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YR5 Specialties > Paeds emergencies, genetics and neonatology COPY > Flashcards

Paeds emergencies, genetics and neonatology COPY Flashcards

1
Q

Recall 2 causes of neonatal collapse

A

Sepsis
CHD

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2
Q

Recall 4 possible causes of jaundice in the neonate 24h-2w

A

Breast milk/ physiological
Infection e.g. UTI
Bruising (instrumental delivery)
Polycythaemia

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3
Q

2 causes of neonatal jaundice <24h from birth

A

Haemolytic disorders: RhD, ABO, G6PD, HS
Congenital infection

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4
Q

7 causes of prolonged neonatal jaundice (>2w)

A

Bile duct obstruction- Biliary Atresia
Congenital hypothyroidism
Haemolytic disorders
Infection e.g. UTI /Congenital
High GI obstruction: Pyloric stenosis
Neonatal hepatitis
Breast milk/ physiological

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5
Q

Recall 4 common causes of rash in the neonate

A

Nappy rash
Milia
Erythema toxicum
Mongolian blue spot

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6
Q

Recall 2 causes of seizures in the neonate?

A

Hypoglycaemia
HIE

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7
Q

Recall 4 milestones that should be reached by one year

A

Walks unsteadily/ cruises
Pincer grip
“mama, dada, no”
Waves bye bye

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8
Q

Recall 4 milestones that should be reached by 18 months

A

Runs
Stack 4 blocks, scribbles
Point at objects they want + know 6+ words
Symbolic play

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9
Q

Recall 5 milestones that should be reached by 2 years

A

Up stairs 2 foot/ step
8 blocks + Draws Vertical line
Link 2 words in sentences + understand 2 step commands
Dry by day

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10
Q

Recall the milestones that should be reached by 3 years

A

GM: Hop on 1 foot, walk upstairs 1 foot per step, downstairs 2 feet per step

FM: Draws circle, bricks in a bridge, makes single cuts in paper with scissors, string of beads

S+L: understands negatives + adjectives. Talks in 3-4w sentences

Social: begins to share toys, plays alone without parents, parallel play, eats with fork + spoon, bowel control

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11
Q

What are the 4 domains of development?

A

Gross motor skills (develop head to toe)
Fine motor skills
Language + speech
Social skills

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12
Q

In what period of life should primitive reflexes be present?

A

From birth, to no later than 6 months

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13
Q

Recall the 5 primitive reflexes

A

Moro (sudden head drop –> arms outstretched)
Stepping
Rooting
Palmar and plantar grasp
Atonic neck (fencing posture)

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14
Q

Why do gross motor skills develop from head to toe?

A

That is how myelination develops

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15
Q

What are the limit ages for gross motor developmental milestones?

A

Head control 4m
Sits unsupported 9m
Stands independently 12m
Walks independently 18m

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16
Q

What are the limit ages for fine motor developmental milestones?

A

Reaches for objects: 6m
Transfers: 8m
Pincer grip: 12m

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17
Q

At what age should children say 6 words with meaning?

A

18 months

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18
Q

At what age should children be able to smile?

A

6 weeks
Limit age 8w

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19
Q

How can abnormal progression be classified?

A

Slow but steady
Plateau,
Regression
Acute insult

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20
Q

What is tested in the full physical exam (first 72 hours)?

A

Heart, hips, eyes, testes

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21
Q

When is the Guthrie heel prick test done?

A

7 days

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22
Q

When is the new baby review done and what does it involve?

A

2 weeks: safe sleeping, vaccination, feeding, caring, development

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23
Q

How is hearing tested in the neonate, and when is this done?

A

Automated Otoacoustic Emission/ AOAE
At 4 weeks

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24
Q

When is the second full physical exam, and what does it involve?

A

At 6 weeks (done by GP) - DDH testing, testicles, heart, weight, length, vaccination discussion

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25
Q

Recall the timings of the immunisations done within the 1st year of life and what is included in each one

A

1st: 8 weeks: Men B, rotavirus, 6-in 1 DTaP/IPV/Hib/HepB

2nd: 12 weeks: also ‘6-in-1’, rotavirus + pneumococcal

3rd: 16 weeks: ALSO 6-in-1 + a repeat MenB

4th: 1 year: 1st MMR + boosters

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26
Q

When is HBV given, and to which infants?

A

At birth, to those whose mother is infected

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27
Q

When is BCG given to eligible infants?

A

At birth

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28
Q

What is included in a health review?

A

Development
Behaviour
Healthy eating

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29
Q

When are the health reviews conducted?

A

1 + 2 years

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30
Q

When are the 5th immunisations and what do they include?

A

3 years 4 months
DTP, polio, 2nd MMR

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31
Q

What is checked at 4 years?

A

Vision

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32
Q

What is checked on school entry?

A

Height, weight, hearing

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33
Q

When are the 6th and 7th immunisations and what do they include?

A

6th immunisations are at 12-14 years: 2 x HPV (6,11,16,18)

7th immunisations = at 14 years, DTP, MenACWY

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34
Q

Which paediatric milestones are checked at the 1 year health review?

A

GM: should be walking unsteadily + standing independently

FM: pincer grip (check for no hand dominance)

Hearing/ speech/ language: 2/3 words other than dada/ mama with intent

Social/emotional/ behavioural: drink from cup with 2 hands

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35
Q

What is the mnemonic for remembering the components of the 6-in-1 vaccine?

A

Parents Will Immunise Toddlers Because Death -
Polio
Whooping cough
Influenzae B
Tetanus
B (hepatitis)
Diptheria

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36
Q

What colours of skin would be a red flag in the traffic light system?

