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RESPIRATORY PAEDS Flashcards

1
Q

What is Bronchiolitis and what is usual causative agent?

A

Infection of the bronchioles

Usually caused by RESPIRATORY SYNCYTIAL VIRUS (RSV)

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2
Q

BRONCHIOLITIS: Age of presentation

A

Usually infants under 1 year - most common in infants under 6 months
Can rarely be diagnosed in children up to 2 years (ex-premature babies with CLD)

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3
Q

BRONCHIOLITIS: Presentation

A
  • Coryzal symptoms
  • Signs of resp distress
  • Dyspnoea
  • Tachypnoea
  • Poor feeding
  • Apnoeas
  • Wheeze and crackles
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4
Q

BRONCHIOLITIS: Signs

A
  • Raised RR
  • Use of accessory muscles
  • Intercostal and subcostal recessions
  • Nasal flaring
  • Head bobbing
  • Tracheal tugging
  • Cyanosis
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5
Q

Define WHEEZE

A

Whistling sound
Narrowed airways
EXPIRATION

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6
Q

Define GRUNTING

A

Caused by exhaling with the glottis partially closed due to increased positive END-EXPIRATORY pressure

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7
Q

Define STRIDOR

A

High pitched INSPIRATORY noise
Obstruction of upper airway
E.g. croup

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8
Q

BRONCHIOLITIS: Treatment

A

Most recover in 2-3 weeks, most managed at home
Supportive management:
- adequate intake
- saline nasal drops

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9
Q

BRONCHIOLITIS: Reasons for admission

A 
Aged UNDER 3 MONTHS or any pre-existing condition such a prematurity, downs, CF 
50-75% or less of normal milk intake 
Clinical dehydration 
RR >70 
O2 sats <92%
Moderate to severe respiratory distress- e.g. deep recessions, head bobbing 
Apnoeas 
Parents unable to manage at home
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10
Q

Blood gases in TYPE 2 respiratory distress

A 
Rising pCO2 
Falling pH (CO2 build up —> acidosis)
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11
Q

BRONCHIOLITIS: preventative injection

A

PALIVIZUMAB - monoclonal antibody against RSV
monthly injection
High risk babies

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12
Q

How is VIRAL INDUCED WHEEZE different to ASTHMA

A 
Caused by: RSV or rhinovirus
Prevention: Before the age of 3
No atopic history 
Occurs during viral infections 
Evidence of viral infection 1-2 days preceding onset of SOB, respiratory distress, expiration wheeze
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13
Q

ACUTE ALLERGIC ASTHMA type of hypersensitivity reaction

A

Type 1 hypersensitivity

IgE

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14
Q

Signs of SEVERE ACUTE ASTHMA

A 
Peak flow <50%
Sats <92%
unable to complete full sentences 
Signs of respiratory distress 
RR >40 (1-5 years) 
RR >30 (5 years+)
HR >140 (1-5 years)
HR >125 (5 years+)
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15
Q

Signs of LIFE THREATENING ACUTE ASTHMA

A 
Peak flow <33% predicted 
Sats <92% 
Exhaustion or poor respiratory effort 
Hypotension 
Silent chest 
Cyanosis 
Altered consciousness or confusion
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16
Q

Management of acute asthma (or viral induced wheeze!)

A

1) Supplementary oxygen if sats low
2) Bronchodilators (e.g. salbutamol, ipratropium, magnesium sulphate)
3) steroids: prednisone (oral) hydrocortisone (IV)
4) Antibiotics if bacterial infection suspected (Amoxixillin or erythromycin)

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17
Q

Stepped up management of bronchodilators

A

1) Inhaled or nebulised SALBUTAMOL (Beta-2 agonist)
2) Inhaled or nebulised IPRATROPIUM BROMIDE (anti-muscarinic)
3) IV MAGNESIUM SULPHATE
4) IV AMINOPHYLLINE

