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Paediatrics (Y4) > 3- Paediatric respiratory - breath sounds (2/3) > Flashcards

3- Paediatric respiratory - breath sounds (2/3) Flashcards

1
Q

Lower respiratory tract infections

A
  • Pneumonia
  • Acute bronchitis
  • Bronchiectasis exacerbation
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2
Q

Pneumonia
Background

A
  • Infection of lung tissue
  • Can be seen as consolidation on chest x-ray
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3
Q

causes of pneumonia

A

Bacteria
- Streptococcus pneumonia (most common)
- Group A strep (e.g. streptococcus pyogenes)
- Group B strep (in pre-vaccinated infants, often contracted during birth)
- Staphylococcus aureus (x-ray): round air filled cavities
- Haemophilus influenza
- Mycoplasma pneumonia (atypical)
o Extra-pulmonary manifestation such as Erythema multiforme

Virus
- Respiratory syncytial virus (RSV)
- Influenza and parainfluenza virus

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4
Q

pathophysiology of pneumonia

A
  • Infection causes inflammation of lung tissue and sputum filling the airways and alveoli
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5
Q

presentation of pneumonia

A
  • Cough (typically wet and productive)
  • High fever (> 38.5ºC)
  • Tachypnoea
  • Tachycardia
  • Increased work of breathing
  • Lethargy
  • Delirium (acute confusion associated with infection)
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6
Q

signs of pneumonia

A

There may be a derangement in basic observations. These can indicate sepsis secondary to the pneumonia:
* Tachypnoea (raised respiratory rate)
* Tachycardia (raised heart rate)
* Hypoxia (low oxygen)
* Hypotension (shock)
* Fever
* Confusion

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7
Q

Characteristics of chest signs of pneumonia:

A
  • Bronchial breath sounds these are harsh breath sounds that are equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway.
  • Focal coarse crackles caused by air passing through sputum similar to using a straw to blow into a drink.
  • Dullness to percussion due to lung tissue collapse and/or consolidation.
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8
Q

Investigations for CXR

A
  • Chest xray (not routinely required) – but the gold standard
  • Sputum cultures
  • Throat swabs for culture and viral PCR

Sepsis
- Blood cultures
- Capillary blood gas analysis and blood lactate

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9
Q

management of pneumonia

A

Antibiotics according to local guidelines
- E.g. PO Amoxicillin +- Macrolide (erythromycin/ clarithromycin) (will cover atypical pneumonia)
- If penicillin allergic can treat with just macrolide monotherapy
- IV Abx if sepsis or problems with intestinal absorption
- Oxygen if sats <92%

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10
Q

Complicated pneumonia

A

Background
- Parapneumonic effusion e.g.transudate/ exudate
- Empyema e.g. presence of pus in the pleural space

Investigation
- CXR

Management
- Long course of antibiotics
- Chest drain and intrapleural fibrinolytic agent (urokinase)
- VATS (video assisted thoracoscopic surgery)

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11
Q

Bronchiectasis

Background

A
  • Abnormal dilatation of the airways with associated destruction of bronchial tissue
  • Potentially reversible in children
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12
Q

Pathophysiology of bronchiectasis

A
  • Usually caused by severe infection which leads to structural damage within bronchial walls, which causes dilation.
  • Scarring which arises as a consequence of immune response, reduces the number of cilia within the bronchi-> further predisposing the individual to further infections
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13
Q

causes of bronchiectasis

A
  • Most associated with cystic fibrosis
  • Non-CF causes
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14
Q

NON-CF causes of bronchiectasis

A

Post-infections
- Streptococcus pneumonia
- Staphylococcus aureus
- Adenovirus
- Measles
- Influenza
- Mycobacterium tuberculosis

Immunodeficiency
- Antibody deficiency e.g. agammaglobulinemia, common variable immune deficiency of IgA/IgG deficiency
- HIV infection
- Ataxia telangiectasia

Primary ciliary dyskinesia e.g. Kartagener’s
- Autosomal recessive genetic defect -> causes reduced efficacy of bronchial cilia
- Reduces Mucociliary clearance – susceptible to infection