A

Pale/ mottled/ ashen/ blue

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37
Q

At what age is a child with fever always considered a red flag in the traffic light system?

A

<3 months

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38
Q

Recall how CPR differs in adults compared to children and neonates

A

Adults: 30:2
Children: 15:2
Neonates: 3:1

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39
Q

In the ABCDE formulation, what comes under ‘disability’?

A

AVPUG - Alert, voice, pain, unresponsive, glucose

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40
Q

What is the most common surgical emergency in newborn babies?

A

Necrotising enterocolitis

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41
Q

Describe the decorticate and decerebrate positions

A

Decorticate = bending wrists up to neck
Decerebrate = wrists pointing out, arms straight down by sides

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42
Q

What is SIRS?

A

Generalised inflammatory response, defined by >/= 2 criteria:
Must inculde 1 of:
- Abnormal temp (<36, >38.5)
- Abnormal WCC
The other criteria are:
- Abnormal HR
- Raised RR

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43
Q

How is a high risk sepsis diagnosed?

A

CVS: hypotension, prolonged cap refil, O2 needed to maintain SpO2
Blood lactate >2
Pale, mottled or non-blanching purpuric rash
RR abnormal or grunting

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44
Q

What is the sepsis 6 pathway in adults?

A

Oxygen
Blood + blood cultures
IV Abx
IV fluids
Check serial lactates
Check urine output

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45
Q

What is the difference between Sepsis and SIRS?

A

Sepsis = SIRS with infection

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46
Q

How is severe sepsis defined?

A

Sepsis with CV dysfunction, ARDS or dysfunction 2 or more organs

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47
Q

How is septic shock defined?

A

Sepsis with CV dysfunction persisting after >, 40mL/kg of fluid resuscitation in 1 hour

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48
Q

What are the common organisms implicated in early onset neonatal sepsis?

A

GBS
E coli
L monocytogenes

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49
Q

Which organism is most likely to cause late onset neonatal sepsis?

A

Coagulase-negative staphylococcus (CoNS) eg. Staph. Epidermis

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50
Q

Which children with sepsis should have an LP?

A

<1 month old
1-3 months who appear unwell/ have WCC <5 or >15

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51
Q

What is the sepsis 6 pathway in children?

A

Give:
1. High-flow O2
2. Abx
- Early-onset neonatal = cefotaxime, amikacin + ampicillin
- Late-onset neonatal =meropenem+ amikacin + ampicillin
- >3m old = ceftriaxone)
3. Early senior input
4. Early inotropic support
5. Fluid resus if indicated (20mls/kg 0.9% NaCl over 5-10 mins)

Take:
1. Bloods:
FBC (abnormal WCC?)
U&E + CRP (?urosepsis)
Glucose
Clotting (?DIC)
ABG + lactate

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52
Q

Which Abx are most useful in meningococcal sepsis?

A

IM benzylpenicillin (in community)
or
IV cefotaxime (in hospital)

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53
Q

Which Abx are most useful in early onset neonatal sepsis?

A

Most likely to be GBS, L. monocytogenes or E coli so:
IV cefotaxime + amikacin + ampicillin

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54
Q

Which Abx are most useful in late onset neonatal sepsis?

A

Most likely to be CoNS (s. epidermis) so:
IV meropenem + amikacin + ampicillin

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55
Q

What is opisthotonos?

A

Hyperextension of neck + back

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56
Q

What are the two ‘signs’ indicative of meningitis?

A

Kernig’s sign: pain on leg straightening
Brudzinski’s sign: supine neck flexion –> knee/ hip flexion

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57
Q

What type of rash is often present in meningitis and what type of meningitis is this most common in?

A

Non-blanching: meningococcal

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58
Q

How does the HR change throught the course of illness in meningitis?

A

Starts high to compensate for brain ischaemia, then drops to as baroreceptors sense high BP

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59
Q

What symptoms make up Cushing’s triad of high ICP?

A

High BP
Low HR
Irregular RR

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60
Q

In what order should meningitis investigations be done?

A

First: LP if not contraindicated to identify source of infection
Next:
1. VBG: including glucose + lactate
2. Blood cultures (BEFORE empirical abx started)
3. FBC, CRP, U+E and creatinine
(After this: give broad spec abx at highest possible dose without delay)

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61
Q

As well as sepsis 6 pathway + Abx, what should the management be in meningitis in children?

A

Steroids (dexamethosone) if CSF shows purulent CSF, WBC >10000, WCC + protein >1g/L, bacterial gram stain + ONLY if it’s not meningococcal

Mannitol (to reduce ICP)

IV saline NaCl

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62
Q

What potential longterm complications of meningitis might need to be discussed with a child’s family?

A

Hearing loss, renal failure, neurodevelopmental conditions
Purpura fulminans: haemorrhagic skin necrosis from DIC

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63
Q

What are the most common causes of viral meningitis?

A

Coxsackie Group B
Echovirus

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64
Q

What is encephalitis?

A

Inflammation of the brain parenchyma

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65
Q

What are the 3 possible aetiologies of encephalitis?

A
  1. Direct invasion of cerebellum (eg HSV)
  2. Post-infectious encephalopathy = delayed brain swelling following neuroimmunological response to antigen
  3. Slow virus infection (eg HIV or SSPE following measles)
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66
Q

What are the signs and symptoms of encephalitis?

A

Same as meningitis: might not be able to tell the difference clinically! If behavioural change is more likely to be encephalitis

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67
Q

What are some contraindications for LP?

