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TAS Neonatal Medicine ✅ > Causes of Jaundice ✅ > Flashcards

Causes of Jaundice ✅ Flashcards

1
Q

What can the causes of hyperbilirubinaemia be divided into?

A
  • Increased bilirubin production due to high red cell turnover
  • Delayed bilirubin clearance
  • Conjugated hyperbilirubinaemia
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2
Q

What forms of bilirubin clearance can be delayed?

A
  • Conjugation
  • Biliary excretion
  • Faecal/urinary elimination
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3
Q

What are the causes of high red cell turnover?

A
  • Physiological
  • Polycythaemia
  • Immune haemolysis
  • RBC enyzme defects
  • RBC membrane abnormalities
  • Other causes of haemolysis
  • Haematomas
  • Maternal diabetes
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4
Q

Why might red cell turnover be high physiologically in a neonate?

A

High haemoglobin and red cell mass at birth and short RBC lifespan

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5
Q

What might cause immune haemolysis in a neonate?

A

Rb/ABO/other isoimmunisation

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6
Q

Give 2 examples of RBC enzyme defects

A
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency

- Pyruvate kinase deficiency

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7
Q

Give 2 examples of RBC membrane abnormalities?

A
  • Hereditary spherocytosis

- Hereditary elliptocytosis

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8
Q

Give 2 examples of causes of haematoma that can lead to jaundice in neonates

A
  • Extensive bruising

- Cephalohaematoma

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9
Q

Give an example of another cause of haemolysis that can cause jaundice in neonates?

A

Sepsis

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10
Q

What are the causes of delayed bilirubin clearance?

A
  • Gilbert’s syndrome
  • Decreased activity of glucuronyltransferase enzyme
  • Drugs needing conjugation for excretion
  • Increased enterohepatic circulation
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11
Q

What happens in Gilbert’s syndrome?

A

There is a poor uptake of bilirubin by hepatocytes

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12
Q

What can cause decreased activity of glucuronyltransferase enzyme?

A
  • Genetic
  • Hypoxia
  • Infection
  • Thyroid deficiency
  • Hypothermia
  • Prematurity
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13
Q

Give a genetic cause of decreased activity of glucuronyltransferase enzyme

A

Crigler-Najjar syndrome

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14
Q

Why might drugs needing conjugation for excretion cause delayed bilirubin excretion?

A

They compete for transferase enzymes

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15
Q

What can cause increased enterohepatic circulation?

A
  • Prolonged gut transit time
  • Delayed passage of meconium
  • Poor enteral feeding
  • Prematurity
  • Antibiotic treatment
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16
Q

What can cause conjugated hyperbilirubinaemia in neonates?

A
  • Congenital infections
  • Neonatal hepatitis
  • Obstructive
  • Parenteral nutrition induced cholestasis
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17
Q

What are the obstructive causes of conjugated hyperbilirubinaemia in neonates?

A
  • Biliary atresia

- Choledochal cyst

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18
Q

What is physiological jaundice?

A

Common, generally harmless jaundice occurring a high proportion of newborn babies in the first weeks of life for which there is no underlying cause

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19
Q

What kind of hyperbilirubinaemia is seen in physiological jaundice?

A

Unconjugated

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20
Q

What is the normal cord blood level of unconjugated bilirubin?

A

20-35µmol/L

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21
Q

What usually happens to levels of bilirubin in the first few days of life?

A

They rise by less than 85µmol/L/day

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22
Q

When does jaundice become clinically apparent?

A

When serum bilirubin is 80-90µmol/L

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23
Q

When do bilirubin levels peak after birth in term infants?

A

Day 4-5

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24
Q

When do bilirubin levels peak after birth in preterm infants?

A

Day 7-8

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25
Q

Who is more likely to develop physiological jaundice?

A

Breastfed babies

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26
Q

Why are breastfed babies more likely to develop physiological jaundice than formula fed babies?

