Neonatal jaundice

Prepared by first group

introduction
Jaundice :
INTRODUCTION
is defined as a yellow discoloration of the body tissue resulting
from the accumulation of excess bilirubin.

Neanatal Jaundice :
is the yellowish discoloration of the eyes, skin and mucous
membranes in the first month of life due to elevated level of
bilirubin in the blood.
(normal serum bilirubin is 1 mg/dl). Neonate appear jaundiced at
serum Bilirubin 7 mg/dl.

it is a common and, in most cases, harmless problem in

neonates.

The yellow discoloration may be as a result of elevation of either

the uncongugated or conjugated bilirubin.
 INTRODUCTION

Bilirubin may have a physiologic role as an antioxidant but

elevations of indirect,
unconjugated bilirubin are potentially neurotoxic.

Even though the conjugated form is not neurotoxic, direct

hyperbilirubinemia indicates a potentially serious hepatic
disorders or a systemic illness.

or management can result into either death or serious

neurological
problems.
Epidemiology
 Epidemiology
• Neonatal jaundice first been described in a Chinese textbook 1000
years ago.

• It is extremely common because almost every newborn develops an

unconjugated serum bilirubin level of more than 30 µmol/L (1.8
mg/dL) during the first week of life.

• Incidence varies with ethnicity and geography,Incidence is higher in

populations living at high altitudes.

• Risk of developing significant neonatal jaundice is higher in male

infants.

• Generally, the prevalence in hospital practice is estimated at

between 50-80%, being more common in preterm about 8%than in
term infants about 50%.
pathophysiology
classification
 classification
Neonatal jaundice classified based on etiology into:
Patholoical Jaundice:Classified based on tybe of
hyperbilirubineamia into:
1_Conguate hyperbilirubinimia
2_Unconguate hyperbilirubinemia
2_Physiological jaundice.
3_Breast feeding jaundice.
4_Hemolytic
Unconjugated jaundice.
Hyperbilirubinemia
High Total Serum Bilirubin (TSB) & conjugated bilirubin < 15 % of TSB
Causes: 2. Defective uptake
1-Bilirubin over production 3. Defective conjugatio
Increased rate of hemolysis (Reticulocyte count elevated) Glucoronyle transferase
Non hemolytic causes (normal reticulocyte count.) enzyme may be:
Extra vascular hemorrhage : Cephalhematoma & Internal hemorrhageo Absent
o Deficient
Elevated RBCs load (Polycythemia)
o Immature
Enhanced enterohepatic circulation of bilirubin 2ry to gastro intestinal stasis.
o Under stimulated
 classification
Conjugated Hyperbilirubinemia
Definition: Rise of total serum bilirubin with the
conjugated fraction > 15% of total Or > 2 mg/dl
Causes:
1.Defective secretion of conjugated bilirubin by
hepatocytes
a .Genetic
b. Acquired: (Neonatal hepatitis) due to:
Infections :
- Neonatal sepsis.
- Viral hepatitis .
- Idiopathic neonatal hepatitis
Metabolic :
- Galactosemia
- Tyrosinemia
 classification
2-Defective excretion due to bile flow obstruction
.

• Intrahepatic:
- Congenital intrahepatic biliary atresia.
-
• Extrahepatic:
- Congenital extrahepatic biliary atresia.
- Inspissated bile syndrome (Bile plu g

Etiology
Hemolysis of neonatal RBC’s due to transplacental passage of maternal
antibodies active against fetal RBCs. It includes:
1. Rh incompatibility; the mother is Rh negative and the baby is Rh positive
2. ABO incompatibility; the mother is usually group O and the fetus group A or B

Haemolytic Disease of the Newborn (HDN) (Erythroblastosis Foetalis)

 classification
2. Moderate hemolytic; present by:-
- Anemia at birth worsening rapidly over the 1st day with hepatosplenomegaly
- Marked indirect hyperBilirubinaemia develops within few hours and
progresses rapidly.
- Cases untreated usually die due to either kernicterus or anemic heart failure.
3. Mild hemolysis
- Mild hemolysis o mild anemia peaking at end of 3rd week.
- Unconjugated hyperbilinibinaemia at range of 16-20 mg/dl.
- May be splenomegaly
Breast Milk Jaundice:
Etiology :Unknown ; Breast milk may contain:
- Pregnandiole ĺ inhibit glucoronyle transferase enzyme.
- E glucoronidase: enhance entero hepatic circulation of bilirubin
 classification

Physiologic Jaundice
Etiology :
• Transient glucuronyl transferase enzyme immaturity .
• Metabolism of extra hemoglobin formed intrauterine
• Shorter life span of neonatal RBC’s
• Reduced Z & Y proteins (Ligandins) during the 1st week

Characters:
• Unconjugated hyperbilirubinemia (Direct bilirubin <1mg/dl)
• No pallor, organomegaly nor risk of kernicterus
• Diagnosed by exclusion (Well baby, No hemolysis, nor anemia)
Clinical features
 Clinical features
1-Yellowish discoloration of Skin and sclera:
that usually start on the face and once the bilirubin levels rise
in the blood, the yellow color moves to chest, abdomen and
finally the legs and arms.