A

Cardiorespiratory instability
Signs of raised ICP
Thrombocytopaenia
Focal neurology
Coagulopathy
Meningococcal meningitis

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68
Q

How should encephalitis be managed?

A

IV acyclovir (high dose) for 3 weeks
HSV is a rare cause but complications are major so treat empirically

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69
Q

What should be added to the treatment regime if it’s a CMV encephalitis?

A

Ganciclovir + Foscarnet

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70
Q

What is anaphylaxis?

A

Type 1 hypersensitivity reaction
IgG cross-linking with IgE membrane-bound Ab of mast cell/ basophil

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71
Q

What is the most common cause of anaphylaxis in children?

A

Food allergy (85%)

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72
Q

What is the dose of IM adrenaline in paediatric anaphylaxis?

A

1:1,000

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73
Q

When can a repeat dose of IM adrenaline be given in paediatric anaphylaxis treatment?

A

If response after 5 mins is insufficient

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74
Q

After giving adrenaline, how should anaphylaxis be managed?

A

Establish airway + high flow O2
IV fluids (crystalloids)
IV chlorpheniramine
IV hydrocortisone
Salbutamol if wheeze

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75
Q

What is the first thing that must be done on observation of a dry baby at delivery?

A

Note time!

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76
Q

What must be done within the first 30 seconds of a neonatal resuscitation?

A

Assess tone, RR, HR (femoral + brachial) + colour

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77
Q

What must be done within the first 60 seconds of a neonatal resuscitation?

A

If not breathing, open airway, do 5 INFLATION BREATHS
Reassess + repeat until chest movement seen

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78
Q

Once chest movement is seen in a neonatal resuscitation, what should be done next?

A

Ventilate for 30s
Then chest compression + ventillation with a rate of 3:1

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79
Q

If HR remains undetectable/ slow in a neonatal resuscitation, what should be considered?

A

Consider venous access + drugs

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80
Q

When should the Apgar score be used?

A

At 1 + 5 mins after delivery, + every 5 mins after if condition remains poor

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81
Q

What apgar score is considered normal?

A

> 7

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82
Q

What are the components of the apgar score?

A

Appearance (colour)
Pulse
Grimace
Activity (muscle tone)
Respiratory

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83
Q

What should be considered if, after tracheal intubation, HR does not increase and good chest movement is not achieved in a neonatal resuscitation?

A

DOPE:
Displaced tube
Obstructed tube
Patient (tracheal obstruction? Lung disorder? Shock? Choanal atresia?)
Equipment failure

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84
Q

When should 5 rescue breaths be given in paediatric BLS?

A

DR AB RESCUE BREATHS CDE

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85
Q

At what BPM should chest compressions be done in paediatric BLS?

A

100-120

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86
Q

What classifies as a stillbirth (rather than a miscarriage)?

A

Foetus born with no signs of life >24 weeks of pregnancy

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87
Q

What is the difference between the perinatal and neonatal mortality rate?

A

Perinatal = stillbirths + deaths within 1st week
neonatal = deaths of live-born infants in first 4 weeks after birth

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88
Q

For how long is a baby considered a neonate?

A

Up to 28 days old

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89
Q

What is considered ‘term’?

A

27-41 weeks old

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90
Q

Recall the cutoff rates for low, very low and extremely low birthweight

A

Low = <2500g
Very low = <1500
Extremely low = <1000

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91
Q

How is small/large for gestational age calculated?

A

Small = in <10th centile, large = >90th centile

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92
Q

What does a routine neonate inspection exam include?

A

Head to toe systematic:
1. Birthweight + gestational age
2. General observation - posture? Pallor? Rash?
3. Head (many things to look for)
4. Breathing, HR + peripheral saturations
5. Femoral pulses + genitalia
6. Musle tone, DDH, whole of back + spine, DDH/ Club feet?
7. Reflexes

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93
Q

What is being looked for upon examination of the neonatal head ?

A

Head circumference (macrocephaly?)
Eyes (red reflex?)
Cephalohematoma (benign, self-resolving)
Caput Succedaneum = Cross Suture lines (self-resolving)
Tense fontanelle (raised ICP?)
Depressed fontanelle (dehydrated?)

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94
Q

What are the primitive reflexes?

A

Moro
Stepping
Asymmetric tonic
Palmar
Babinski’s

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95
Q

What are the components of the test for DDH?

A

Barlow’s (abduct and push joint posteriorly)
Ortolani’s (lift and externally rotate)

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96
Q

What is the Guthrie test?

A

Biochemical screening

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97
Q

When should the Guthrie test be done?

A

At 7 days old

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98
Q

What is included in the Guthrie test?

A

Congenital hypothyroidism
SCD
CF
6 metabolic diseases:
- PKU
- MCADD
- Maple Syrup Urine disease
- IVA (isovaleric acidaemia)
- Glutaric aciduria type 1
- HCU (homocysteinuria )

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99
Q

Which type of infection can cause sensorineural hearing loss in neonates?

A

CMV

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100
Q

What is the 1st and 2nd line options for testing hearing at birth?

A

1st line: Evoked otoacoustic emission- If earphone doesn’t produce an echo…
2nd line: Automated auditory brainstem response- Computer analyses the EEG wave forms evoked in response to a series of clicks

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101
Q

What features of FAS would be seen in the neonatal examination?

A

Microcephaly
Absent philtrum
Cardiac abnormalities
Reduced IQ
IUGR
Small upper lip

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102
Q

What is the triad of features seen in Rubella syndrome?

A

Cataracts
Deafness
Cardiac abnormalities

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103
Q

What abnormalities would be seen in a baby who is born to a mother with syphillis?