A

Pathogenesis unclear, but proposed mechanisms;

  • Increased ß-glucuronidase in breast milk
  • High free fatty acid in breast milk
  • Certain factors in breast milk may inhibit the enzyme responsible for conjugation the liver
  • Inadequate milk intake
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27
Q

Why does the increased beta-glucuronidase in breast milk increase the risk of jaundice?

A

It can increase enteric absorption of bilirubin and hence the hepatic bilirubin load

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28
Q

Why does the high free fatty acid in breast milk increase the risk of jaundice?

A

It may compete for albumin binding sites for transport to the liver

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29
Q

How does inadequate milk intake lead to jaundice in breastfed babies?

A

Leads to sluggish gut action which increases enterohepatic circulation of bilirubin

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30
Q

Why do formula-fed babies have lower bilirubin levels?

A

Due to increased clearance of bilirubin from the gut

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31
Q

When does jaundice in term infants resolve?

A

Usually by 2 weeks of age

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32
Q

When does jaundice in preterm infants resolve?

A

Usually by 3 weeks

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33
Q

How long might jaundice persist in breastfed infants?

A

4-10 weeks

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34
Q

Should breastfeeding be continued in jaundiced infants?

A

Yes

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35
Q

What are the types of haemolytic disease of the newborn?

A
  • Rh incompatibility

- ABO incompatibility

36
Q

What is rhesus haemolytic disease?

A

When there is incompatibility of the Rh blood group between the mother and fetus

37
Q

What are the potential antigens in the Rh blood group?

A
  • D
  • C
  • Kell
38
Q

When can rhesus haemolytic disease occur, in terms of the blood groups of the mother and fetus?

A

If the mother is rhesus negative and the baby is rhesus positive

39
Q

Why might a rhesus negative mother have a rhesus positive child?

A

If the child inherited the antigen from it’s father

40
Q

What kind of antibodies can the mother generate against the baby in rhesus haemolytic disease?

A

IgG

41
Q

Where are antigens generated in rhesus haemolytic disease?

A

In the mothers bloodstream

42
Q

How does IgG generated in the mothers bloodstream get to the baby in rhesus haemolytic disease?

A

It crosses the placenta

43
Q

What happens when maternal IgG against crosses the placenta in rhesus haemolytic disease?

A

It causes fetal red cell haemolysis

44
Q

What can fetal red cell haemolysis lead to in rhesus haemolytic disease?

A
  • Jaundice
  • Anaemia
  • Hydrops
  • Hepatosplenomegaly
45
Q

Can rhesus haemolytic disease occur in the first pregnancy?

A

Occasionally

46
Q

Why does rhesus haemolytic disease not usually occur in the first pregnancy?

A

As the mother needs to be sensitised to the rhesus-positive antigen, which usually occurs during the first pregnancy

47
Q

What causes sensitisation of the mother to rhesus-positive antigen in rhesus haemolytic disease?

A

Feto-maternal haemorrhage

48
Q

When does feto-maternal haemorrhage most commonly occur?

A

During delivery

49
Q

Other than delivery, when might feto-maternal haemorrhage occur?

A
  • Miscarriage
  • Placental abruption
  • Amniocentesis
  • Chorionic villus sampling
50
Q

When can rhesus haemolytic disease occur in a first pregnancy?

A

If the mother has been sensitised, e.g. from blood transfusion

51
Q

What does the prenatal management of rhesus haemolytic disease involve?

A
  • Monitoring of antibody levels

- Referral to specialist centre if indicated

52
Q

How can fetal rhesus genotype be determined?

A

Non-invasively by cell free fetal DNA analysis in maternal serum

53
Q

How can fetal anaemia be monitored?

A
  • Serial ultrasound scanning of middle cerebral artery Doppler waveform
  • Measurement of fetal haematocrit from cordocentesis
54
Q

What may be necessary in the prenatal management of rhesus haemolytic disease?

A

Intrauterine blood transfusion

55
Q

What is required after birth in rhesus haemolytic disease?

