Neonatal Jaundice: Addisu An

Neonatal Jaundice
 Jaundice is yellow discoloration of the sclera, skin, and

mucous membranes due to bilirubin deposition.
 Appears when total bilirubin is more than 5-7 mg /dl
 Jaundice is seen in the first week of life in 60% of term
and 80 % of preterm babies
 Hyperbilirubinemia is an increase in the serum
bilirubin manifested clinically by jaundice.
Addisu An 04/24/2021
Jaun…
2
 Bilirubin- degradation product of heme

Unconjugated(Indirect acting)
Conjugated (Direct acting)
 Bilirubin has physiologic role in the body as anti

oxidant but indirect or unconjugated bilirubin has
neurotoxic effect when elevated.
 Even though its not neurotoxic, the direct is a sign of
serious systemic or hepatic disorder.
Destruction of RBC none RBC components
Hemoglobin
globin heme 3
heme oxygenase
biliverdin
biliverdin redactase
bilirubin (IX alpha)
Albumin
bilirubin, IX alpha + albumin
Ligandin ( Y protein & Z protein) entro-hepatic circulation

Uridine diphosphate glucornyl
transferase enzyme
bilirubin glucuronide (conjugated bilirubin)
intestine( stercobilin + urobilinogen)
Classification of Jaundice
4
 Physiologic jaundice
 Pathologic jaundice
i.Direct (conjugated).
ii. Indirect(unconjugated).
 Breast Milk jaundice
 Breast Feeding jaundice
Physiologic Jaundice(Icterus Neonatorum)
5
 Jaundice that appears by the 2nd or 3rd day of life

 Peak bilirubin occurs at 3–5 days of age, with a total
bilirubin of no more than 15 mg/dl.
 Rate of rise of bilirubin is <5mg/dl/24hrs
 Direct bilirubin <2mg/dl
 Declines by the 5-7th day of life to below 2mg/dl
 TSB level in the low-risk zone.
 Onset and resolution may be delayed in premature
infants
Cause of physiologic jaundice
6
 Increased bilirubin production

Increased fetal RBC value

 Shorter life span of RBC(70-90days)
 Increased enterohepatic circulation

• Increased beta glucuronidase activity
 Decreased hepatic uptake, conjugation and excretion

 Y protein (ligandin) is diminished
 UDPG enzyme activity is decreased
Management of physiologic jaundice
7
 no specific treatment is generally required

 Adequate feeding
 Careful observation of newborn will help to distinguish
b/n healthy babies with normal physiological response
 In premature babies, rising bilirubin level to critical
level require use of phototherapy or phenobarbital
administration
Breast Milk Jaundice
8
 Develops in about 2% of breast fed infants after 7th day

 Concentration may reach as high as 10-30mg/dl on 2nd
-3rd week of life
 Believed to be due to glucuronidase in breast milk
 Cessation of breast milk for 1-2 days results in decline of
bilirubin level
 Resuming BF doesn’t cause return of hyperbilirubinemia.
Breast Feeding Jaundice
9
 Occurs in the 1st week

 May be due to;
-- milk intake with dehydration or E-H circulation
--- caloric intake
 Frequent BF, rooming in with night feeding, and

discouraging 5% dextrose/water supplementation may
reduce the incidence
Pathologic Hyperbilirubinemia
10
 Time of appearance is with in first 24-36 hrs. of life

 The rate of rise of bilirubin is > 5mg/dl/24hr
 Serum bilirubin is greater than 12mg/dl in term and
greater than 10-14mg/dl in preterm babies
 If jaundice persists after 10-14days of life
 If direct bilirubin is >2mg/dl
Physiological vs. Pathological Jaundice
11
No Features Physiologic Pathological
Jaundice Jaundice
1 Clinical onset of jaundice (after >24 hrs <24 hrs

birth)
2 Jaundice still clinically visible Term < 8 days Term ≥8 days

(day after birth) Preterm < 14 days Preterm > 14 days
3 Peak TSB Term < 12 mg/dl Term > 12 mg/dl

