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Year 4 Paediatrics > Paediatric Neonatology > Flashcards

Paediatric Neonatology Flashcards

1
Q

Neonatal resuscitation

A
  1. Dry the baby
  2. Keep baby warm - heat lamp/plastic bag
  3. APGAR Score
  4. Stimulate breathing - neutral position of head, check for aiway obstruction
  5. 5 inflation breaths
  6. 30 chest compressions, 2 inflation breaths
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2
Q

When to do APGAR scores

A

1, 5 and 10 minutes after birth

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3
Q

What does prolonged hypoxia cause

A

Hypoxic ischaemic encephalopathy

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4
Q

How to treat hypoxic ischaemic encephalopathy

A

Therapeutic hypothermia with active cooling

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5
Q

APGAR Score

A 
Appearance - skin colour 
Pulse 
Grimmace - response to stimulation 
Activity - muscle tone 
Respiration
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6
Q

Delayed umbilical cord clamping

A

Uncompromised neonates - delay of at least 1 min before clamping

Neonates that require resus - clamp sooner

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7
Q

Benefits and disadvantages of delayed cord clamping

A

Advantages:

  • increases neonatal haemoglobin and iron stores
  • improves blood pressure
  • decreases the incidence of intraventricular haemorrhage and necrotising enterocolitis

Disadvantages:
- neonatal jaundice increases

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8
Q

Care immediately after birth

A 
Skin to skin 
Clamp the umbilical cord 
Dry the baby 
Keep baby warm with hat and blanket 
Vitamin K intramuscular injection 
Label the baby 
Measure weight and height
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9
Q

When to take oral vitamin K

A

Dose at birth, 7 days and 6 weeks

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10
Q

When to do a newborn examination

A

Within 72 hours after birth

Repeated at 6 - 8 weeks by GP

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11
Q

When is the blood spot test done?

A

Day 5 (latest day 8)

Results take 6 - 8 weeks to come back

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12
Q

Pre ductal and post ductal saturations

A

Pre ductal - right hand - receives blood from the right subclavian artery before the ductus arteriosus

Post ductal - foot - recieves blood from the descending aorta after the ductus arteriosus

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13
Q

3 questions to ask in the newborn examination

A
  1. Are they feeding
  2. FHx of heart, hip or eye problems
  3. Have they passed meconium
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14
Q

If a mother is posivtive for group B streptococcus, what is the management?

A

Prophylactic IV benzylpenicillin and gentamycin for neonate

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15
Q

Risk factors for neonatal sepsis

A 
Vaginal GBS colonisation 
GBS sepsis in a previous child 
Maternal sepsis 
Chorioamnionitis 
Maternal fever of > 38 celsius 
Prematurity 
PROM
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16
Q

Clinical features of neonatal sepsis

A 
Fever 
Reduced tone and activity 
Poor feeding 
Respiratory distress or apnoea 
Vomiting 
Hypoxia 
Jaundice within 24 hours 
Seizures 
Hypoglycaemia
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17
Q

Treatment for suspected neonatal sepsis

A

1 risk factor/ feature - monitor for at least 12 hours

2 + Risk factors/ features - antibiotics

1 red flag sign - antibiotics

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18
Q

Antibiotics for neonatal sepsis

A

Benzylpenicillin and gentamyin

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19
Q

Caput succeddaneum features - cause, suture lines, colour

A
  • Caused by pressure to the scalp e.g. forceps delivery
  • oedema outside the periosteum
  • does cross the suture lines
  • resolves within a few days
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20
Q

Cephalohaematoma features - cause, suture lines, colour

A
  • collection of blood between the skull and the periosteum
  • caused by damaged blood vessels due to trauma
  • does NOT cross the suture lines
  • discolouration to skin
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21
Q

Pathophysiology of Erbs Palsy

A

Injury to C5/C6 nerves in the brachial plexus often due to shoulder dystocia because of macrosomnia, instrumental delivery or trauma

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22
Q

Erbs palsy presentation

A

Weakness of shoulder abduction, external roation, arm flexion and finger extension - waiters tip

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23
Q

Management of erbs palsy

A

Function normally returns within a few months but may require neurosurgical input if persists

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24
Q

What is a fractured clavicle during delivery associated with?

A

Shoulder dystocia
Instrumental delivery
Trauma
Macrosomia

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25
Q

How does a fractured clavicle after delivery present?