A

Saddle nose
Rhinitis
Deafness
Hepatosplenomegaly
Jaundice

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104
Q

What is the NIPE and when should it be done?

A

Neonatal + infant Physical Examination

<72 hours AND 6-8 weeks

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105
Q

What are the 4 major areas of the NIPE?

A

Heart, Eyes, Testes, Hips

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106
Q

What is positional talipes, and what causes it?

A

Feet remaining in in-utero position, due to intrauterine compression

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107
Q

How should positional talipes be managed?

A

Physiotherapy

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108
Q

What is club foot known as medically?

A

Talipes equinovarus

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109
Q

How should club feet be managed?

A

Ponsetti method (plaster casting and bracing)
Surgery if severe

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110
Q

What is the cause of hypoxic ischaemic encephalopathy ?

A

Perinatal asphyxia - may be due to placental abruption, interruption of umbilical blood flow (eg shoulder dystocia –> cord compression), maternal hypotension, IUGR or failure to breathe at birth

111
Q

If hypoxic ischaemic encephalopathy continues post-natally, what will it cause?

A

Cerebral palsy

112
Q

What are the key features of mild hypoxic ischaemic encephalopathy ?

A

Staring eyes, hyperventilation, hypertonia

113
Q

What are the key feature of moderate hypoxic ischaemic encephalopathy ?

A

Cannot feed, possible seizures, hypotonic

114
Q

What are the key features of severe hypoxic ischaemic encephalopathy ?

A

No normal movement in response to pain, tone fluctuates between hypertonic and hypotonic, seizures refractory to treatment, MODS

115
Q

How should hypoxic ischaemic encephalopathy be managed?

A

Supportively
Resp support, anticonvulsants, fluid restriction (transient renal impairment), inotropes (to treat hypotension), therapeutic hypothermia (requires NICU)

116
Q

At what age does brain injury classify as ‘acquired brain injury’ and not cerebral palsy?

A

2 years old

117
Q

How can cerebral palsy be aquired post-natally?

A

Perventricular leukomalacia secondary to ischaemia (eg meningitis, very prem birth)

118
Q

Recall some features of abnormal posture/tone due to cerebral palsy

A

Stiff legs which scissor
Hypotonia or spasticity
Inability to lift head
Rounded back when sitting
Fisted hands

119
Q

Other than postural/ limb tone abnormalities, what abnormalities might be seen in cerebral palsy?

A

Feeding difficulties, abnormal gait, hand preference before 1 year old

120
Q

How is gross motor function classified?

A

GMFCS (gross motor funtion classification system!)

121
Q

What are the subtypes of cerebral palsywith their relative prevalences?

A

Spastic CP (90%)
Dyskinetic CP (6%)
Ataxic CP (4%)

122
Q

What is the cause of spastic cerebral palsy?

A

Damage to UMN pathway (pyramidal tracts)

123
Q

What is one of the pathognomonic features of spastic cerebral palsys opposed to other types of cerebral palsy?

A

Clasp knife rigidity - increased tone suddenly gives way under pressure

124
Q

What are the 3 main types of spastic cerebral palsy?

A

1) unilateral/ hemiplegia:
- unilateral arm + leg, face spared
- tiptoe walk on affected side
- likely to have an unremarkable Mx + birth

2) BL/ quadriplegia: all 4 limbs, often severe
- poor head control –> low central tone + seizures - often have LD

3) Diplegia (legs affected to a greater degree)
- Abnormal walk
- A/w pre-term birth damage

125
Q

What are the possible causes of dyskinetic cerebral palsy?

A

HIE or kernicterus

126
Q

What is kernicterus?

A

Brain damage due to hyperbilirubinaemia

127
Q

Describe the phenotype of dyskinetic cerebral palsy

A

Variable muscle tone predominated by primitive motor reflexes:
- Chorea
- Athetosis (fanning fingers)
- Dystonia (twisted appearance)

128
Q

What is the cause of ataxic cerebral palsy?

A

Damage to cerebellum - most geneticly determined

129
Q

How should cerebral palsy be investigated?

A

History, clinical examination and developmental progress - if cause is not clear, MRI

130
Q

What one clinical sign is always an indication for referral for cerebral palsy investigation?

A

Persistent toe walking

131
Q

What are some red flags for other neurological conditions when considering a diagnosis of cerebral palsy?

A

Absence of other risk factors
FHx of progressive neurological disorder
Loss of already attained cognitive/ developmental abilities
MRI suggestive of progressive neurological disorder

132
Q

How should cerebral palsy be managed?

A

Very MDT orientated
- Info about prognosis: eg children who can sit by age 2 are likely to be able to walk unaided by 6
- SCOPE disability charity
- Medication: stiffness = diazepam, sleeping = melatonin, constipation = movicol, drooling = anticholinergic

133
Q

Recall some important things to say in PACES counselling of a cerebral palsy child’s parents

A

Explain that brain damage has occurred in early development
Explain that damage doesn’t get worse, but will change its manifestation as the child gets older
Refer to MDT - especially paediatrician
Longterm management = physiotherapy, SALT + SEN
Medication options

134
Q

Which babies are at highest risk of developing NEC?

A

Premature/ LBW

135
Q

What is the aetiology of NEC?

A

Mostly unknown but thought to be a combination of poor blood flow + infection

136
Q

What are the early signs of NEC?

A

Biliary vomiting (green)
Feeding intolerance

137
Q

What will be seen on AXR in NEC?

A

Gas cysts

138
Q

What are the appropriate investigations to do in NEC?

A

AXR
Blood cultures

139
Q

What are the criteria used to decide management of NEC?