2-Color of stool:
unconjugated hyperbilirubinemia(Dark )
conjugated hyperbilirubinemia(pale)
3-color of urine:
-usually normal unconjucated
hyperbilirubinemia.
-Dark conjugated
hyperbilirubinemia.
 Clinical features

4-possible concurrent problems: (Absent in physiological jaundice)

 risk of kernicterus: lethargy, fever, poor sucking &feeding, loss

of motor reflex, and high pitch-cry ( that's occur in unconjugated hype
emia)
 risk of anemia: pale and increase rate of breathing

 malabsorption and failure to thrive.

 hepatosplenomegaly.
Causes
 Causes
Physiological causes :
1/ Decrease RBC survival less than 90 days,
increase RBC Vol/kg , polycythemia of NB.

2/ Poor hepatic intake due to immature liver.

3/Increase entrohepatic circulation due to

high level of intestinal beta-glucuronidase.
delayed colonization by bacteria.
decrease gut motility
 Pathological causes

Unconjugated hyperbilirubinemia (hemolytic

/non-hemolytic )
conjugated hyperbilirubinemia (hepatic/post
hepatic )
 Causes
Unconjugated
hyperbilirubinemia
Hemolytic Non-Hemolytic
• Coombs test
postive • Breast milk
• ABO incompatibility
• Rh incompatibility jaundice.
• Coombs test • Cirggler Najjar
negative syndrome
• Spherocytosis ,
eplliptocytosis type1 and 2.
• G6PD • Gilbert
• Hemoglobinopathie syndrome.
s • Hypothyroidism
• Spesis
 Causes
conjugated hyperbilirubinemia
Hepatic Post Hepatic

• Idiopathic neonatal
Biliary atresia
hepatitis. .
• Dubin Jonhson
Bile duct
syndrome. .stenosis
• Infections CMV and
HIV,sepsis. Choledochal
.cyst
• Rotor's syndrome
 DIAGNOSIS
History and physical examination
 History
Family and maternal history is important for diagnosing neonatal
jaundice and the management approach.

For the family history, the following should be evaluated:

○ History of previous sibling developed neonatal jaundice
○ Family history of jaundice
○ Family history of hereditary hemolytic disorders
○ Family members with liver disease

○ For the maternal history, the following should be evaluated:

○ The history of pregnancy and delivery
○ Any maternal complications or illness during the pregnancy
○ Breastfeeding history
○ Usage of any drugs
 Physical Examination
Complete physical exam including evidence of hepatomegaly, splenomegaly.

Appearance of the patient

Patients with neonatal jaundice may appear drowsy in severe cases.[1]
○ Skin
○ Yellow skin due to deposition of bilirubin , Petichia
○ Eyes
○ Jaundice is usually best seen in the conjunctiva
○ Abdomen
○ Hepatomegaly ,splenomegaly may be present
○ Neurologic
○ A flapping tremor may be present
○ Changes in muscle tone
○ Seizures
○ Microcephaly in some cases
Investigations
 Investigations
 Bilirubin measurement
to determine the type of hyperbilirubinemia
• Serum bilirubin level (total and direct).
• Transcutaneous (bilirubinometer):
which uses a special light to measure bilirubin
in the skin.

 Full blood count

• Hemoglobin value.
• WBC count .

 CRP
 Reticulocyte count.
 Blood grouping (ABO and Rh) for baby and mother.
 Direct Coomb's test to detect maternal antibodies
that coat the baby's RBCs.

 Peripheral blood film for erythrocyte morpholygy.

 Enzyme assay: G6PD deficiency.

 Liver function test.

 Ultrasound if indicated .

 Thyroid function tests.

complications
 complications
Common complications of neonatal jaundice include the following:

1.Acute bilirubin encephalopathy:

Bilirubin is toxic to the brain and high levels may cause acute
bilirubin encephalopathy.
In the beginning, it may be asymptomatic or the infant is sleepy
and hypotonic.

