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Y5 Paediatrics > Neonatal > Flashcards

Neonatal Flashcards

1
Q

What figure constitutes an unconjugated (indirect) jaundice?

A

CB less than 15% of total bilirubin

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2
Q

What figure constitutes a direct/conjugated jaundice?

A

Conjugated bilirubin greater than 15% of total or over 20mmol/L

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3
Q

What constitutes prolonged jaundice in term and preterm babies?

A 
Term = 2 weeks of age plus
Preterm = 3 weeks of age plus
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4
Q

6 areas of causes of conjugated hyperbilirubinaemia?

A 
Sepsis
Extrahepatic biliary obstruction
TPN jaundice
Toxic e.g. Aspirin, paracetamol, rifampicin, alcohol, steroids
Neonatal hepatitis
Metabolic or genetic
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5
Q

What type of jaundice is TPN associated jaundice?

A

Conjugated

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6
Q

6 areas of causes of unconjugated hyperbilirubinaemia?

A

Sepsis
Physiologic e.g. Breast milk
Haemolytic e.g. Rhesus/ABO
RBC defects e.g. G6PD def, hereditary spherocytosis/eliptocytosis or pyruvate kinase deficiency
Conjugation defects - Gilbert’s or Crigler Najjar
Other - galactosaemia, delayed cord clamping, cephalhaematoma/bruising, pyloric stenosis

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7
Q

What type of jaundice does congenital hypothyroidism cause?

A

Conjugated

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8
Q

What type of jaundice is breastfeeding/physiological jaundice?

A

Unconjugated

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9
Q

Why is jaundice more likely in neonates?

A

Increased bilirubin production due to higher haematocrit and higher red cell turnover due to decreased life span (85 days)
Decreased conjugation
Increased enterohepatic circulation due to reduced gut motility

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10
Q

What type is most neonatal jaundice and therefore what is more worrying?

A

Most is unconjugated

So conjugated potentially concerning

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11
Q

What is the typical pattern of physiological jaundice in neonates?

A

Occurs after 24 hours, peaks at 2-4 days and resolves within 1-2 weeks

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12
Q

Why does TPN cause jaundice? Which type?

A

Lower gut motility so increased enterohepatic circulation and increased absorption of conjugated bilirubin into blood

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13
Q

What does early (less than 24 hours after birth) jaundice often reflect?

A

Severe haemolysis e.g. ABO or rhesus
Other red cell or membrane defects
Or severe cephalhaematoma

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14
Q

What is more likely the cause of prolonged jaundice?

A

Infection or metabolic disease incl hypothyroidism

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15
Q

What type of hyperbilirubinaemia is worse for neurological function and can cause acute neonatal encephalopathy?

A

Unconjugated

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16
Q

What is kernicterus?

A

Chronic sequelae of often acute hyperbilirubinaemia (usually unconjugated), consisting of choreoathetoid CP (dyskinetic), SN hearing loss and loss of upgaze plus dental enamel dysplasia

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17
Q

Early to late signs of acute bilirubin encephalopathy?

A

Early hypotonia and high pitched cry
Febrile, poor feeding, lethargic
Later retrocolis, opisthotonos, apnoeas, seizures, hypertonic and death

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18
Q

What type of hyperbilirubinaemia is managed by UV phototherapy and why?

A

Unconjugated - converts unconjugated to water soluble photo-isomers which are then excreted in urine

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19
Q

What cause of unconjugated hyperbilirubinaemia is UV phototherapy often not very effective for?

A

Haemolysis

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20
Q

Side effects and considerations for UV phototherapy for neonatal jaundice?

A

Need to be well hydrated to maintain urine output
Can get eye damage, diarrhoea, skin rash, overheating
Also lack of parental contact

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21
Q

When might exchange transfusions or IVIg be used for hyperbilirubinaemia?

A

If very very high or quick rise

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22
Q

What is NRDS? After what gestation is it rare?

A

Lung disease in newborns due to surfactant deficiency - mostly a disease of the very premature, rare after 32 weeks

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23
Q

Give 4 metabolic disturbances that can inhibit surfactant production?

A

Acidosis
Hypothermia
Hyperglycaemia
Sepsis

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24
Q

How is NRDS prevented?