A

Bell’s staging

140
Q

Recall the elements of NEC management

A
  1. Bowel rest: stop oral feed + switch to parenteral nutrition
  2. Broad-spectrum Abx (eg Tazocin): duration depends on stage
  3. Laparotomy (if perforation is seen on AXR)
141
Q

Give some reasons for physiological jaundice at birth

A
  1. Hb release from RBCs as there is high [Hb] at birth
  2. RBC lifespan being 70 days rather than 120 days
  3. Breast milk jaundice (but not until after >24 hours)
  4. BR metabolism being less efficient in first few days of life
142
Q

What is the main danger of uBR buildup in neonates?

A

Kernicterus (a form of encephalopathy): it’s caused by a deposit of uBR in the basal ganglia
May develop into dyskinetic CP, LD + sensorineural deafness

143
Q

How can uBR buildup in neonates be treated before any damage is done?

A

Phototherapy +/- IvIG and exchange transfusion

144
Q

What would be the difference in clinical presentation between uBR buildup and cBR buildup?

A

uBR buildup –> kernicterus
cBR buildup –> dark urine + pale stools

145
Q

In what situations should phototherapy be stopped?

A

If bronzing occurs: it means the child has a buildup of cBR, rather than uBR, which cannot be treated using phototherapy

146
Q

How should investigations begin in neonatal jaundice?

A
  1. Check transcutaneous or serum BR levels
  2. Do a split BR to check uBR/cBR
  3. May want to do a blood film analysis
147
Q

Recall some pathological causes of neonatal jaundice in babies <24 hours old

A

GRAPHIC DOG
- Gilbert’s
- Rhesus disease
- ABO incompatability (–> haemolysis)
- PK deficiency
- Hereditary spherocytosis
- Infection
- Crigler-Najjar
- Dubin-Johnson
- Other…
- G6PD deficiency

148
Q

Recall 3 physiological causes of jaundice in a 2 day to 2 week old baby

A

Physiological jaundice
- due to immature liver, peaks at 3-5 days
Breastfeeding jaundice
- less milk intake –> more enterohepatic recycling
Breastmilk jaundice
- Decreased UGT1A1 activity (occurs following physiological jaundice)

149
Q

What haemolytic and metabolic causes for jaundice might present in a 2 day to 2 week old baby?

A

Metabolic = Gilbert’s, Crigler-Najjar, Dubin-Johnson
Haemolytic: G6PDD, PK deficiency, hereditary spherocytosis (less likely to be ABO at this point)

150
Q

What may be the cause of jaundice in a 2 day to 2 week old baby that didn’t present in first 24 hours?

A

Congenital hypothyroidism
Dehydration
Bruising (cephalohematoma)
Polycythaemia

151
Q

How should jaundice be investigated in a baby over 2 weeks old?

A

Direct and indirect serum BR

152
Q

Which of the conditions that cause jaundice in a 2 day to 2 week old baby might continue to the >2 weeks stage?

A

All - but physiological + breastmilk is most common

153
Q

Recall 2 further causes of a buildup of uBR in a baby over 2 weeks old

A

Pyloric stenosis (presents at 2-4 weeks)
Congenital hypothyroidism*

154
Q

Systematically recall the causes of a raised cBR in the neonate (>2w old)

A

Endocrine: Congenital hypothyroidism

GI: Billiary atresia, ascending cholangitis (can be caused by lipids on TPN)

Metabolic: Gal-1-PUT, A1AT deficiency, Tyrosinaemia type 1, peroxisomal disease

Other: CF, idiopathic neonatal hepatitis

155
Q

For how long does jaundice have to persist in order to be defined as ‘prolonged’?

A

> 14 days if term
21 days if pre-term

156
Q

At what age should investigations include a split BR rather than just a total BR?

A

2 weeks

157
Q

What is a worrying BR in a baby >37w gestation (red flag for kernicterus)?

A

> 340

158
Q

Recall the clinical features of kernicterus

A

Poor feeding, extreme letahrgy, hypotonia, high-pitched cry

159
Q

Recall some investigations you might do to find the underlying cause of jaundice in a baby

A

TC/ serum BR within 6 hours of presentation

Haematocrit

DAT/ Coombs (haemolysis?)

G6PD levels (depending on ethnic origin)

TSH (hypothyroid?)

LFTs (ascending cholangitis? Biliary atresia?)

Blood group of M and B (ABO incompatible? Rhesus?)

Blood film + osmotic fragility (hereditary spherocytosis?)

MC&S of urine/ CSF (if ? infection cause)

160
Q

How is treatment of neonatal jaundice guided?

A

There are thresholds at which phototherapy/ exchange transfusion are indicated

161
Q

What are the options for treatment of neonatal jaundice?

A

Phototherapy +/- IV Ig
Exchange transfusion + phototherapy +/- IV Ig

162
Q

How does phototherapy work?

A

Converts uBR to a water-soluble pigment that is excreted in urine

163
Q

What important checks should be done during/ after phototherapy?

A

During: temperature, BR levels every 4-6 hours (with regular feed breaks)
After (12-18 hours post): check for a rebound hyperbilirubinaemia

164
Q

When should intensive phototherapy be given?

A
  1. Rapidly rising BR
  2. Serum BR within 50mmol of exchange tranfusion threshold (after 72 hours life)
  3. BR level doesn’t respond after 6 hours of therapy
165
Q

What are the 2 indications for exchange transfusion to treat neonatal jaundice?

A
  1. BR threshold reached
  2. Signs of kernicterus
166
Q

What is an important thing to remember when giving an exchange transfusion?