Post obstructive
- Foregin. Body aspiration

Congenital syndromes
- Youngs
o Bronchiectasis
o Reduced fertility
o Rhinosinusitis
- Yellow -nail syndrome
o Pleural effusions
o Lymphoedema
o Dystrophic nails
o Bronchiectasis’s (40%)

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15
Q

bronchiectasis presentation

A
  • Chronic , productive cough
  • Chest pain
  • Wheeze
  • Breathlessness on exertion
  • Haemoptysis
  • Recurrent or persistent infections of lower tract
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16
Q

examination findings bronchiectasis

A

Examination
- Finger clubbing
- Inspiratory crackles
- Wheezing

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17
Q

investigations for bronchiectasis

A

Two-fold investigations: diagnosis and cause
- Imaging
- bronchoscopy

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18
Q

imaging for bronchiectasis

A

Chest X-ray
- Bronchial wall thickening
- Airway dilation
- Can appear normal

High res CT (HRCT)- gold standard
- Bronchial wall thickening, diameter of bronchus larger than accompanying bronchial artery – signet ring sign
- Cystic fibrosis - bilateral upper lobe bronchiectasis
- Post TB infection- unilateral upper lobe bronchiectasis
- Foreign body inhalation- focal bronchiectasis (lower lobe)

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19
Q

bronchoscopy

A

o Not routine
o For patients with focal bronchiectasis evident on HRCT

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20
Q

Investigating the underlying cause of bronchiectasis

A
  • Chloride sweat test – CF
  • CFTR gene mutation
  • FBC with leucocyte differential
  • Immunoglobulin panel for immunoglobulin deficiency
  • Ciliary biopsy during bronchoscopy
  • HIV test
  • Microbiological assessment
    o E.g. pseudomonas spp colonisation- think CF
  • Lung function- obstructive pattern or mixed obstructive and restrictive pattern- scarring compromises lung compliance
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21
Q

Management of bronchiectasis

A

Aim: relieve symptoms, prevent progression of disease and ensure normal growth and development

  • Chest physiotherapy
    o Mucus clearing techniques
  • Bronchodilators for those with a wheeze
  • Exacerbations and abxs
    o Non encapsulated haemophilus, streptococcus pneumonia and Moraxella catarrhalis
    o Some children need short courses and others more continuous treatment
  • Follow up regularly
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22
Q

Complications of bronchiectasis

A
  • Recurrent infection
  • Life-threatening haemoptysis
  • Lung abscess
  • Pneumothorax
  • Poor growth and development
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23
Q

Prognosis of bronchiectasis

A
  • Depends on the cause
  • E.g. if post -infective- treatment should halt disease
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24
Q

CF background

A

Cystic fibrosis is an autosomal recessive disease caused by a mutation in the CF transmembrane conductance regulator gene (CFTR) resulting in multisystem dysfunction. In 2000 the life expectancy of a child born in 2000 was 50 years

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25
Q

pathophysiology of CF

A

CTFR is a protein chloride channel which is found in many epithelial tissues.
- Cl- moves down its conc gradient using ATP
- This fault also affects sodium reabsorption (ENaC) which reduces the amount of water in secretions
- This reduces airway surfactant liquid and impedes mucus clearance and immunological functions
- Different organs have different sensitivity to loss of CFTR protein function e.g. vas deferens very sensitive

26
Q

which organs are specifically affected by CF

A

respiratory system
pancreas
GI
reproductive

27
Q

respiratory system and CF

A
  • Reduced mucus clearance and reduction in effectiveness of Mucociliary escalator impedes immunological function
  • Provides a niche for bacterial growth with biofilm mode of growth providing ideal conditions to protect bacteria from host immune system and antibiotics
  • Pro-inflammatory cascade -> tissue damage
28
Q

Pancrease and CF

A
  • Pancreatic duct occluded in-utero -> permanent damage to exocrine pancreas -> pancreatic insufficiency
  • CF-related diabetes mellitus
29
Q

GI and CF

A
  • CTFR defect causes small intestine to secrete viscous mucus which can cause bowel obstruction in utero -> meconium ileus
  • Cholestasis in-utero can cause neonatal jaundice
  • Can cause CF-related liver disease later in life
30
Q

reproductive systema and CF

A

o 98% of men are infertile due to congenital absence of vas deferens
o Nutrition important predictor of successful pregnancy. Must be carefully planned -> can be associated in deterioration of lung health

