Neonatal jaundice Flashcards

1
Q

What is jaundice?

A

Clinical sign - Yellow colouration of skin and sclerae due to accumulation of bilirubin

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2
Q

Normal factors in the neonate that make them more susceptible to jaundice

A
  • Neonates: high haematocrit / RBC volume; shorter life span of RBC (70 -90 days)
  • High bilirubin production
  • Slow bilirubin clearance
  • Immature hepatic glucuronyl transferase
  • High beta glucoronidase (increased bilirubin re-absorption)
  • Absent colonic bacteria
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3
Q

Why neonates more susceptible to developing kernicterus?

A

BBB permeable to bilirubin for first 10-14 days of life

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4
Q

Features of acute bilirubin encephalopathy

A

Lethargy, poor feeding, high pitched cry

Opisthotonus, seizures

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5
Q

Features of chronic bilirubin encephalopathy

A
  1. Kernicterus - histological accumulation of pigment in basal ganglia
  2. BIND (bilirubin induced neurological dysfunction) - subtle intellectual impairment
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6
Q

Clinical features of Kernicterus

A

Athetoid cerebral palsy
Hearing loss
Paralysis of upward gaze

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7
Q

Criteria for pathological jaundice

A
  • Any increase in conjugated bilirubin
  • Early jaundice: before 24 hours of life
  • Extremely high
  • Prolonged
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8
Q

Criteria suggesting physiological jaundice

A
  • Elevated unconjugated bilirubin
  • TSB generally peaks at about 100umol/L on day 3-4 and then declines to adult levels by day 10 (Asian infants peak at higher values)
  • Exaggerated physiologic (up to 290umol/L)
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9
Q

How is a diagnosis of physiological jaundice made?

A

Never appears in first 24 hours of life
Diagnosis of exclusion in active, well fed and are not ill.
TSB usually not >200umol/l (275 in breastfed)

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10
Q

What is breastmilk jaundice?

A

Prolonged unconjugated physiological jaundice in a breast fed newborn
Good growth/ weight
?beta-glucuronidase increases enterohepatic circulation?

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11
Q

What does beta-glucuronidase do?

A

Deconjugates glucuronic acid causing more bilirubin to be re-absorbed in the small intestine.

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12
Q

Causes of an unconjugated pathological jaundice in the neonate

A
  • Breast feeding jaundice
  • Haemolysis
  • Internal haemorrhage
  • Polycythaemia
  • Infant of diabetic mother
  • Hypothyroidism
  • Rare (Crigler-Najjar, Gilbert syndrome)
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13
Q

Causes of a conjugated pathological jaundice in the neonate

A
  • Congenital infections (CMV, syphilis, herpes, rubella)
  • Hepatitis (TPN, viral)
  • UTI
  • Sepsis
  • Rare: biliary atresia, cystic fibrosis, inborn errors of metabolism
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14
Q

What is breastfeeding jaundice?

A

Poor breastfeeding - dehydration and weight loss.

Delayed GIT bilirubin clearance = more re-absorption

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15
Q

Treatment of breastfeeding jaundice

A

Rehydration and more frequent feeding

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16
Q

Causes of heamolysis in the neonate

A

Common
- Blood group incompatibility: haemolytic disease of the newborn (ABO, Rhesus, minor antigens)
- Infections / sepsis
Rare:
- Haemoglobinopathy (thalassaemia)
- RBC enzyme deficiency (glucose 6 phosphatase deficiency, pyruvate kinase deficiency)
- RBC membrane defects (spherocytosis, ovalocytosis)

17
Q

Causes of heamorrhage in the neonate

A

Common
- Bruising (traumatic delivery / resuscitation)
- Pre term / NVD
- Vaginal breech
- Cephalhaematoma, subaponeurotic haemorrhage
Rare
- Internal haemorrhage

18
Q

Most common cause of heamolytic disease of the newborn

A

ABO incompatibility

19
Q

ABO incomatibility pathophysiology

A

Maternal blood group O has IgG against A and B antigens. If child has A or B then they develop mild haemolysis. Once born placenta can no longer remove bilirubin. Therefore, accumulates.

20
Q

How do we diagnose ABO incompatibility?

A

All children born to group O mothers have TSB measured at 8 hours. If TSB > 80umol/l then phototherapy started and grouping and Coombs test is performed.

21
Q

What must the resus status of the mother and father be to get Rh disease of the newborn?

A
Mother = negative
Father = positive
22
Q

What are the major threats to the Rh diseased infants life?

A

Profound anaemia
Respiratory distress, cardiac failure
Bilirubin encephalopathy

23
Q

Features of severe Rh disease

A

Massive extra medullary haematopoiesis
Hydrops fetalis
IUD

24
Q

Why is jaundice not always seen at birth in Rh disease?

A

Placenta can remove excess biliruin

25
Q

How is Rh disease prevented?

A
IM anti-D immunoglobulin given to Resus negative woman within 72 hours following:
Delivery
Miscarriage
Amniocentesis
APH
ECV
26
Q

Clinical features of Rh disease

A
Pale large placenta
Anaemia
Jaundice (rapid onset)
HSM
Oedema
Blueberry muffin rash
27
Q

Rx for Rh disease

A

Resuscitate (Respiratory, metabolic disturbances)
Phototherapy (Start immediately, TSB every 2-4 hours)
Exchange transfusion (If cord TSB >120/ HB <30%)
Straight blood transfusion
IV immunoglobulin

28
Q

How does phototherapy work?

A

Bilirubin converted to metabolically inert, water soluble Lumiruin by blue light

29
Q

Side effects of phototherapy

A
  • Hyper / hypothermia
  • Skin rashes
  • Diarrhoea
  • Maternal anxiety / bonding
30
Q

What are the indications for exchange transfusion?

A
Cord TSB > 120
Cord Hb < 10
PCV < 30 %
Hydrops fetalis
Phototherapy failure
Signs of bilirubin encephalopathy
31
Q

What TSB level correlates to recognition of clinical jaundice?

A

> 70 umol/l

32
Q

Causes of prolonged jaundice

A

Breastmilk jaundice
Hypothyroidism
Galactosaemia
Hepatitis