A

Maternal steroids

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25
Q

What is transient tachypnoea of the newborn TTN? What does it usually present following?

A

Due to delayed surfactant clearance or absorption of surfactant - commonly in the setting of elective CS

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26
Q

How do babies get congenital pneumonia and what bugs therefore usually cause it?

A

Inhalation of infected amniotic fluid e.g. Chorioamnionitis or maternal illness
Usually caused by GBS, E Coli, listeria, chlamydia etc.

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27
Q

What are the 3 main pathogenic features of meconium aspiration syndrome?

A

Mechanical airway blockage
Barrier preventing airway exchange
Chemical pneumonitis

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28
Q

What are exam findings for meconium aspiration syndrome?

A

Diffuse wet crackles, rhonchi
Respiratory acidosis
In setting of stained liquor

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29
Q

What infection can be related to meconium aspiration syndrome?

A

Listeriosis

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30
Q

What is bronchopulmonary dysplasia? Definition in terms of gestation?

A

Impaired alveolar development sometimes defined as oxygen requirement after 36 weeks gestation

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31
Q

What reduces the incidence of nec?

A

Breastfeeding

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32
Q

4 RFs for nec?

A

Prematurity
VLBW/IUGR causing gut ischaemia
Hypoxia
Polycythaemia or exchange transfusions

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33
Q

What part of the bowel does nec often affect?

A

Terminal ileum/caecum

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34
Q

What structural findings of the bowel characterise nec?

A

Subserosal gas on mesenteric border of bowel

Gangrenous necrosis on antemesenteric border

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35
Q

When does nec generally present? What makes it present later?

A

Usually presents in 2nd week of life - 8 to 10 days

Can be later in very premature babies

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36
Q

Early signs of nec?

A

Change in feeding tolerance - increased aspirates and gastric retention (residual milk in stomach pre feed)
Abdominal distension and vomiting

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37
Q

Later progressive signs of nec?

A 
General illness and fevers
Abdo tenderness
Blood stained stool
Ileus, perforation
Shock, DIC, organ failure
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38
Q

What does XR show for nec?

A

Pneumatosis intestinalis and hepatic portal venous gas

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39
Q

What criteria is used to stage nec? Briefly outline them?

A

Bell’s staging criteria
Stage 1 is suspected nec - non specific illness, early GI signs in predisposed infant, XR shows dilated bowel
Stage 2 is definite nec - as above plus mild to moderate acidosis, thrombocytopenia, gross GI bleeding plus gas and thickened wall on XR
Stage 3 is advanced nec - shock, severe acidosis, DIC, significant bleeding, pneumoperitoneum etc.

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40
Q

What fbc disturbance is common and possibly severe in nec?

A

Thrombocytopenia

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41
Q

Management of nec?

A

Supportive initially - pass free drainage NG tube
Broad spec Abx for 2 weeks
Surgery as indicated - beware risk of short bowel syndrome

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42
Q

Where does caput succedaneum form and what is it?

A

Oedematous region forming between skin and galeal aponeurosis/periosteum

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43
Q

How can you tell a caput succedaneum?

A

It crosses suture lines

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44
Q

Which neonatal haematoma crosses suture lines?

A

Caput succedaneum

45
Q

What is a cephalohaematoma and where does it form?

A

Traumatic subperiosteal bleed just deep to epicranial/galeal aponeurosis

46
Q

How can you tell a cephalohaematoma?

A

Doesn’t cross suture lines

47
Q

Which neonatal haematoma doesn’t cross suture lines?

A

Cephalhaematoma

48
Q

3 risks/possible sequelae of cephalohaematoma?

A

Unconjugated hyperbilirubinaemia
Ossification or calcification and subsequent deformation
Infection

49
Q

What is a chignon?

A

A temporary swelling on baby head following ventouse delivery

50
Q

What is the term for a temporary baby head swelling following ventouse delivery?

A

Chignon

51
Q

What is a subgaleal haematoma?

A

Bleed between periosteum and galeal aponeurosis

52
Q

Which is potentially the most serious neonatal haematoma and why?

A

Subgaleal haematoma

As it can cause large intravascular loss and shock

53
Q

What usually causes a subgaleal haematoma?