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18
Q

MODERATE to SEVERE acute asthma stepwise treatment

A

1) SALBUTAMOL inhaler via spacer device (10 puffs every 2 hours)
2) Nebulisers with SALBUTAMOL/IPRATROPIUM BROMIDE
3) oral PREDNISONE (1mg per kg weight OD for 3 days)
4) IV HYDROCORTISONE
5) IV MAGNESIUM SULPHATE
6) IV SABUTAMOL
7) IV AMINOPHYLLINE

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19
Q

MILD asthma

A

SALBUTAMOL inhaler via spacer (e.g. 4-6 puffs every 4 hours)

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20
Q

Side effects of Salbutamol

A

Hypokalaemia

Tachycardia

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21
Q

CHRONIC ASTHMA diagnosis

A

Spirometry with bronchodilator reversibility testing (FEV1 improvement by >12%)
Direct bronchial challenge test with histamine or Mehta hotline
Fractional exhaled NO (FeNO)
Peak flow variability measured by keeping a diary

22
Q

Management stepwise approach CHRONIC ASTHMA in UNDER 5s

A
  1. Short acting beta-2 agonist (e.g. salbutamol) PRN
  2. Add low dose corticosteroid inhaler or leukotriene antagonist (ie oral monteleukast)
  3. Add other option from step 2
  4. Refer to specialist
23
Q

Management CHRONIC ASTHMA in children AGED 5-12

A
  1. (Same) Salbutamol
  2. (Same) Low dose corticosteroid inhaler
  3. LONG ACTING BETA-2 AGONIST inhaler (e.g. SALMETEROL)
  4. Titration up the corticosteroid inhaler
  5. Consider adding
    oral MONTELUKAST
    THEOPHYLLINE
  6. Increase corticosteroid to high dose
  7. Refer to specialist
24
Q

