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child and family > neonatal jaundice > Flashcards

neonatal jaundice Flashcards

1
Q

where do babies get jaundice first

A

face

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2
Q

bilirubin metabolism

A

unconjugated bilirubin is metabolised by the liver to conjugated bilirubin which can be excreted into the gut

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3
Q

why are babies inefficient at managing bilirubin

A
  • liver metabolism relies on bilirubin uptake via ligandin and then conjugation by uridine diphosphoglucuronyltransferase (UDPGT)
  • both ligandin and UDPGT are low in the new born making newborns inefficient
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4
Q

what is enterohepatic cirulation

A

in newborns a percentage reverts to unconjugated bilirubin and is recirculated into the blood stream

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5
Q

how can gilberts disease affect jaundice

A
  • mutation of the UGT1A1 gene
  • reduces bilirubin-UGT
  • makes jaundice worse
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6
Q

what happens when bilirubin crosses the BBB

A
  • causes encephalopathy which can lead to kernicterus

- small risk of cerebral palsy with high levels

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7
Q

risk factors for brain damage by bilirubin

A
  • decreasing gestation
  • asphyxia
  • acidosis
  • hypoxia
  • hypothermia
  • meningitis
  • sepsis
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8
Q

causes of neonatal jaundice

A

physiological (normal)

pathological

  • haemolysis
  • sepsis
  • metabolic disorders
  • liver disease
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9
Q

at what hours is jaundice seemed pathological

A

0-24 hours

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10
Q

when is jaundice seemed physiological

A

24-72 hours

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11
Q

what causes physiological jaundice

A
  • increased production
  • decreased uptake and binding by liver cells
  • decreased conjugation
  • decreased excretion
  • increased enterohepatic circulation of bilirubin
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12
Q

causes of pathological jaundice

A
  • due to haemolysis
  • hepatitis
  • ABO incompatibility
  • Rh immunisation
  • sepsis
  • red cell enzyme defects
  • red cell membrane defects
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13
Q

investigation of early pathological jaundice

A
  • total bilirubin concentration
  • maternal blood group and antibody titres
  • baby’s blood group
  • full blood count
  • CRP if maybe infection
  • measure conjugated bilirubin if clinical concern
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14
Q

what does bilirubin encephalopathy present with

A
  • lethargy
  • temperature instability
  • hypotonia
  • arching of the head, neck and back
  • spasticity
  • seizures
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15
Q

what is jaundice at 24 hours - 10 days

A

jaundice that is physiological but its so so high that it is pathological
called ‘too high’ jaundice

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16
Q

causes of ‘too high’ jaundice

A
  • mild dehydration
  • insufficient milk supply
  • breakdown of extravasted blood
  • some is haemolysis
  • infection
  • gut obstruction causing increased extrahepatic circulation
17
Q

what is prolonged jaundice

A

> 14 days term
or
21 days preterm

18
Q

causes of persistent unconjugated hyperbilirubinaemia

A
  • breast milk jaundice
  • poor milk intake
  • haemolysis
  • infection (especially UTI)
  • hypothyroidism (babies are screened for this)
19
Q

causes of persistent conjugated hyperbilirubinaemia

A

NOT NORMAL

  • hepatitis (caused by injection or metabolic disorders)
  • biliary atresia
20
Q

what is biliary atresia

A
  • rare disorder causing obstructive jaundice which is fatal if not treated
  • infants usually have pale stools and dark urine
  • requires surgery
21
Q

presentation of breast milk jaundice

A
  • persistent jaundice in otherwise healthy breast fed baby
  • normal conjugated portion
  • normal FBC and blood group
  • no sign of infection
  • thriving
  • reassurance and no further action
22
Q

treatment of jaundice

A
  • treat cause if there is one
  • adequate feeding/hydration
  • enteral feeding
  • breast milk is best, may need formula
  • sometimes tube feeding
  • phototherapy is mainstay
  • exchange transfusion
  • IV immunoglobulin
23
Q

signs that the jaundice is likely physiological

A
  • onset day 2
  • peak day 5
  • resolve by day 10-14
  • otherwise well infant
24
Q

signs that the jaundice is likely pathological

A
  • onset day 1
  • peak day is variable
  • prolonged after day 14
  • symptoms and signs of aetiological cause

child and family (20 decks)

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