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resp Flashcards

1
Q

why is prompt recognition and treatment of acute epiglottitis important?

A

airway obstruction can develop

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2
Q

what is acute epiglottitis caused by?

A

Haemophilus influenzae type B

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3
Q

what are the features of acute epiglottitis?

A
  1. rapid onset
  2. high temperature, generally unwell
  3. stridor
  4. drooling of saliva
  5. ‘tripod’ position: pt finds it easier to breathe if leaning forward and extending neck in seated position
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4
Q

how is the diagnosis of acute epiglottitis made?

A

direct visualisation via laryngoscopy

X-rays can be done, especially if there is concern about a foreign body

(lateral view: ‘thumb sign’ swelling of epiglottis)

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5
Q

how is acute epiglottitis managed?

A
  1. immediate senior involvement + anaesthetics, ENT (emergency airway support): ET may be necessary to protect airway
  2. if suspected, DO NOT examine the throat due to risk of acute airway obstruction
  3. oxygen
  4. IV abx
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6
Q

what should you NOT do if you suspect acute epiglottitis and why?

A

examine the throat as this can cause acute airway obstruction

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7
Q

what is croup and what is it characterised by?

A

an URTI seen in infants and toddlers

characterised by stridor caused by a combination of laryngeal oedema and secretions

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8
Q

what is croup caused by?

A

parainfluenza viruses

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9
Q

what is the peak incidence for croup?

A

6 months to 3 years

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10
Q

what are the features of croup?

A
  1. stridor
  2. barking cough (worse at night)
  3. fever
  4. coryzal symptoms
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11
Q

what are the different severity of croup?

A
  1. mild
  2. moderate
  3. severe
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12
Q

what defines mild croup?

A
  • occasional barking cough
  • no audible stridor at rest
  • no / mild suprasternal +/- intercostal recession
  • child is happy, prepared to eat, drink and play
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13
Q

what defines moderate croup?

A
  • frequent barking cough
  • easily audible stridor at rest
  • suprasternal and sternal wall retraction at rest
  • no / little distress or agitation
  • child can be placated and is interested in its surroundings
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14
Q

what defines severe croup?

A
  • frequent barking cough
  • prominent inspiratory (and occasionally, expiratory) stridor at rest
  • marked sternal wall retractions
  • significant distress and agitation / lethargy / restlessness (a sign of hypoxaemia)
  • tachycardia occurs with more severe obstructive symptoms and hypoxaemia
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15
Q

when do you admit a child with croup?

A

moderate / severe croup

other features:

  • <6 months age
  • known upper airway abnormalities (e.g. Laryngomalacia, Down’s)
  • uncertainty about dx
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16
Q

what are other important differentials to consider for croup?

A
  1. acute epiglottitis
  2. bacterial tracheitis
  3. peritonsillar abscess
  4. FB inhalation
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17
Q

what is the management for croup?

A

single dose of oral dexamethasone (0.15 mg/kg) to all children regardless of severity

[prednisolone is an alternative]

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18
Q

what should be given in an emergency for croup?

A
  1. high-flow oxygen
  2. nebulised adrenaline
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19
Q

when do you start low dose inhaled corticosteroid (ICS) in chidren > 5 years old?

A

Not controlled on previous step (with SABA only)
OR
Newly-diagnosed asthma with symptoms >= 3 / week or night-time waking

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20
Q

what is bronchiolitis and what is the pathogen responsible?

A

a condition characterised by acute bronchiolar inflammation.

Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases.

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21
Q
  • most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against the pathogen
  • higher incidence in winter
A

bronchiolitis

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22
Q

what are the other causative organisms for bronchiolitis?

A

other causes: mycoplasma, adenoviruses

may be secondary bacterial infection

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23
Q

what comorbidities could a child have that makes bronchiolitis more serious?

A
  • bronchopulmonary dysplasia (e.g. Premature)
  • congenital heart disease
  • cystic fibrosis
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24
Q

what are features of bronchiolitis?

A
  • coryzal symptoms (including mild fever) precede
  • dry cough
  • increasing breathlessness
  • wheezing, fine inspiratory crackles (not always present)
  • feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission
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25
Q

when should you consider referring a child with bronchiolitis to hospital?

A
  • a respiratory rate of over 60 breaths/minute
  • difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume ‘taking account of risk factors and using clinical judgement’)
  • clinical dehydration.
26
Q

how do you investigate for bronchiolitis?

A

immunofluorescence of nasopharyngeal secretions may show RSV

27
Q

how is bronchiolitis managed?

A

largely supportive!

  • humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92%
  • nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
  • suction is sometimes used for excessive upper airway secretions
28
Q

In a child aged < 5 years with asthma not controlled by a SABA + paediatric low-dose ICS, what is the next step in Mx?

A

add a leukotriene receptor antagonist

29
Q

in children > 5 years old with asthma, what is the next step in management if SABA + paediatric low dose ICS + LTRA does not work?

A

(stop LTRA)

SABA + paediatric low dose ICS + LABA

30
Q

what does a normal pCO2 indicate in acute asthma attack?

normal pCO2 is 4.8-6kPa

A

indicates reduced respiratory effort

is therefore a life-threatening sign

31
Q

what are the criteria for a severe asthma attack?