Preterm < 15 mg/dl Preterm > 15 mg/dl
4 Rise in TSB < 5mg/dl/24 hrs > 5mg/dl/24 hrs
5 Conjugated serum bilirubin level <2mg/dl >2mg/dl or 15 % of

TB
Direct/Conjugated Hyperbilirubinemia
12
 Is due to failure to excrete CB from the hepatocytes into

the duodenum.
 It is manifested by a CB level > 15-20% of the total
bilirubin level.
 It may be associated with hepatomegaly, splenomegaly,
pale stools, and dark urine.
Indirect/Unconjugated Hyperbilirubinemia
13
 Unconjugated hyperbilirubinemia may be caused/

increased by any factor that:
1. Increases the load of bilirubin to be metabolized by the
liver
 Hemolytic anemia, polycythemia, bruising or internal
hemorrhage, shortened red blood cell life as a result of
immaturity or transfusion of cells, increased enter-
hepatic circulation, infection
Etiolog…
14
2. Damages or reduces the activity of the transferase

enzyme or other related enzymes (genetic deficiency,
hypoxia, infection, hypothermia, thyroid deficiency)
3. Competes for or blocks the transferase enzyme ,drugs
and other substances requiring glucuronic acid
conjugation for excretion
4. Absence or decreased amounts of the enzyme or to
reduction of bilirubin uptake by liver cells (genetic defect,
and prematurity).
Risk factors for unconjugated hyperbilirbinemia
15
 Jaundice visible on the first day of life

 A sibling with neonatal jaundice/anemia
 Unrecognized hemolysis(RH/ABO etc. )
 Non optimal feeding(breast/formula)
 Deficiency of UDP-glucuronyl transferase def.(Crigler-
Najar, Gillbert disease.
 Infection (viral/bacterial), Infant of diabetic mother,
Immaturity
 Cephalhematoma/bruising, central Hct>65%
 East Asian, Mediterranian,Native American
Evaluation
16
 Laboratory Tests
 Totaland direct serum bilirubin level
 Blood type (ABO, Rh)
 Direct antibody test (Coombs’ test)

 Serum albumin
 CBC with differential

 Peripheral blood smear for RBC morphology and
 Reticulocyte count
17
Management of unconjugated Bilirubin
18
 Regardless of the cause the first goal of therapy is

• To prevent the UCB from reaching neurotoxic level
• To prevent severe anemia & hypoxia
 Modes of treatment
 phototherapy,
 exchange transfusion and
 pharmacotherapy
A. Phototherapy
19
 Uses blue-green spectrum light of wavelength 425–475

nm which is absorbed by unconjugated bilirubin in the
skin and converted to a water-soluble stereoisomer that
can be excreted in bile without conjugation.
 Is not a replacement for exchange transfusion
 Phototherapy decreases the need for exchange
transfusion
 Its effect is seen with in the first 6-12hrs of use
Photothera…
20
 Phototherapy works by infusing discrete photons of

energy similar to the molecules of a drug.
 These photons are absorbed by bilirubin molecules in
the skin and subcutaneous tissue, just as drug molecules
bind to a receptor.
 The bilirubin then undergoes photochemical reactions
(isomerization) to form execrable isomers and
breakdown products that can bypass the liver’s
conjugating system and be excreted without further
metabolism.
 Some photo products also are excreted in the urine.
Photothera…
21
Technique
 Infant
is usually placed at 45-60cm distance from the
light with skin exposed.
 Largest surface area possible exposed
Indications
 Pathologic jaundice
 Prophylactic in VLBW infants
Phototherapy Precautions
22
Cover eyes and genitalia

Repositioned the new born at least every 2 hours to
permit the light to reach all surface of the skin
Discontinue phototherapy and remove eye patches at
least once per 8 hour shift or at the time of feeding (6hrs
on and 6hrs off).
Monitor fluid and electrolyte status
Monitor temperature every 4-8 hours
Determine TSB 6 hourly
Side effects of Phototherapy
23
Dehydration -- increased insensible water loss

