Jaundice Flashcards

1
Q

Neonatal jaundice

A

Jaundice is the yellow discolouration of the skin, sclera and mucus membranes caused by deposition of bilirubin.

Visible when bilirubin is > 5mg/dl
Occurs in 60% of term babies and 80% of preterm babies

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2
Q

What I’d biliburin

A
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3
Q

Indirect/Unconjugated

A

Insoluble in water
Binds to albumin and travels to the liver where it becomes conjugated/water soluble
Can cross blood-brain barrier
Toxic to the brain in high levels

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4
Q

Direct conjugated

A

Direct/Conjugated
Soluble in water and is made by liver from indirect bilirubin
Conjugated with glucoronic-acid
Excreted in urine and stools
Not

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5
Q

Mechanism of neonatal jaundice

A

Increased bilirubin load due to high haemoglobin concentration
- The normal newborn infant.
- Hemolysis
- Cephalohematoma or bruising

  1. Decreased bilirubin conjugation in liver
    • Decreased uridine glucoronyl transferase activity
    • Glucoronyl transferase deficiency
  2. Defective bilirubin excretion
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6
Q

Types of jaundice

A

Physiological jaundice
Appears between 24-72hrs of age.
Peaks on 4th to 5th day of life in term neonates and 7th day in preterm.
Disappears by day 10-14 of life.
Unconjugated bilirubin is the predominant form
Its serum level is usually less than 15mg/dl.
Clinically not detectable after 14 days.

Pathologic jaundice
Appears within 24 hours of life,
Due to an increase in serum bilirubin beyond 5mg/dl per day.
Persists for more than 2 weeks of life
Conjugated form is predominant.
Pale stools, dark urine.
Signs of underlying

Breastfeeding jaundice
Jaundice that occurs in exclusively breastfed babies, appearing between 24-72 hrs of life.
Caused by decreased frequency of breastfeeding which leads to elevated bilirubin levels due to increased reabsorption of bilirubin by the intestines.
Management includes encouraging mother to breastfeed frequently

Breastmilk jaundice
Commonest cause of prolonged jaundice in term neonates. Noted in the 3rd week of life
Caused by prolonged increased enterohepatic circulation of bilirubin
Enzyme B-glucoronidase deconjugates bilirubin remaining in intestines which is returned to liver for reconjugation.
But because neonates have a higher level of this enzyme, higher levels of unconjugated bilirubin occurs and leads to increased enterohepatic circulation.
Encourage mothers to feed frequently & bilirubin levels diminish gradually.

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6
Q

Types of jaundice

A

Physiological jaundice
Appears between 24-72hrs of age.
Peaks on 4th to 5th day of life in term neonates and 7th day in preterm.
Disappears by day 10-14 of life.
Unconjugated bilirubin is the predominant form
Its serum level is usually less than 15mg/dl.
Clinically not detectable after 14 days.

Pathologic j

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6
Q

Types of jaundice

A

Physiological jaundice
Appears between 24-72hrs of age.
Peaks on 4th to 5th day of life in term neonates and 7th day in preterm.
Disappears by day 10-14 of life.
Unconjugated bilirubin is the predominant form
Its serum level is usually less than 15mg/dl.
Clinically not detectable after 14 days.

Pathologic j

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7
Q

Causes of neonatal jaundicr

A
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8
Q

Pathological jaundice

A
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9
Q

Unconjugated jaundice

A

Hemolysis
RH, ABO and other blood group incompatibilities
Red blood cell membrane defects i.e Spherocytosis
Sepsis, DIC
Hematomas
Polycythemia

  1. Non-hemolysis
    Breast milk jaundice
    Crigler Najjar syndrome
    Gilbert syndrome
    Hypothyrodism
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10
Q

Conjugated bilirubin

A
  1. Hepatic causes
    Idiopathic neonatal hepatitis
    Infections – TORCHES, Sepsis
    Inborn errors of metabolism – galactosemia
    Dubin Johnson syndrome/ Rotor’s syndrome
  2. Post hepatic
    Biliary atresia
    Bile duct stenosis
    Choledochal cyst
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11
Q

Risk factors of jaundice

A

J – jaundice within 1st 24 hrs of life or prematurity
A -a sibling that was jaundiced as a neonate
U - unrecognized hemolysis ( AB0 )
N – Non optimal nursing/sucking
D – deficiency of G6PD , drugs
I – infections
C – cephalohematoma /bruising
E – East Asian/North Indian

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12
Q

Clinical presentation

A

Yellow discolouration of the eyes or body
Fever
Vomiting
Inability to suck
Features of failure to thrive
Abdominal distension
Passage of pale stools and dark urine

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13
Q

History

A

Birth weight, gestation and postnatal age
Onset/duration/progression
Colour of stools and urine
Feeding history
Weight progression
Maternal hx
Antenatal
-booking, illnesses, infections
Drugs
- herbal, NSAIDS
Medical
- blood group, haemolytic disease
- Birth history – trauma

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14
Q

Clinical examination

A

Pallor
Dehydration
Weight loss/failure to thrive
Fever
Hepatosplenomegaly
Evidence of birth trauma
Neurological fallout

15
Q

Investigations

A

Bilirubin measurement – total and conjugated serum levels
Full blood count and blood smear
Reticulocyte count
Blood grouping of mother & baby
Coombs test
Urinalysis & MCS
Electrolytes
Liver function tests
Septic markers
Thyroid function tests
Ultrasound

16
Q

Kernicterus

A
  • Pathological diagnosis referring to yellow staining of the brain caused by bilirubin deposition associated with neuronal necrosis and gliosis.
    It is the direct consequence of very high level of unconjugated bilirubin.
    Parts commonly affected – Basal ganglia, brain stem nuclei, cerebellar nuclei, hippocampus, anterior horn cells of spinal cord.
    It develops in 30% of infants with untreated hemolytic disease and bilirubin > 25-30mg/dl
    More than 75% of infants die and 80% of affected have bilateral choreoathetosis with involuntary spasms.
    Later in life, delayed motor skills, hearing loss, movement disorders etc
17
Q

Manifestations of kernius

A

Stage 1 – hypotonia, lethargy, high pitched cry and poor suck
Stage 2 – hypertonia, rigidity, fever, seizures oculogyric crisis
Stage 3 – hypotonia replaces hypertonia after first week