A

Give folic acid afterwards to prevent anaemia

167
Q

What is one thing to be cautious of if delivering high oxygen levels to a neonate?

A

Retinopathy of prematurity

168
Q

Recall some signs of respiratory distress in babies

A

High RR (>60)
Laboured breathing
Chest wall recessions
Nasal flaring
Expiratory grunting
Cyanosis (if severe)

169
Q

What is the most common cause of respiratory distress in term infants?

A

Transient tachypnoea of the neonate

170
Q

Recall 4 conditions that PPHTN can be secondary to

A

Birth Asphyxia
Meconium aspiration
Septicaemia
RDS

171
Q

What is the pathophysiology of PPHTN?

A

High pulmonary vascular resistance –> right to left shunting within lungs at atrial and ductal levels

172
Q

Recall some signs and symptoms of PPHTN

A

Cyanosis after birth
Absent heart murmurs + signs of HF

173
Q

What investigations are appropriate in PPHTN and what would they show if pos?

A

CXR: normal heart size but some pulmonary oligaemia
Echo: to ensure no cardiac defect

174
Q

How should PPHTN be treated?

A

Oxygen, NO (inhaled), sildenafil (!!) Ventilation: mechanical, high frequenct (oscillatory) OR, if severe, extracorporeal membrane oxygenation (ECMO) +/- heart/lung bypass

175
Q

What is the cause of TTotN?

A

Delay in resorption of lung fluid

176
Q

How is a diagnosis of TTofN made?

A
  1. CXR - shows fluid in horizontal fissure
  2. Other causes excluded
177
Q

What are the possible causes of paediatric chronic lung disease?

A

Infection, barotrauma, iatrogenic injury

178
Q

What is the pathophysiology of paediatric chronic lung disease?

A

Lung damage due to pressure and volume trauma from artificial ventilation, O2 toxicity and infection

179
Q

What are appropriate investigations in paediatric chronic lung disease and what would pos results show?

A

CXR: widespread opacification

CBG/VBG: acidosis, hypercapnia, hypoxia

180
Q

How can paediatric chronic lung disease be managed?

A

Respiratory support (!): prolonged artificial ventilation –> wean to CPAP –> wean to additional O2

Corticosteroid therapy - dexamethosone is useful for short-term clinical improvement (but concerns limit use)

181
Q

What is the cause of RDS in neonates?

A

Deficiency of surfactant (common if born <28 weeks gestation)

182
Q

Recall some risk factors for RDS

A

DM mother
2nd born of premature twin

183
Q

How is RDS diagnosed?

A

It’s a clinical diagnosis
Can be supported by:
- Pulse oximetry
- CXR showing pneumothorax (from ventilation), ground-glass appearance

184
Q

How can RDS be managed antenatally and postnatally?

A

Antenatal: steroid therapy + tocolytic therapy so steroids have at least 24 hours to work
Postnatal: oxygen and ventilation (caution: CLD), CPAP

185
Q

What is the cause of pneumothorax in children, and what is the best way to prevent them?

A

Ventilation which causes pulmonary interstitial emphysema

Can be prevented that infants are ventilated on the lowest possible pressures with adequate chest movement and blood gaes

186
Q

How should infant pneumothorax be treated?

A

Immediate decompression
Oxygen therapy
Chest drain if tenion pneumothorax

187
Q

When does meconium aspiration occur?

A

Exclusively in immediate neonatal period

188
Q

What is the biggest RF for meconium aspiration?

A

Increased GA

189
Q

What are the signs and symptoms of meconium aspiration?

A

Respiratory distress, chest retraction, hypoxia

190
Q

How is meconium aspiration diagnosed?

A

CXR: shows overinflated lungs, patches of collapse and consolidation
May show pneumothorax or pneumomediastinum (from air leak)

191
Q

How is meconium aspiration managed?

A

Observation: there will be meconium-stained amniotic fluid and no history of GBS

IV ampicillin and IV gentamicin (to treat features of infection)

CPAP (for severe cases)

192
Q

What is meconium ileus?

A

Thick, sticky meconium that has a prolonged passing time

193
Q

What is the normal period of delivery of meconium?

A

Within 24 hours

194
Q

Recall 2 associations of meconium ileus

A

CF
Biliary atresia

195
Q

How should meconium ileus be managed?

A

1st line: Gastrograffin enema
2nd line: surgery

196
Q

Recall some differentials for billious vomiting in the neonate

A

NEC
Duodenal/ jejunal/ ileal atresia
Meconium ileus
Malrotation volvulus

197
Q

What is the most important investigation to do in investigating billious vomiting, and what results might it show?

A

AXR: “Double bubble” sign = duodenal atresia
Air-fluid levels - jejunal/ ileal atresia
Dilated bowel loops –> NEC

198
Q

How are duodenal/ jejunal/ ileal atresia managed?

A

Duodenal atresia –> duodenoduodenostomy
Jejunal/ ileal atresia –> laparotomy

199
Q

How is malrotation volvulus managed?

A

Ladd’s procedure

200
Q

When does malrotation volvulus present, and how is it diagnosed?

A

3-7 days
Upper GI contrast or USS

201
Q

What is the pathophysiology of cleft lip/ palate?

A

Failure of fusion of the frontonasal and maxiliary processes

202
Q

Recall one condition that babies with cleft lip/ palate are at an increased risk of

A

Secretory otitis media

203
Q

Recall 2 maternal risk factors for cleft lip/ palate

A

Antiepileptic/ BDZ use

204
Q

What are some pre-surgical concerns to bear in mind in cleft lip/ palate?