31
Q

Risk factors for CF

A

Genetic
- Autosomal recessive
- More than 2000 identified mutations in CTFR gene
- Categorised into 5
- E.g. Class 1 – nonsense mutation and no complete CFTR protein formed
- E.g. Class 5 completes CTFR protein but deficiency in number

32
Q

presentation of CF in neonates

A

Meconium ileus
- Abdominal distension and delayed passage of meconium and bilious vomiting in first day of life
- Failure to thrive
- Prolonged neonatal jaundice

33
Q

presentation of CF in infancy

A

o Failure to thrive
o Recurrent chest infractions
o Pancreatic insufficiency: steatorrhea

34
Q

presentation of CF in adults

A

o Rectal prolapse
o Nasal polyps
o sinusitis

35
Q

presentation of CF in adolescents

A

o DM secondary to pancreatic insufficiency
o Chronic lung disease
o DIOS, gallstones, liver cirrhosis

36
Q

examination of CF patient

A
  • Hands: finger clubbing
  • Face: nasal polyps
  • Chest: hyperinflated, crepitiations, portacath (indwelling vascular access device)
  • Abdomen: faecal mass (if constipated/DIOS), may have
37
Q

Investigations (diagnosis and monitoring) for CF

A
  • Chest radiograph: to assess for hyperinflation, there may be evidence of bronchial thickening (undertaken annually as part of annual assessment)
  • Chloride sweat test (at diagnosis and annually) - >60mmol/L
  • Microbiological assessment e.g. cough swab/sputum sample (at every clinical encounter)
  • Glucose tolerance test(at annual assessment at teenage and beyond)
  • Liver function test and coagulation (at annual assessment)
  • Bone profile(at annual assessment)
  • Lung function testing– spirometry / lung clearance index
38
Q

the chloride sweat test

A
  • This test measures the electrolyte concentration in sweat
  • Sweat sample is collected by pilocarpine iontophoresis. Careful technique must be employed to ensure and adequate sample is collected to avoid inaccurate results. A common reason for failure of the test is an insufficient sample in a small baby (limit 3kg).
39
Q

interpreting a chloride sweat test

A
  • A sweat chloride >60mmol/L is suggestive of CF. A sweat chloride of 40-60mmol/L is borderline and should be repeated
  • A single sweat test is not sufficient to diagnose CF, a second test or identification of genetic mutation should confirm the diagnosis.
  • There are a number of reasons for a false positives/negatives.
40
Q

complications of CF: resp

A

o Allergic bronchopulmonary aspergillosis (ABPA
o Bronchiectasis (do CT)
o Haemoptysis
o Pulmonary hypertension
o Pneumothorax
o Nasal polyps

41
Q

complications of CF: GI

A
  • Rectal prolapse (frequent passage of bulky stools)
  • Distal intestinal obstruction syndrome (DIOS)
    –>Obstruction of distal ileum and affects up to 10% of children with CF
    –>Due to slower intestinal transit
    –>Colicky abdominal pain
  • CF related liver disease
    –>Cholestasis
    –> Gallstones
    –> Liver cirrhosis
42
Q

complications of CF: endocrine

A
  • CF related diabetes (CFRD)- older children
    o DKA rarer due to not an absolute lack of insulin
  • Delayed puberty
  • Osteoporosis
    Sub or infertility
43
Q

managment of CF

A

MDT approach e.g. GP, resp paediatrician, CF nurse, dietician, physiotherapist, psychologist and SW
- education
- resp
- GI
- preventing chest infections

44
Q

CF managment: education

A
  • Patient and family
  • Segregation to reduce cross-infection
  • When admitted in a side room
  • Patiens who are pseudomonas naïve attened diff clinics to those with chronic infection
45
Q

CF management: respiratory

A
  • Physiotherapy
    o Mucus clearance via twice-daily
  • Mucolytics and DNase
    o DNase (dornase alpha) is inhaled and reduces viscosity of mucus by digesting DNA which is abundant in the sputum of patients with CF
    o Hypertonic saline can aid airway clearance (and can be used at time of physiotherapy to further aid clearance)(limited evidence to support use in under 12 yrs).
  • Small molecule therapy- Ivacaftor/ lumicaftor
  • Physical exercise
46
Q

