axons with retrograde uptake
into the cell body
 DANGER OF HYPERBILIRUBINAEMIA
CONTED

 Damage may become permanent with the

destruction of cell body, pyknosis, death and then
phagocytosis
 Damage is localized to basal ganglia, the
hippocampus, the thalamus and other areas may be
due to regional blood flow and preferential binding
of bilirubin found in synaptic and dentritic regions
of the brain.
WHAT ARE THE FACTORS
INFLUENCING TOXICITY?
 FACTORS INFLUENCING TOXICITY

 Complex and incompletely understood

 Total bilirubin level.
 Serum albumin concentration
 Binding of bilirubin to albumin
 Penetration of bilirubin into the brain
 Vulnerability of brain cells to the toxic effects of
bilirubin
FACTORS INFLUENCING TOXICITY CONTED

 Drugs can displace bilirubin in albumin binding

sites
 Anoxia
 Hypercarbia
 Hyperosmolality can open up blood brain barrier.
COMPLICATION OF BILIRUBIN TOXICITY

BILIRUBIN ENCEPHALOPATHY
(KERNICTERUS)
 Yellow nuclear staining of the brain
Three clinical stages;

STAGE 1
Lettargy, poor feeding, vomiting, high pitched cry, decreased
tone and poor moro’s reflex
BILIRUBIN ENCEPHALOPATHY CONTED

 STAGE II
Fever, Rigidity, opisthotonous, seizures, oculolgyric
crisis, paralysis of upward gaze

STAGE III
Decreased spasticity after about a week.
 COMPLICATIONS OF
KERNICTERUS

 Extra-pyramidal disturbances
 Auditory impairments
 Upward gaze paralysis
 Dental enamel dysplasias
 Athetosis
 Cerebral palsy
 High frequency sensorineural deafness.
Management

The primary focus of management of

hyperbilirubinaemia is to reduce the incidence of
severe hyperbilirubinaemia and prevent bilirubin
encephalopathy
History
Physical Examination
 MANAGEMENT

Approximate clinical Assessment;

 Manifestation on the face at serum level of 5mg/dl

 Yellow staining of the trunk correlate with 10-15mg/dl

 Palms and soles stained correlate15mg/dl and above

 Such progression less well appreciated in preterm infants.

 MANAGEMENT CONTED

 Severity related to depth of jaundice

 Despite improvement of the mechanism of bilirubin

neurotoxicity ,ability to predict which babies are
greater risks remains imprecise.

 Most common reason for readmission of babies back to

hospital after discharged
Management contd.

Investigations
Total bilirubin
Conjugated bilirubin
FBC
Retic counts
Blood film report
G6PD status
Management cont'd

Blood group
Combs test
Urinalysis
 MANAGEMENT CONTED

Mainly two methods;

 Phototherapy
 Exchange blood transfusion (EBT)

PHOTOTHERAPY
 Main indication is pathologic jaundice
 For preterms, prophylactic phototherapy is encouraged
and advocated
 COMPLICATIONS OF PHOTOTHERAPY

1. Dehydration
2. Bronze baby syndrome
3. Diarrhoea (green loose stool)
4. Abdominal distention
5. Eye damages
6. Hypothermia
7. Dermatitis
 MECHANISM OF PHOTOTHERAPY

1. Photo-oxidation
2. Configurational isomerization
3. Structural isomerization

 In configurational isomerization, the ZZ isomers of bilirubin is converted to the

ZE,EZ and EE isoforms

 The ZE isoforms maintain the polar groups at one end of bilirubin molecule and
enables it to be excreted in the bile.
MECHANISM OF PHOTOTHERAPY CONTED

 The structural isomer, lumirubin, major excretory product of phototherapy

 This structural change is irreversible and allows the more polar bilirubin to be
excreted in bile and urine

 Blue lights most effective for phototherapy with wavelength (450nm) minimum
irradiance of 6μw/cm/nm
PRACTICAL STEPS FOR ADMINISTERING
PHOTO THERAPY

1. Place baby naked under phototherapy

2. Cover eyes (blindfold) and genitals (in males) and lower abdomen (in female)

3. Mother should be encouraged to remove her baby and breastfeed every 2-3hours
4. Whenever baby is put back, the posture should be changed every time from
prone to supine and vice versa
PRACTICAL STEPS FOR ADMINISTERING
PHOTO THERAPY CONTED

5. Hydration ,fluid and electrolyte (especially in preterm babies) should be

monitored.