CHRONIC ASTHMA management 12 years +

A

SAME AS ADULT

25
Metered dose inhaler technique WITHOUT SPACER
Remove cap Shake inhaler Sit or stand up straight Lift chin slightly Fully exhale Make tight seal around inhaler between lips Press canister and take steady breath in Continue breathing for 3-4 seconds after pressing canister Hold breath for 10 SECONDS Wait 30 seconds before next dose Rinse mouth after steroid inhaler
26
Metered dose inhaler WITH A SPACER
``` Assemble spacer Shake inhaler Attach inhaler Sit/stand up straight List chin slightly Make seal with lips/mask Spray dose into inhaler Take steady breaths in and out 5 times until the mist fully inhaled ```
27
Characteristic signs of PNEUMONIA
Bronchial breath sounds (harsh breath sounds equally loud on inspiration and expiration - caused by consolidation of lung tissue around airway) Focal coarse crackles (air passing through sputum - like straw blowing into drink) Dullness to percussion (consolidation)
28
Common bacterial causes of PNEUMONIA
``` Strep. Pneumonia Group A Strep (e.g. strep pyogenes) Group B strep (pre-vaccinated infants) Staph. Aureus H. Influenza Mycoplasma pneumonia (atypical bacteria - extra pulmonary manifestations e.g. erthyema multiforme) ```
29
Viral causes of PNEUMONIA
RSV (most common) Parainfluenza virus Influenza virus
30
Management of pneumonia
AMOXICILLIN Add macrolide (e.g. ERYTHROMYCIN, CLARITHROMYCIN or AZITHROMYCIN ) - covers atypical bacteria Penicillin allergy - MACROLIDES AS MONOTHERAPY
31
RECURRENT LRTI: Pontential underlying problems
Reflux, aspiration, neurological disease, heart disease, asthma, cystic fibrosis, primary ciliary dyskinesia, immune deficiency
32
CROUP: causative agents
PARAINFLUENZA Influenza Adenovirus RSV
33
CROUP: age of presentation
6 months - 2 years
34
CROUP: presentation
Barking cough Hoarse voice STRIDOR Low grade fever
35
CROUP: management
Can be managed at home - SUPPORTIVE ``` Oral DEXAMETHASONE - single dose, can be repeated after 12hrs if required If not improving, stepwise: - Oral Dex - Oxygen - Nebulised budesonide - Nebulised adrenaline - intubation/ventilation ```
36
EPIGLOTTITIS: Infective agents
HAEMOPHILIUS INFLUENZA TYPE B | - rare now due to vaccination
37
EPIGLOTTITIS: X-ray signs
Lateral X-ray of neck: THUMB SIGNS - soft tissue shakedown that looks like thumb pressed against trachea caused by oedematous swollen epiglottis
38
EPIGOTITTIS: management
``` Medical emergency!! Do not distress child Secure airway - most don’t need intubation but there is a risk of sudden airway closure, so prepare for intubation or tracheostomy IV antibiotics (e.g. CEFTRIAXONE) Steroids (DEXAMETHASONE) ```
39
Laryngomalacia characteristics
CHRONIC STRIDOR - during inspiration (larynx flops across airway as child breaths in) - harsh whistling sound - intermittent, more prominent when feeding, upset, during URTI Peak presentation at 6MONTHS
40
WHOOPING COUGH: causative agents
Bordetella Pertussis (gram neg bacteria)
41
WHOOPING COUGH: presentation
Initially: Coryzal symptoms, low grade fever, mild dry cough A week +: More severe coughing fits, PAROXYSMAL cough Loud inspiratory WHOOP when coughing ends as out of breath Can cough so hard they faint, vomit, develop pneumothorax +/- apnoeas NOTIFIABLE DISEASE
42
WHOOPING COUGH: management
Notify public health! Simple supportive care Macrolide antibiotics: AZITHROMYCIN, ERYTHROMYCIN, CLARITHROMYCIN (within first 21 day) Alternative: Co-trimoxazole Close contacts: Prophylactic antibiotics
43
CYSTIC FIBROSIS: genetic mutation
Cystic fibrosis transmembrane conductance regulatory gene Chromosome 7 Codes for a type of chloride channel
44
CYSTIC FIBROSIS: prevalence
1 in 2500 children have CF | 1 in 25 are carriers for the mutation
45
CYSTIC FIBROSIS: key consequences
1) THICK PANCREATIC and BILIARY secretions - block ducts, lack of digestive enzymes such as pancreatic lipase in the digestive tract 2) Low volume THICK AIRWAY SECRETIONS - reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections 3) Congenital bilateral absence of the VAS DEFERENS in males - male infertility as sperm have no way of getting from the testis to ejaculate
46
CYSTIC FIBROSIS: Diagnosis
Screening: Newborn bloodspot test (shows high immune reactive trypsinogen levels) SWEAT TEST - gold standard for diagnosis (high conc. of chloride ions >60mmol/L) GENETIC SCREENING - for the GFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling or blood test after birth
47
CYSTIC FIBROSIS: the sweat test
PILOCARPINE applied to skin Electrodes placed wither side of the patch and small current passed between electrodes - causing skin to sweat Sweat absorbed by gauze/filter paper and a analysed for chloride ion concentration
48
CYSTIC FIBROSIS: microbial colonisers
``` Most common: Staph Aureus H. Influenza Pseudomonas aeruginosa (BAD - often becomes resistant and increases mortality) Other: Klebsiella pneumoniae E Coli ```
49
CYSTIC FIBROSIS: Management
Chest PHYSIOTHERAPY Exercise High Calorie diet CREON tablets - to digest fats due to pancreatic insufficency Prophylactic FLUCLOXACILLIN tablets Bronchodilators Nebulised DNase - can breakdown DNA material in respiratory secretions - making secretions less viscous and easier to clear vaccinations: PNEUMOCOCCAL, INFLUENZA and VARICELLA
50
CYSTIC FIBROSIS: Monitoring
Follow up every 6 months Regular monitoring for colonisation of bacteria in sputum (e.g. pseudomonas) Screening for: diabetes, osteoporosis, VitD deficiency, liver failure
51
PRIMARY CILIARY DYSKINESIA: also known as?
Kartagner’s syndrome
52
KARTAGNER’S TRIAD
Paranasal sinusitis Bronchiectasis Situs Inversus (Not all patients will have all 3)

PAEDIATRICS (18 decks)

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