CF management: GI

A
  • Creon
    o Pancreatic enzyme supplementation for meals which contain fat
  • Fat soluble vitamins (ADEK)
  • Monitor growth
    o Metabolic demand may eb higher and so nutrition followed carefully for optimal growth
    o May have poor weight gain – supplement meals. May need gastrotomy in extreme malnutrition
47
Q

CF management: common chest infections

A

e.g. S.aureus, H. influenzae and Pseudomonas aeruginosa
- Sputum culture
- 2 weeks of antibiotics even if child asymptomatic
- High doses
- IV may be required if oral not responsive
- Prophylactic antibiotics recommended until age of 3
- Regular azithromycin recommended to improve lung function

48
Q

Chronic infections in CF

A

e.g. pseudomonas aeruginosa
 Associated with poor lung function
 Biofilms aid colonisation and protection from host immunity and antibiotics
 Long term antibiotics
 Inhaled antibiotics

49
Q

Annual review CF:

A

microbiological assessment, blood tests, lung functions tests, CXR, oral glucose tolerance test (OGTT)

50
Q

Tracheobronchomalacia

A

Background
- “Floppy” airways
- Flaccidity of supporting cartilage

Types 3 groups
- Congenital
- Extrinsic compression
- Acquired

Management
- Nothing
- Prophylactic Antibiotics/physio
- CPAP
- Surgery

Prognosis very good (usually)!

51
Q

Obstructive sleep apnoea background

A
  • Apnoea is defined as a lack of breathing.
  • Obstructive apnoea refers to a lack of airflow in the face of respiratory effort.
  • It is most often associated with sleep.
  • The obstructive sleep apnoea syndrome (OSAS) may be due to tonsillar/adenoidal hypertrophy, macroglossia, or micrognathia.
52
Q

obstructive sleep apnoea causes

A

Causes
- Upper airway obstruction e.g. Adenotonsillar enlargement
- Genetic conditions e.g. Pierre Robin syndrome, trisomy- 21

53
Q

OSA presentation

A

Presentation
- Snoring and sleep disturbance.
- Daytime sleepiness or inattention.
- Enuresis.
- Only about 15% of snoring children have significant airway obstruction.

54
Q

investigations for OSA

A
  • Sleep study
    o Overnight pulse oximetry
  • Chest x-ray and ECG
    o To examine for secondary heart cardiac consequences of airway obstruction
55
Q

Management

A
  • Depends on aetiology
  • Surgery
    o Tonsillectomy or adenoidectomy
  • CPAP (positive airway pressure support)
56
Q

Paediatric long term ventilatory support

Who is eligible?

A

Any child below the age of 17 who is
- Medically stable
- Requires a mechanical aid for breathing either invasively by tracheostomy or by non-invasive mask interface for all or part of the 24 h day (after a failure to wean)
- For longer than 3 months

57
Q

what may cause a child to require long term ventilatory support

A
  • Neuromuscular
  • Upper airway obstruction
  • Obesity syndrome
  • Hypoventilation
    o Neuromuscular weakness
    o Mechanical e.g. scoliosis
  • Central
    o Brainstem lesions
    o Neurological disorders
  • Trauma
58
Q

goal/ types of long term ventilation

A

Goal
- Maintain adequate ventilation/ oxygenation

Types:
- Maintain open airways (pressure only i.e. CPAP)
o Upper airway obstruction
o Tracheobronchomalacia

- Provide artificial ventilation (pressue and rate i.e. BiPAP)
o Neuromuscular conditions
o Central hypoventilation

59
Q

considerations for LTV

A

Interface
- Non-invasive e.g. facemask/ nasal
- Invasive e.g. tracheostomy

Duration
- Overnight only
- 24/7
- Somewhere in between

Modality
o CPAP
o BiPAP

60
Q

considerations for LTV

A

Interface
- Non-invasive e.g. facemask/ nasal
- Invasive e.g. tracheostomy

Duration
- Overnight only
- 24/7
- Somewhere in between

Modality
o CPAP
o BiPAP

Paediatrics (Y4) (42 decks)

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