6. Mother should be reassured about the transient benign nature of greenish loose
stools and rashes that may be seen.

7. Irradiance meter efficacy should be checked every 2months

8. Not recommended for conjugated hyperbilirubinaemia.

EXCHANGE BLOOD TRANSFUSION (EBT)

INDICATIONS
 Absolute
 Relative

ABSOLUTE INDICATIONS
1. Cord bilirubin of 4mg/dl or more
2. Cord haemogram of 10mg/dl or less
3. Bilirubin level ≥10mg/kg
EXCHANGE BLOOD TRANSFUSION
(EBT)CONTED
4. Rate of rise of bilirubin ≥ 0.75mg/hour

5. Rate of rise of bilirubin ≥ 5mg in the first 24hours or per day

6. For full term neonates bilirubin level ≥ 20mg/dl

7. For preterm neonates bilirubin level ≥ 15mg/dl

8. Kernicterus.
 RELATIVE INDICATIONS

1. Sepsis

2. Priapism

3. Stroke in sickle cell disease

 COMPLICATIONS

Early complications
 Hypovolaemia
 Hypervolaemia
 Apnoea, bradycardia, vasospasm, hypoglycaemia,
hypomagnesaemia, hypothension
 Congestive cardiac failure
 Anaemia
 Infections
 thrombosis
 COMPLICATIONS CONTED

Late complications
 Hepatitis
 Inspissated bile syndrome
 Malaria infections
 HIV infections
 TECHNIQUE (Procedure)

TECHNIQUE:
 Fresh whole blood
 Must not be older than 3days
 Properly cross matched blood against mother’s blood
 Screen for HIV, Hepatitis, malaria
 The in- out method
 The continuous flow method
 Double volume exchange is 2x80ml/kg is 160ml/kg
 TECHNIQUE CONTED

 Infusion of calcium gluconate 1ml after every

100ml of blood is given
 Time for procedure not less than75mins and not
more than 90mins
 CONCLUSION
(Hyperbilirubinaemia) can be mild, moderate, and severe.
Severe consequences can arise leading to long term complications in the child and
agony in the family if not properly and timely addressed. Time is of essence both
on the part of parents noticing it early and reporting or assessing health care
immediately, and the health care giver to recognize it immediately and immediately
do the needful. This is to avoid the unpleasant long term complications and
consequences that may arise.

Always remember “A stitch in Time saves nine”.

 REFERENCES

1. Kramer IT. Advancdement of dermal icterus in the jaundice newborn. Amer. J.

Dischild 1969;118;454-458.

2. Seidman DS, Stevenson DK, Zivanti E, Gala G. Hospital readmission due to

neonatal hyperbilirubinaemia Peadriatrics 1995;96:726-729.

3. Ives KN. Neonatal jaundice. Rennice JM, Robert NC(Eds). Testbook of

Neonatology,3rd edition. Churchill livingstone ;Edinburgh 1999;715-732
 REFERENCES CONTED

4. Narang A., Geeta G, Praveen K. Neonatal jaundice. An analysis of 551cases.

Indian Pediatr 1997;34;429-432

5. Cloherty JP. Neonatal Hyperbilirubinaemia In: Manual of neonatal care. 3 rd

Edn.Philadephia, Lippincott, 1991;298-334
THANK YOU FOR
LISTENING!!!