If the encephalopathy not diagnosed early, more complications

will develop as lethargy, seizures, inability to feed, and apnea in
severe cases.
It is better to diagnose it early in order not to develop severe
cases of encephalopathy.
 complications
2.Kernicterus:

Kernicterus is the chronic neurologic dysfunction that

results from high levels of bilirubin that occurs due to
damage of the basal ganglia.

Kernicterus can present with the following features:

Hearing impairement
Gaze abnormality
Cerebral palsy like features(mental
retardation,seizure,speech impairment and
developmental delay)

The neurological manifestations of Kernicterus are

reversible with exchange transfusion and decreasing
Treatment
 Treatment
TREATMENT OF UNCONJUGATED HYPERBILIRUBINEMIA
 Aim of treatment
 1- reduce the incidence of severe hyperbilirubinaemia
2- Prevent bilirubin encephalopathy (kernicterus)
 Modalities include:
• Phototherapy
• Exchange blood transfusion
• . Pharmacotherapy

Phototherapy :

Is the use of high intensity light energy to reduce bilirubin levels on the skin
surface

Light is used in the white,blue, turquoise,and green wavelengths the range from
420-470nm2

Mechanism of action:conversation of insoluble bilirubin into soluble bilirubin

1-Photothrapy :
● Indications
Treatment
•TSB >15mg/dl term Technic:
• TSB>12mg/dl preterm • Distance between the light source
•TSB >5mg/dl within24 hours and baby:45 cm
Adjuvant to exchange transfusion
• Maximum amount of skin exposed
• Cover only eye and genital
● Contraindications:
• Porphyria
• Conjugated hyperbilirubinaemia - Bronze baby syndrome
• Unconjugated hyperbilirubinaemia (20mg/dl or >)
• Diseases with hypersensitivity to light
 Treatment
2-Exchange blood transfusion

● Done to rapidly lower the serum bilirubin concentration and/or

prevent further rise

● Indications

• Unconjugated hyperbilirubinemia of 20mg/dl and above in term or

15mg/dl and above LBW in preterm

• Serum bilirubin level up to 10mg/kg for other preterms

• Bilirubin level rising rapidly up to 5mg/dl/day

• Serum bilirubin >10mg/dl on the first day of life or 15mg/dl at 48hrs

of life

•Clinical signs of kernicterus

 Treatment
●Procedure
Exchange blood in aliquots and
• Take vital signs
document
• Empty the stomach - prevents aspiration
• Give 1ml of1 0 %calcium gluconate
after every 100ml slowly and listen to
• Ensure right blood is available
the heart alongside
• Maintain asepsis
• Take post EBT PCV and serum
bilirubin
• Catheterize umbilical vein and secure in place
• Replace all drugs given earlier if not
• Take pre EBT PCV and serum bilirubin
time for next dose

• Prevent hypoglycaemia- 200mg/kg

of IV glucose
3- Pharmacotherapy Treatment
• Not routine used because of ineffectiveness

• Phenobartitone

• Metalloprotoporphyrins (eg tin mesoporphirin)

• Oral agar (e.g Cholesteramine)

• Albumin infusion

• Intravenous immunoglobulin

Used for infants with Rh or ABO isoimmunization

-Inhibits haemolysis

Dose = 0.5-1 gm/kg/dose IV, repeat in 12hrs

 Treatment
Treatment of kernicters:

● Treatment of hyperbilirubinaemia

● Counselling/training the parents on coping

with the sequale

● Management of feeding difficulty

● Physiotherapy for limitation of disability

● Speech and language therapy (SAL(

 Treatment
TREATMENT OF CONJUGATED
HYPERBILIRUBINAEMIA

● Mainly supportive

• Parenteral vitamin k

• Vitamin A and D supplementation - prevents rickets

• Diet - low fat, medium chain triglyceride

• Phenobarbitone - helps bile exceretion

conclusion
 conclusion
 Jaundice presents with yellowness of skin
and mucous membranes
 The cause can be physiological or
pathological due to abnormalities in
bilirubin metabolism
 Unconjugated bilirubin is neurotoxic to the
brain and hence needs urgent attention
 Prompt diagnosis and management helps
to prevent severity and complications like
kernicterus
 Modalities of treatment include
 conclusion
Neonatal jaundice still contributes significant
to neonatal morbidity, mortality and long-
term handicap especially in the developing
countries. This is made worse by ignorance
on the part of parents and health workers
which contributes to delay in seeking proper
medical care.

However, education at primary health care

level, prompt diagnosis and referral to
appropriate specialist will go a long way to
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