--- loose stools
Skin rashes
Retinal injury
Bronze Baby Syndrome
 Dark grayish discoloration of skin
 Occur in infants with significant elevation of direct-
reacting bilirubin
 May last for many months
Photothera…
24
 Phototherapy D/C when

1. Bilirubin level is lower enough to eliminate the risk
of kernicterus
2. the risk factor for the newborn is resolved
3. the neonate is older enough to handle the bilirubin
load
For infants receiving intensive phototherapy:
25
 If TSB ≥25 mg/dL, repeat TSB within 2–3 hr

 If TSB 20–25 mg/dL, repeat within 3–4 hr.
 If TSB <20 mg/dL, repeat in 4–6 hr.
 If TSB continues to fall, repeat in 8–12 hr
 If TSB is not decreasing or is moving closer to level for
exchange transfusion consider it.
 When TSB is <13–14 mg/dL, discontinue phototherapy.
B. Exchange Transfusion
26
 Double-volume exchange transfusion is most often

used in infants with extreme hyperbilirubinemia.
Indication:
 TSB > 25mg/dL
 Infant has signs of kernicterus
 When intensive phototherapy has not lowered TSB by at least
0.5 mg/dL/h after 4 hrs & risk of kernicterus > risk of the
procedure.
Exchange Transfus…
27
 The amount of blood volume to be exchanged is

equivalent to 2x the blood volume of the baby (85ml/kg )
 Use fresh blood less than 24 hours
 Do procedure after umbilical catheterization using
aseptic technique
 The amount of blood to be removed at a time is 5ml to
20 ml
28
 Double volume exchange transfusion

- replaces 85% of circulating newborn RBC
- reduces bilirubin level by half of the previous pre
exchange value
- Besides removing bilirubin corrects anemia
 Baby needs to continue phototherapy after exchange
transfusion
 O negative blood is the most preferred type of blood for
exchange transfusion.
29
Monitor V/S
Post transfusion HCT 4-6 hours after the procedure.
Bilirubin 4 hourly after the procedure.
 RBS every 30-60 minutes during the procedure and 2-4
hourly for the first 24 hours after procedure.
Calcium gluconate slowly via a peripheral vein under
strict cardiac monitoring after every 100ml of blood is
exchanged.
Cloxacillin 50mg/Kg bid for 2- 3 days and gentamicin
5mg/kg BID for 2-3 days.
Keep baby NPO for 4 hours before and after procedure.
Recommendations for the management of hyperbilirubinemia in preterm infants
30
Complications
31
 Thrombocytopenia
 Portal vein thrombosis/perforation
 Necrotizing Enterocolitis
 Cardiac arrythmias, volume overload
 Hypocalcemia, Hypomagnesemia, Hypoglycemia, and
Hyperkalemia
 Acidosis
 Respiratory & metabolic acidosis
 HIV, Hepatitis B & C infection
 Death
C. Pharmacologic Therapy
32
 Pharmacologic agents
 to interfere with heme degradation and bilirubin
production,
 accelerate the normal metabolic pathways for
bilirubin clearance,
 inhibit the enterohepatic circulation of bilirubin
Pharmacologic…
33
 Phenobarbital
 Accelerates metabolic pathways for bilirubin clearance
 Protoporphyrins
 Inhibit heme oxygenase
 Tin and zinc protoporphyrin or mesoporphyrin (Sn-PP,
Zn-PP; Sn-MP, Zn-MP).
 IV gamma globulin
 inhibits
hemolysis
 Act. Charcoal
 binds bili in the intestine decreased E-H circulation
Bilirubin Toxicity
34
 Unconjugated bilirubin anion is the agent of bilirubin

neurotoxicity. The anion binds to the phospholipids
(gangliosides) of neuronal plasma membranes causing
injury, which then allows more anion to enter the
neuron.
 Intracellular bilirubin anion binds to the membrane
phospholipids of subcellular organelles, causing
impaired energy metabolism, altered excitatory amino
acid homeostasis, excitotoxic neuronal injury, and cell
death.
Acute Bilirubin Encephalopathy(ABE)
35
 Acute Bilirubin Encephalopathy: clinical nervous

system manifestations caused by bilirubin toxicity
ABE describes the signs and symptoms of brain damage
in the newborn.
Typical Features:
 Lethargy, poor feeding.
 Irritability, high-pitched cry.
 Arching of the neck (retrocollis) and trunk