A

Close bilirubin and haemoglobin monitoring

56
Q

Why is close bilirubin monitoring required after birth in rhesus haemolytic disease?

A

Bilirubin level may rise very rapidly to dangerously high levels

57
Q

Why has rhesus D alloimmunisation become rare?

A

As maternal blood group and antibody status is routinely tested, and if rhesus negative mothers are given anti-D IgG immunoglobulin

58
Q

What does anti-D IgG immunoglobulin do?

A

Clears any felt red blood cells that may have leaked into the maternal circulation

59
Q

How has the use of anti-D immunoglobulin changed the type of rhesus haemolytic disease that occurs?

A

Most cases are now anti-cell and anti-c

60
Q

What is the difference between rhesus haemolytic disease caused by anti-Kell and anti-c compared to anti-D?

A

Anti-Kell and anti-c lead to much less severe fetal anaemia and hyperbilirubinaemia

61
Q

What are the types of haemolytic disease of the newborn?

A
  • Rh incompatibility

- ABO incompatibility

62
Q

When does ABO incompatibility arise, in terms of the blood group of the mother and fetus?

A

When a mother with blood type O has a fetus with a different blood type (A, B, or AB)

63
Q

What kind of antibodies are the anti-A/anti-B produced in ABO incompatibility?

A

IgG

64
Q

Is hyperbilirubineamia more severe in ABO incompatibility or rhesus haemolytic disease?

A

Rhesus haemolytic disease

65
Q

Why is hyperbilirubinaemia less severe in ABO incompatibility?

A

As fetal RBCs express low ABO blood group antigens compared with adult levels

66
Q

When is the onset of haemolysis and jaundice in ABO incompatibility?

A

After birth

67
Q

How is ABO incompatibility diagnosed?

A

Direct antibody test is positive

68
Q

What is the most common cause of severe neonatal jaundice and kernicterus worldwide?

A

G6PD deficiency

69
Q

What is G6PD deficiency?

A

An X-linked recessive disorder characterised by low levels of glucose-6-phosphate dehydrogenase

70
Q

What is the function of G6PD?

A

It is involved in red blood cell metabolism

71
Q

Is G6PD deficiency more common in males or females?

A

Male s

72
Q

Why is G6PD deficiency more common in males?

A

Due to it’s X-linked inheritance

73
Q

How might carrier females be affected with G6PD deficiency?

A

They may have a milder form

74
Q

Why might carrier females have a milder form of G6PD deficiency?

A

As a result of lyonization

75
Q

What ethnicity is G6PD more common in?

A
  • Mediterranean
  • Middle or Far Eastern
  • African
76
Q

What might trigger patients with G6PD deficiency to haemolyse?

A

A number of stressors, e.g.;

  • Infection
  • Certain medications
  • Fava beans
77
Q

How is G6PD deficiency diagnosed?

A

By measuring G6PD activity in RBCs

78
Q

What causes Crigler-Najjar syndrome?

A

Deficiency of the enzyme uridine diphosphate glucuronyl-transferase (UGT)

79
Q

What is the inheritance of Crigler-Najjar syndrome?

A

Autosome recessive

80
Q

When does Crigler-Najjar syndrome present?

A

In the early neonatal period

81
Q

How does Crigler-Najjar syndrome present?

A

Rapid rise in serum bilirubin to very high levels despite phototherapy

82
Q

What can develop as a result of the jaundice in Crigler-Najjar syndrome?

A

Kernicterus

83
Q

Is type 1 or type 2 Crigler-Najjar syndrome more severe?

A

Type 1

84
Q

What are the peak bilirubin levels in type 1 Crigler-Najjar syndrome?

A

Up to 850µmol/L

85
Q

Can Gilbert’s syndrome cause severe unconjugated hyperbilirubinaemia?

A

It can contribute

86
Q

What % of the population is homozygous for Gilbert’s syndrome?

A

5-10%

87
Q

What % of the population is heterozygous for Gilbert’s syndrome?

A

40%

TAS Neonatal Medicine ✅ (35 decks)

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