A

Ventouse assisted delivery

54
Q

When is IVH most common and why?

A

In very premature babies (27-30 weeks or less)

Because blood vessels in brain strengthen over last 10 weeks of gestation

55
Q

What is the natural history/progression of IVH?

A

Starts as periventricular subependymal germinal matrix (PVH) before extending into lateral ventricles (IVH)

56
Q

Complications of IVH?

A

Post-haemorrhagic ventricular dilatation (PHVD) - wide cranial sutures
Apnoeas
Seizures
Setting sun eyes

57
Q

What measurement is used to track IVH for PHVD?

A

Ventricular index/Levine measurement

58
Q

What 2 complications of IVH may lead to risk of cerebral palsy?

A

Parenchymal infarct

PHVD

59
Q

When does IVH most commonly occur?

A

First few days of life

60
Q

3 descriptions of bleeding distribution in IVH and how do these relate to grades?

A

Subependymal only = grade 1 germinal matrix haemorrhage
IVH +/- ventricular dilatation
IVH +/- parenchymal involvement = grade 4 parenchymal haemorrhage

61
Q

What is periventricular leukomalacia?

A

Severe haemorrhagic periventricular infarct and HIE can lead to cortical necrosis, basal ganglia injuries, focal infarcts or subcortical leukomalacia
High risk of spastic diplegic cerebral palsy

62
Q

What processes typically underlie PVL?

A

Labile BP e.g. Shock or hypotension

63
Q

What are signs of TOF/OA?

A

Polyhydramnios in mum
Mucousy baby, choking on feeding
Unable to pass NG tube - try this then CXR

64
Q

What are the 5 types of TOF/OA by Gross classification?

A

A - proximal and distal oesophageal buds with missing mid segment, no TOF (long gap OA)
B - proximal and distal oesophageal buds, proximal TOF
C - proximal OA with distal TOF at carina
D - proximal oesophagus terminates at proximal trachea, distal oesophagus arises from lower trachea
E - TOF without OA

65
Q

What is H type TOF/OA?

A

Isolated TOF, no OA

66
Q

What is the most common type of TOF/OA?

A

C - proximal OA with distal TOF

67
Q

Management of a TOF/OA?

A

Regular aspiration of proximal oesophageal pouch and IV fluids
Urgent surgery if child needs mechanical ventilation

68
Q

Long term sequelae of TOF/OA?

A

Tracheomalacia, respiratory disease incl early aspiration, oesophageal obstruction when moving to solids, GORD

69
Q

Bilious vomiting in neonates is what until proven otherwise?

A

Midgut malrotation with volvulus

70
Q

Differentials for bilious vomiting in neonates?

A 
Malrotation +/- midgut volvulus
Duodenal atresia
Jejuno-Ileal atresia
Meconium ileus
Hirschprungs disease
Nec
71
Q

How does retinal vasculature develop in foetus and newborn?

A

Starts developing around 16 weeks duration from optic disc

Finishes vascularising to edge of peripheral retina by around 1m post birth

72
Q

Why does retinopathy of prematurity occur?

A

Retinal vessels are used to growing in relatively hypoxic conditions, so if born prem the retina becomes hyperoxic which reduces VEGF production
This halts vascular growth, vessels vasoconstrict and obliterate
Eye continues to grow and periphery becomes hypoxic again, inducing VEGF
This leads to angiogenesis of tortuous vessels, fibrovascular prolfieration and intravitreal fibrosis eventually leading to retinal detachment

73
Q

Risk factors for ROP?

A

LBW/VLBW
Born under 32 weeks gestation
O2 therapy
Respiratory distress and IVH are predictive

74
Q

Describe screening process for ROP?

A

All babies born at 32 weeks or less or BW less than 1500g
32-27 weeks are screened at 28-35 d of life
Less than 27 weeks are screened at 30-31 weeks gest age
Then weekly or fortnightly as clinically appropriate

75
Q

Management options for ROP?

A

Laser photocoagulation/cryotherapy
Anti-VEGF for aggressive posterior ROP
Vitrectomy or vitreoretinal surgery to reattach detached retina (stage 5)

76
Q

What is stage 5 ROP?