(opisthotonos).
 Apnea, seizures, coma (late).
Chronic Bilirubin Encephalopathy(Kernicterus)
36
 Kernicterus is the pathologic finding of staining of basal

ganglia and brainstem nuclei associated with chronic
permanent brain injury.
Clinical Features
 Extrapyramidal movement disorder (choreoathetoid
cerebral palsy).
 Gaze abnormality, especially limitation of upward gaze.
 Auditory disturbances.
 Dysplasia of the enamel of the deciduous teeth.
BIND Scoring System
37
1 Point 2 Points 3 Points

(Nonspecific, (Progressive (Advanced
Subtle) Toxicity) Toxicity)
Mental status Sleepy, poor feeding Lethargy + Semi-coma,

irritability seizures, apnea
Muscle tone Slight decrease Hypertonia or Markedly

hypotonia, increased
depending on (opisthotonus) or
arousal state decreased
or or
Mild arching Bicycling
Cry High-pitched Shrill Inconsolable
38
Addisu An
THANK U!!! 04/24/2021

Neonatal Jaundice: Addisu An

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Neonatal Jaundice

 Jaundice is yellow discoloration of the sclera, skin, and

 Bilirubin- degradation product of heme

 Bilirubin has physiologic role in the body as anti

Ligandin ( Y protein & Z protein) entro-hepatic circulation

bilirubin glucuronide (conjugated bilirubin)

intestine( stercobilin + urobilinogen)

 Jaundice that appears by the 2nd or 3rd day of life

 Increased bilirubin production

 Shorter life span of RBC(70-90days)

 Increased enterohepatic circulation

 Decreased hepatic uptake, conjugation and excretion

 UDPG enzyme activity is decreased

 no specific treatment is generally required

 Develops in about 2% of breast fed infants after 7th day

 Occurs in the 1st week

--- caloric intake

 Frequent BF, rooming in with night feeding, and

 Time of appearance is with in first 24-36 hrs. of life

 If direct bilirubin is >2mg/dl

1 Clinical onset of jaundice (after >24 hrs <24 hrs

2 Jaundice still clinically visible Term < 8 days Term ≥8 days

3 Peak TSB Term < 12 mg/dl Term > 12 mg/dl

4 Rise in TSB < 5mg/dl/24 hrs > 5mg/dl/24 hrs

5 Conjugated serum bilirubin level <2mg/dl >2mg/dl or 15 % of

 Is due to failure to excrete CB from the hepatocytes into

 Unconjugated hyperbilirubinemia may be caused/

2. Damages or reduces the activity of the transferase

 Jaundice visible on the first day of life

 Direct antibody test (Coombs’ test)

 CBC with differential

 Regardless of the cause the first goal of therapy is

 Uses blue-green spectrum light of wavelength 425–475

 Phototherapy works by infusing discrete photons of

 Prophylactic in VLBW infants

Cover eyes and genitalia

Dehydration -- increased insensible water loss

 Phototherapy D/C when

 If TSB ≥25 mg/dL, repeat TSB within 2–3 hr

 Double-volume exchange transfusion is most often

 The amount of blood volume to be exchanged is

 Double volume exchange transfusion

 Unconjugated bilirubin anion is the agent of bilirubin

 Acute Bilirubin Encephalopathy: clinical nervous

 Irritability, high-pitched cry.

 Arching of the neck (retrocollis) and trunk

 Kernicterus is the pathologic finding of staining of basal

 Dysplasia of the enamel of the deciduous teeth.

1 Point 2 Points 3 Points

Mental status Sleepy, poor feeding Lethargy + Semi-coma,

Muscle tone Slight decrease Hypertonia or Markedly

Mild arching Bicycling

Cry High-pitched Shrill Inconsolable

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