A

Asymmetry
Lack of movement of arm on affected side
Pain and distress when moving affected arm

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26
Q

Investigations and management for a fractured clavicle during delivery

A

Ix: USS or Xray

Mx: conservative or immobilisation - usually heals well

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27
Q

Pathophysiology of hypoxic ischaemic encephalopathy

A

Occurs due to prolonged or severe hypoxia in neonates that causes ischaemia and brain damage

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28
Q

Complications of HIE

A

Cerebral palsy due to permanent damage

Death

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29
Q

Causes of HIE

A

Maternal shock
Intrapartum haemorrhage
Prolapsed cord
Nuchal cord

30
Q

Presentation of mild HIE

A

pH < 7 on umbilical artery blood gas
Poor APGAR score

Poor feeding
Irritable
Hyper alert
Resolves within 24 hours

31
Q

Presentation of moderate HIE

A

pH < 7 on umbilical artery blood gas
Poor APGAR score

Poor feeding
Lethargic and hypotonic 
Seizures 
Weeks to resolve 
40% develop cerebral palsu
32
Q

Presentation of severe HIE

A

pH < 7 on umbilical artery blood gas
Poor APGAR score

Reduced consciousness
Apnoea
Flaccid and reduced or absent reflexes
50% mortality/ 90% cerebral palsy

33
Q

Management of HIE

A

MDT

Supportive - resus, ventilation, nutrition

Seizures - therapeutic hypothermia (33 - 34 celsius) for 72 hours

34
Q

Physiological jaundice

A

Occurs at 2 - 7 days

Fetal haemoglobin is more fragile
Neonatal liver is less well developed

35
Q

Causes of neonatal jaundice - increased production

A 
Haemolytic anaemia 
ABO incompatability 
Haemorrhage 
Cephalo - haematoma 
Polycythaemia 
Sepsis or DIC 
G6PD deficiency
36
Q

Causes of neonatal jaundice - decreased excretion

A 
Prematurity 
Breast milk jaundice 
Neonatal cholestasis 
Biliary atresia 
Gilbert syndrome 
Hypothyroidism
37
Q

Jaundice within 24 hours

A

Always pathological

Common cause - sepsis, treat with antibiotics and phototherapy

38
Q

Kernicterus

A

Accumulation of bilirubin in the basal ganglia which can cause brain damage, cerebral palsy, learning disabilities and deafness

39
Q

Breast milk jaundice pathophysiology

A

Components of breast milk inhibit the ability of the liver to conjugate bilirubin

More likely to become dehydrated if not feedinf adequately which can lead to constipation - increasing the absorption of bilirubin in the intestines

40
Q

Haemolytic disease of the newborn pathophysiology

A

Mother - rhesus negative - no rhesus antigens, has the rhesus antibodies

Baby - rhesus positive - rhesus antigens, no antibodies

Occurs in second pregnancy

41
Q

Prolonged jaundice

A

More than 14 days - term baby

More than 21 days - premature baby

42
Q

Causes of prolonged jaundice

A

Biliary atresia
Hypothyroidism
G6PD deficiency

43
Q

Investigations for prolonged jaundice

A 
Bloods - TFTs, FBC 
Blood film - polycythaemia
Blood type testing 
Direct Coombs test - haemolysis 
Blood and urine cultures - sepsis 
G6PDehydrogenase levels - G6PD deficiency
44
Q

Management of neonatal jaundice

A

Plot bilirubin levels on treatment threshold chart

If above the line, phototherapy is given or if extremely high, blood transfusion given

45
Q

Prematurity

A

Less than 37 weeks of gestation at birth

Under 28 weeks - extremely preterm
28 - 32 weeks - very preterm
32 - 37 weeks - moderate to late preterm

46
Q

Associations with prematurity

A 
Maternal alcohol, smoking or drug use 
Social deprivation 
Over or underweight mother 
Maternal co-morbidities 
Twins 
FHx of prematurity
47
Q

Managment of prematurity to delay birth

A
  • prophylactic vaginal progesterone

- prophylactic cervical cerclage

48
Q

USS result for women that are suspected to have preterm deliveries

A

Cervical length of 25mm or less before 24 weeks gestation - give prophylaxis to delay birth

49
Q

Management to improve outcomes in preterm babies

A

Tocolysis - nifedipine to delay labour
Maternal corticosteroids - before 35 weeks gestation
IV magnesium sulphate - before 34 weeks gestation - protects brain
Delayed cord clamping