A

Retrolental fibroplasia - retinal detachment

77
Q

What is the surgical management of biliary atresia and how does this vary?

A

If completely obstructed requires liver transplant

If incomplete can do Kasai procedure - hepatoportoenterostomy

78
Q

How does biliary atresia present?

A

‘Late’ prolonged conjugated jaundice

Eventually progressing to cirrhosis, ascites, liver failure

79
Q

2 alternative names for biliary atresia?

A

Extrahepatic ductopenia

Progressive obliterative cholangiopathy

80
Q

Investigations for biliary atresia?

A

Bloods incl deranged LFTs
Liver biopsy
Imaging incl USS

81
Q

What do they do in a Kasai procedure?

A

Attach part of small intestine directly to liver

Attach the rest of small intestine (from stomach - proximal end) to this small intestine to form a Roux en Y connection

82
Q

What is the most common cause of congenital/infantile stridor?

A

Laryngomalacia

83
Q

4 examples of central wall defects?

A

Ectopia cordis
Cloacal exstrophy
Exomphalos
Gastroschisis

84
Q

Which abdominal wall defect is associated strongly with other syndromes? Which ones?

A

Exomphalos
E.g. Trisomies 13, 18, 21 and other chromosomal
Beckwith-Wiedemann
Penatology of Cantrell
Cloacal exstrophy and other caudal defects

85
Q

Which side does Gastroschisis usually occur on?

A

Right side

86
Q

When does the diaphragm usually close in gestation?

A

8 weeks

87
Q

What is the most common type of Congenital Diaphragmatic Hernia?

A

Bochdalek - postero-lateral CDH which affects back left of diaphragm

88
Q

What are the 5 most important parts of newborn screening?

A 
Eyes
Ears
Heart
Hips
Testes
89
Q

When is newborn check usually done?

A

Between 6 and 24 hours of birth to give time for nappy changes, feeds, circulatory adaptations etc

90
Q

What is normal feeding amount for an established baby up to around 6m? How often is this split up into?

A

150ml/kg/day, often starting at around 60ml/kg/day

Split into 3 to 4 hourly feeds

91
Q

How often does breast feeding tend to occur and how long does it last?

A

Every 2-3 hours lasting 10-20 mins

92
Q

What is the first breast milk called and when does normal breast milk after this come in?

A

Colostrum

Normal milk comes in around 3 days

93
Q

Normal newborn baby heart rate?

A

120-160

94
Q

Normal newborn resp rate?

A

40-60

95
Q

What would you do if suspecting TTN but not cleared by 6 hours?

A

CXR and start empirical Abx

96
Q

How and when is surfactant given after birth?

A

At the time of birth when intubation occurs, down the tube

And again at 12 hours if necessary

97
Q

From what gestation can babies normally coordinate oral feeds?

A

34 weeks

98
Q

How and when is TPN given and how is it weaned?

A

Normally given pre 32 weeks gestation via UVC
Balance with breast milk and reduce TPN over time, giving bolus feeds from 32 weeks and moving on to oral by 34 weeks
Aiming for the total of 150-175ml/kg/day

99
Q

How do you confirm a malrotation?

A

Upper GI contrast

100
Q

When do premature babies have head scans?

A

1 and 6 weeks of age

101
Q

What is vernix caseosum?

A

White slimy stuff that covers babies

102
Q

What is erythema toxicum?

A

Classically white papules with erythematous flare affecting hands, feet, back of trunk etc

103
Q

What are milk spots?

A

Hypertrophic sebaceous glands often on nose

104
Q

What is witches milk?

A

Milk that can come from newborn breast tissue due to withdrawal of hormonal flow from placenta

105
Q

What is a simple naevus?

A

Stork bite (front and back of head)

106
Q

How long does strawberry naevus take to go? When would you decide to treat?

A

Up to 18m

May treat if on eye or nappy area

107
Q

With what disease is a sunflower cataract associated?

A

Wilson’s disease

108
Q

What might be the cause of later onset neonatal sepsis e.g. On SCBU?

A

Coagulase negative staph

109
Q

What is the grading system for HIE? What is its role?

A

Sarnat staging

1-3 mild to severe, suggests the likelihood of subsequent seizures and prognostication

Y5 Paediatrics (13 decks)

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