A

Specialised feeding
Watch out for aiway problems
Pre-surgical lip-tapping/ nasal alveolar modelling to narrow cleft

205
Q

What is the name for a left-sided diaphragmatic hernia?

A

Bochdalek hernia

206
Q

When does diaphragmatic hernia form in utero?

A

At around 6-8 weeks gestation

207
Q

Recall 2 factors affecting prognosis in diaphragmatic hernia

A
  1. Liver position
  2. Lung-to-head ratio
208
Q

What are the signs and symptoms of diaphragmatic hernia?

A

Respiratory distress at delivery
Concave chest at birth

209
Q

How is diaphragmatic hernia diagnosed?

A

Routine USS following resp distress at birth

210
Q

What does CXR show in diaphragmatic hernia?

A

mediastinum displaced to left, collapsed left lung, bowel loops in thorax

211
Q

Recall the 1st and 2nd line management options for diagphragmatic hernia management

A

1st: NG tube and suction - prevents distention of intrathoracic bowel and allows breathing

2nd: Surgical reduction and repair, allowing re-expansion of the lung
- TPN/ ventilation needed for recovery

212
Q

What is oesophageal atresia?

A

Malformation of the oesophagus so that it does not attach to the stomach

213
Q

What is tracheo-oesophageal fistula?

A

Part of the oesophagus is joined to the trachea - often occurs alonsgide OA

214
Q

What is the main risk of oesophageal atresia/ tracheo-oesophageal fistula?

A

Stomach acid can regurgitate into the lungs causing CLD/ BPD (bronchopulmonary dysplasia)

215
Q

How will amniotic fluid be affected by a TOF that is preventing swallow?

A

Polyhydramnios

216
Q

How should tracheo-oesophageal fistula/ oesophageal atresia be investigated?

A

NG tube to aspirate the stomach contents can quickly confirm or exclude

The gold standard = gastragaffin swallow

217
Q

Recall the management of oesophageal atresia/ tracheo-oesophageal fistula

A
  1. Replogle tube to drain saliva from oesophagus
  2. Surgical repair (within a few days of birth) followed by NICU and ventilator support
218
Q

What is biliary atresia?

A

Progressive fibrosis + obliteration of extra- + intra-hepatic trees, leading to chronic liver failure in 2 years

219
Q

What are the subtypes of biliary atresia?

A

T1 - common bile duct atresia
T2 - cystic duct atresia
T3 - full atresia (>90%)

220
Q

What are the signs and symptoms of bililary atresia?

A

Obstructive jaundic picture (pale stools, dark urine) with no vomiting
Hepatosplenomegaly
Normal BW –> faltering growth

221
Q

Once a raised cBR has been identified, how can biliary atresia be diagnosed? What, then, is the gold standard?

A

USS showing triangular cord sign
LFT shows raised GGT
Gold standard: TIBIDA isotope scan (radioisotope scan of bile secretion) confirmed by ERCP and biopsy

222
Q

What is the 1st-line management of biliary atresia?

A

Kasai hepatoportoenterostomy
Ligate fibrous ducts abive the join with the duodenum
Join an end of the duodenum directly to the porta hepatis of the liver
If unsuccessful –> transplant

223
Q

How are the complications of biliary atresia managed?

A

Fat-soluble vitamins (as bile ducts affected)
Usodeoxycholic acid (this promotes bile flow)
Prophylatic Abx (to prevent cholangitis - cotrimoxazole)

224
Q

What is small bowel atresia?

A

Congenital absence or complete closure of part of the lumen of the small bowel

225
Q

Recall 3 associations of duodenal atresia

A

Congenital cardiac abnormalities
Down’s
Polyhydramnios

226
Q

What are the signs and symptoms of small bowel atresia?

A

Bile-stained vomiting is the main one

If non-bilious may be duodenal rather than jejunal/ ileal

Abdominal distention

227
Q

How should small bowel atresia be managed?

A

ABCDE to stabilise neonate+/- NG tube decompression
Surgical:
- primary anastomosis or LADD procedure if malrotation is present
- Need to examine the whole bowel while you’re at it to exclude other multiple atretic segments

228
Q

What is the main gene implicated in CAKUT?

A

PAX 2

229
Q

Recall 4 renal conditions of CAKUT

A

Multicystic kidneys
Renal agenesis
Medullary sponge kidney
Horseshoe kidney

230
Q

Recall 3 non-renal conditions of CAKUT

A

Pelvouteric junction obstruction
Vesicoureteral reflux (in 30% of children presenting with UTIs)
Bladder outlet obstruction

231
Q

Recall some antenatal signs of CAKUT

A

Oligohydramnios
Decreaed foetal UO

232
Q

Recall some postnatal signs of CAKUT

A

Often present with UTI
Intra-abdominal mass
Haematuria
Renal calculi/ renal failure
Hepatosplenomegaly

233
Q

What is Potter’s sequence?

A

BL renal agenesis
Abnormal facies (widely separated eyes, low set ears, receding jaw)
Caused by OLIGOHYDRAMNIOS

234
Q

Recall five important investigations you could do when looking for a cause of CAKUT

A

Renal USS
DMSA scan (Tc-99) - detects scarring + functional defects
MCUG (micturating cystourethrogram) - visualises anatomy (would see VUR)
MAG3 renogram (also Tc-99) - dynamic screen shows MAG3 being excreted into urine using furosemoide
Genetic karyotyping

235
Q

What are some signs of an atypical UTI?

A

Poor UO
Sepsis
Abdo/bladder mass
Failure to respond in <48 hours
Raised creatinine
Infection with non-E coli organisms

236
Q

How do you choose which investigation to use in UTI?