50
Q

Problems with premature babies

A

Respiratory distress - inadequate amounts of surfactant
Hypothermia
Hypoglycaemia
Poor feeding - lack of suckling reflex
Apnoea
Neonatal jaundice - under developed liver
Intraventricular haemorrhage
Retinopathy of prematurity - blood vessels proliferating behind retina
Necrotising enterocolitis

51
Q

Long term affects of prematurity

A 
Chronic lung disease of prematurity 
Learning and behaviour difficulties 
Recurrent infections
Hearing and visual impairment 
Cerebral palsy
52
Q

Apnoea

A

Spontaneous cessation of breathing for more than 20 seconds or shorter periods with oxygen desaturation or bradycardia

53
Q

Management of apnoea

A

Tactile stimulation - prompt baby to restart breathing

IV caffeine

54
Q

Who does retinopathy of prematurity affect?

A

Typically babies born before 32 weeks gestation

55
Q

Complications of retinopathy of prematurity

A

Scarring
Retinal detachment
Blindness

56
Q

Retinopathy of prematurity pathophysiology

A

Retinal blood vessel development starts at 16 weeks and ends at 37 - 40 weeks.

Blood vessels grow from the centre to the outer area and stimulated by hypoxia

When retina are exposed to higher concentrations of oxygen in a preterm baby, blood vessels do not develop but when hypoxic again, produce excessive blood vessels - neurovascularisation and scar tissue

57
Q

Zones of the retina

A

Zone 1 - optic nerve and macula

Zone 2 - zone 1 edge to ora serrata (pigmented border between the retina and the ciliary body

Zone 3 - outside the ora serrata

58
Q

Who is screened for retinopathy of prematurity

A

Babies born before 32 weeks

Under 1.5kg

59
Q

Screening for retinopathy of prematurity

A

Screening starts at:

30 - 31 weeks of gestation - if born before 27 weeks

4 - 5 weeks of age - if born more than 27 weeks

Occurs at least every 2 weeks until the blood vessels reach zone 3

60
Q

Plus disease

A

Tortous vessels

Hazy vitreous humour

61
Q

Treatment for retinopathy of prematurtiy

A

Transpupillary laser photocoagulation - stops and reverses neurovascularisation

2nd line - cryotherapy and injection of intravitreal VEGF inhibitors

Surgery for retinal detachment

62
Q

Necrotising enterocolitis pathophysiology

A

Condition that affects premature neonates where part of the bowel becomes necrotic

Life threatening emergency as can lead to perforation, peritonitis and shock

63
Q

Risk factors for NEC

A
  • Very low birth weight or prematurity
  • Formula feeds
  • Respiratory distress and assisted ventilation
  • Sepsis
  • PDA and other congenital heart disease
64
Q

Investigations for NEC

A

Bloods - FBC, CRP
Blood culture
Blood gas - metabolic acidosis
Abdo xray

65
Q

Management of NEC

A

IV fluids
IV antibiotics
Nill by mouth - NGT or TPN

Surgical emergency

66
Q

Withdrawals fom opiates, SSRIs and alcohol features

A

Present 3 hours - 3 days after birth

CNS: irritable, tremors and seizures

Respiratory: tachypnoea

Metabolic: poor feeding, regurgitation and vomiting, hypoglycaemia, loose stools

67
Q

Management of withdrawals in neonates

A

Monitor in hospital for at least 3 days

Urine testing

Oral morphine - opiate withdrawal

Oral phenobarbitone - non opiate withdrawal

68
Q

Congenital rubella syndrome maternal vaccinations

A

If planning to get pregnant - 2 doses of MMR vaccine, 3 months apart (live attenuated)

Pregnant women - vaccine after birth

69
Q

Chickenpox exposure during pregnancy

A

If not immune, IV varicella immunoglobulins as prophylaxis within 10 days of exposure

70
Q

Risk factors for sudden infant death

A

Prematurity
Low birth weight
Smoking during pregnancy
Male

71
Q

How to minimise SIDS

A
  • Put baby on back when not supervised and sleeping
  • keep their head uncovered
  • place feet at the foot of bed to prevent slipping down
  • keep cot clear of toys and blankets
  • avoid smoking
  • avoid co sleeping
  • Maintain room temperature

Year 4 Paediatrics (19 decks)

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