A
  • spO2 < 92%
  • PEF 33-50% best or predicted
  • too breathless to talk or feed
  • HR >125 (>5years), >140 (1-5 years)
  • RR >30 bpm (>5 years), >40 (1-5 years)
  • use of accessory neck muscles
32
Q

what are the features of a life-threatening asthma attack?

A
  • spO2 <92%
  • PEF <33% best or predicted
  • silent chest
  • poor respiratory effort
  • agitation
  • altered consciousness
  • cyanosis
33
Q

what are the causes of snoring in children?

A
  • obesity
  • nasal problems: polyps, deviated septum, hypertrophic nasal turbinates
  • recurrent tonsillitis
  • Down’s syndrome
  • hypothyroidism
34
Q

what are amber signs in paediatric patients with a fever?

A
  • Nasal flaring
  • Lung crackles on auscultation
  • Not responding normally to social cues
  • Reduced nappy wetting
  • Dry mucous membranes
  • Pallor reported by parent or carer
35
Q

what are red signs in paediatric patients with a fever?

A
  • Moderate or severe chest wall recession
  • Does not wake if roused
  • Reduced skin turgor
  • Mottled or blue appearance
  • Grunting
36
Q

what are your dDx for stridor in children?

A
  1. croup
  2. acute epiglottitis
  3. inhaled foreign body
  4. laryngomalacia
37
Q

what are the sx of foreign body inhalation?

A

depends on site of impaction

sudden onset:

  • coughing
  • choking
  • vomiting
  • stridor
38
Q

what is laryngomalacia and how does it present?

A

congenital abnormalitiy of the larynx

infants present at 4 weeks of age with stridor

39
Q

what is surfactant deficient lung disease (SDLD) also known as?

A

respiratory distress syndrome

40
Q

in whom is SDLD seen in?

A

premature infants

41
Q

what is SDLD caused by?

A

insufficient surfactant production and structural immaturity of the lungs

42
Q

what does the risk of SDLD decrease with?

A

gestation

43
Q

what are the other risk factors for SDLD?

A
  1. male
  2. diabetic mothers
  3. C-section
  4. 2nd born of premature twins
44
Q

what are the clinical features of SDLD?

A

respiratory distress in the newborn

tachypnoea, intercostal recession, expiratory grunting, cyanosis

45
Q

what are the CXR findings for SDLD?

A

‘ground-glass’ appearance

indistinct heart border

46
Q

what is the mx for SDLD?

A
  1. prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation
  2. oxygen
  3. assisted ventilation
  4. exogenous surfactant given via endotracheal tube
47
Q

what is cystic fibrosis (CF)?

A

autosomal recessive disorder

causing increased viscosity of secretions (e.g. lungs and pancreas)

due to defect in CF transmembrane conductance regulator gene (CFTR)

which codes a cAMP-regulated chloride channel

48
Q

what are 80% of CF cases due to in the UK?

A

delta F508 on long arm of chromosome 7

49
Q

how many births does CF affect and what is the carrier rate?

A

affects 1 per 2500 births

carrier rate 1 in 25

50
Q

what are some organisms which may colonise CF pts?

A
  1. staph aureus
  2. pseudomonas aeruginosa
  3. bukholderia cepacia
  4. aspergillus
51
Q

what are the presenting features of CF in the neonatal period?

A

around 20%

  • meconium ileus
  • less commonly prolonged jaundice
52
Q

what are other presenting features of CF

A
  • recurrent chest infections (40%)
  • malabsoption (30%): steatorrhoea, faltering growth
  • other features (10%): liver disease
53
Q

when are most cases of CF picked up?

A

during newborn screening programmes or early childhood

but 5% of pts are dx-ed after 18 years old

54
Q

what are other features of CF?

A
  • short stature
  • DM
  • delayed puberty
  • rectal prolapse (due to bulky stools)
  • nasal polyps
  • male infertility, female subfertility
55
Q

how is CF diagnosed?

A

sweat test

  • pts with CF have abnormally high sweat chloride
  • normal value <40 mEq/l, CF >60 mEq/l
56
Q

what are some causes of false +ve sweat test?

A
  • malnutrition
  • adrenal insufficiency
  • glycogen storage diseases
  • nephrogenic diabetes insipidus
  • hypothyroidism, hypoparathyroidism
  • G6PD
  • ectodermal dysplasia
57
Q

what is the most common reason for false -ve sweat test?

A

skin oedema

due to hypoalbuminaemia/hypoproteinaemia 2˚ to pancreatic exocrine insufficiency

58
Q

how is CF managed?

A
  • multidisciplinary approach
  • regular chest physiotherapy and postural drainage (at least 2x/day)
  • high calorie diet, high fat intake
  • vitamin supplementation
  • pancreatic enzyme supplements
  • minimise contact with other CF pts to prevent cross infection
  • lung transplantation
  • Lumacaftor / Ivacaftor (Orkambi) for pts homozygous for delta F508 mutation
59
Q

what does Lumacaftor do?

A

increases the number of CFTR proteins that are transported to the cell surface

60
Q

what does Ivacaftor do?

A

a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through channel pore

61
Q

what is an important CF-specific contraindication to lung transplantation?

A

chronic infection with Burkholderia cepacia

paediatrics (23 decks)

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