A

If atypical UTI, recurrent UTI, or first UTI
<6m: Renal USS
If recurrent UTI or atypical UTI <3 years old: DMSA scan
If VUR is suspected on USS, obstruction or trauma: MCUG/ VCUG

237
Q

What is the pathophysiology of VUR?

A

The ureters enter the bladder perpendicularly –> shorter intramural course –> VUR

238
Q

What is the main factor affecting prognosis of VUR?

A

Whether there’s a renal cause or not: renal causes have a bad prognosis but non-renal causes have a pretty good prognosis if treated

239
Q

What are the types of anorectal malformation, and how can you tell the difference between them?

A

Low anorectal anomaly = anus closed over - in a different position or narrower than usual + fistula to skin
High anorectal anomaly - bowel has closed end at high level, not connecting with anus - fistula is usually to bladder/ urethra/ vagina

240
Q

What are the symptoms of anorectal malformation?

A

Absent/ delayed meconium
Swollen abdomen
Vomiting
If there’s a fistula they may pass stool from an abnormal area

241
Q

How should anorectal malformation be investigated?

A

Checked on neonatal check - it’s a clinical dx

242
Q

How is anorectal malformation managed in babies?

A

Surgical correction by 9 months

243
Q

What is the normal period of time in which the testes descend?

A

Usually by 3m but can be up to 6m

244
Q

At what point should a referral to a paediatric surgeon be made, if there is UL testicular undescent?

A

3 months

245
Q

At what point should a referral to a paediatric surgeon be made, if there is BL undescent of testes?

A

May have a pituitary cause so immediately refer to paeds/ endo

246
Q

What are the medical and surgical management options for cryptorchidism?

A

Medical: beta-hCG (may or may not be given)
Surgical: orchidopexy

247
Q

What is billious vomit a red flag for?

A

Intestinal obstruction (intussusception, malrotation, strangulated inguinal hernia)

248
Q

What is haematemesis a red flag for?

A

Oesophagitis/ PUD

249
Q

What is projectile vomit at 2-7 weeks a red flag for?

A

Pyloric stenosis

250
Q

What is vomiting at end of paroxysmal coughing a red flag for?

A

Whooping cough

251
Q

What is abdo distention a red flag for in a baby?

A

Intestinal obstruction
Strangulated inguinal hernia

252
Q

What is hepatosplenomegaly a red flag for?

A

Chronic liver disease
Inborn error of metabolism

253
Q

What is blood in stool a red flag for?

A

Intussusception
Gastroenteritis (salmonella, campylobacter)

254
Q

What are bulging fontanelles/ seizures a red flag for?

A

Raised ICP

255
Q

What is a failure to thrive a red flag for?

A

GORD
Coeliac
Chronic GI

256
Q

What is chronic vomiting in an infant most likely to be due to?

A

GORD or a feeding problem

257
Q

What is transient vomiting in a child most likely to be due to?

A

Gastroenteritis
URTI

258
Q

What needs to be excluded urgently when an infant is vomiting?

A

Meningitis
UTI

259
Q

What is a failure to pass meconium in first 24 hours a red flag for?

A

Hirschprung’s

260
Q

What is FTT/ growth failure a red flag for in a constipated child?

A

Hypothyroid/ coeliac

261
Q

What is gross abdo distention with constipation a red flag for?

A

Hirschprung’s/ other GI dysmotility

262
Q

What is abnormal LL neurology/ deformation a red flag for?

A

Lumbosacral pathology

263
Q

What is a red flag for spina bifida?

A

Sacral dimple above nasal cleft

264
Q

What is perianal fistula/ abscess/ fissure a red flag for in infants?

A

Perianal Crohn’s

265
Q

What is the normal feed pattern in newborns?

A

45-90ml per 2-3 hours

266
Q

What is the normal feed pattern in a 2 month old?

A

120-150mls per 3/4 hours

267
Q

What is the normal feed pattern in a 6 month old?

A

Solids should be being introduced

268
Q

By what age should bowel habit be similar for a child as an adult?

A

4 years

269
Q

Recall the most common complication of long-standing constipation in children

A

Over-distention
Lose feeling needed to defaecate
Iinvoluntary soiling with overflow

270
Q

How can constipation be treated in children?

A

Stool softeners (eg movicol)
If unsuccessful consider stimulant laxatives (eg senna)
Movicol can be used as a maintenance therapy

271
Q

How is constipation diagnosed in a child?

A

2+ of the following:
< 3 complete stools per week
Hard, large stool or ‘rabbit dropping’
Overflow soiling 1+ year
Distress, pain, bleeding associated with stool

272
Q

Recall the management protocol for paediatric status epilepticus

A
  1. ABC
  2. Check blood glucose - if <3mmol/L –> IV glucose and then re-check
  3. If vascular access –> IV lorazepam
    If no vascular access –> PR diazepam/ buccal midazolam
  4. If IV access: More lorazepam
    If still no IV access - PR paraldehyde
  5. If previously had IV access to give IV lorazepam but it hasn’t worked, try PR paraldehyde
  6. If no response in 10 mins call for senior help
    If not on oral phenytoin: phenytoin
    If already on oral phenytoin: phenobarbital
  7. If no response within 20 mins, call anaesthetist/ intensivist –>
    Induction with thiopental
    Mechanical ventilation
    –> PICU
273
Q

What is the dose per kg of lorazepam to give to children in status epilepticus?

A

0.1mg/kg

274
Q

What is the dose per kg of diazepam to give to children in status epilepticus?

A

0.5mg/kg

YR5 Specialties (27 decks)

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