Asthma and Wheeze Associated with Viral Episode (WAVE)

Question 1

What is the epidemiology of asthma?

Answer 1

1:12 adults and 1:11 children receiving treatment in the UK

60% report significant persistent symptoms

Pre puberty – boys>girls; post puberty – boys

Question 2

What is suspected aetiology of asthma?

Answer 2

Intrinsic:
Asthma starts in middle age, no trigger identified

Extrinsic:
Usually occurring in atopic individuals (+ve skin prick tests)
90% of childhood cases and 50% of adult asthma
Strong FHx present in these cases

Can also be extrinsic and non-atopic - via sensitisation to certain agents e.g. environmental pollutants, aspirin, Betablockers

Question 3

What is atopy?

Answer 3

A term to describe individuals who have allergies/asthma/hayfever

Runs in families:
ADAM33 gene - links to airway hyperresponsiveness
PHF11 gene - increased IgE production

Individuals have many IgE antibodies to common allergens - present in about 30-40% of population

Question 4

What is the hygiene hypothesis?

Answer 4

Concerns the development of atopy

Lack of early childhood exposure to infectious agents, symbiotic microorganisms and parasites increases susceptibility to allergic disease by suppressing the natural development of the immune system

Question 5

What is the pathology of non-atopic intrinsic asthma?

Answer 5

No T cell involvement (not immunologically mediated)

Associated with recurrent viral RTI’s (esp in early childhood)

Skin tests -ve

Bronchoconstriction secondary to airway hyperresponsiveness > inflammation

Question 6

What is the pathology of aspirin induced asthma?

Answer 6

Unknown

Possibly increases leukotrienes and decreases prostaglandins (due to COX inhibition) = airway irritation

Also why dont give NSAIDs in asthma

Question 7

What is the pathology of occupational asthma?

Answer 7

Hypersensitivity to agent at work

E.g. paints, varnishes - bind to T cells and activate (no IgE needed)

Professions at risk include:
baker, electrician, carpenter, painter etc

Typical onset is 3-6 months after work starts; weekends may be better

Question 8

What is the pathology of atopic asthma?

Answer 8

Common allergens = dust mites/faeces, pollen, pet hair, spores

Antigen exposure leads to CD4 T cell differentiation into T helper cells (Th2) which secrete IL4 + IL-5

IL-4 makes B cells become plasma cells which then secrete IgE

IL-5 sensitises eosinophils and mast cells to the new antigen

IgE binds to mast cells in mucosa - these are at higher concentrations in the lungs of asthmatics - waits until reexposure to antigen then will activate/degranulate

Acute asthma attack:
Degranulation of mast cells releases inflammatory mediators (histamine, prostaglandins, leukotrienes) which cause smooth muscle contraction (bronchoconstriction), increased bronchial secretions and increased vascular permeability

Late phase reaction:
Accumulation of eosinophils at the site - sustained inflammation

Question 9

What are the effects of cold air and exercise on asthmatic lungs?

Answer 9

Both dry out the mucosa - lining becomes hyperosmolar - leads to mast cell degranulation and inflammation

Question 10

What are the effects of bronchoconstriction and inflammation on lung function?

Answer 10

Distal airway hyperinflation and collapse

Mucous plugging of bronchi secondary to high levels of secretions

Thickening of bronchial basement membrane - when smooth muscle does contract, the lumen becomes very narrow

Epithelial dysplasia - ciliated columnar become mucous secreting cells

Smooth muscle hypertrophy - more likely to contract and stay contracted for longer

Question 11

How does asthma present?

Answer 11

Wheezing attacks - precipitated by a variety of triggers (exercise, cold weather, viral illness, allergens, pollutants etc)

Periodic shortness of breath

Night symptoms - SOB, nocturnal cough (can present alone)

Interval symptoms e.g. between acute asthma attacks are important to rule out WAVE

Hx or FHx of atopy

Loss of function/low QoL e.g. cant join in sports or walk to school

Question 12

How do you differentiate between a severe and a life threatening asthma attack according to BTS guidelines?

Answer 12

Severe:
SpO2 <92%
Peak flow - 33-50% of best or predicted 
Too breathless to talk or feed 
HR: >125 @ >5yrs or >140 @ 1-5yrs
RR: >30 @ >5yrs or >40 @ 1-5yrs
Use of accessory neck muscles 

Life threatening:
SpO2 <92%
PEF <33%
Silent chest, poor resp effort, agitation, altered consciousness, cyanosis

Question 13

What lung function tests do you use to investigate asthma?

Answer 13

Peak Expiratory Flow (PEF):
2x readings per day - variability?
2x weeks worth of measurements 
Diurnal variation 
Impact of exercise, addition of bronchodilator etc 

Spirometry:
Obstructive condition = reduced FEV1 and FEV1/FVC ratio <0.7

If >15% improvement in FEV1 or PEF following inhilation of bronchodilator then = reversibility which is highly suggestive of asthma

Can also do treadmill test - PEF - 6mins/HR up to 160 - repeat PEF (again looking for 15% difference)

Can also give trial of 20mg prednisolone PO OD for up to 2wks - should respond better to bronchodilators as well as improve FEV1 >15%

Question 14

What other tests might be helpful in investigating asthma?

Answer 14

Atopy and allergy:
Skin prick test - for allergens
Radioallergosorbent test (RAST) - blood test for specific IgE antibodies
Bloods - high eosinophil count

Question 15

What is some non-pharmacological management of asthma?

Answer 15

Patient education - what condition is, who can be useful, when to come to hospital, how to use inhalers

Identification and avoidance of triggers - allergens? (often dust mite faeces - regular bedding changing) Occupational change?

Flu vaccines

Never take betablockers and NSAIDs

Question 16

What is the first step on the ladder of asthma management?

Answer 16

Short Acting Beta Agonist (SABA)

Salbutamol (or terbutaline)

Self administer 2 puffs PRN (200micrograms)

SE: fine tremor, anxiety, dry mouth, palpitations

Blue inhaler/reliever

Given when occasional symptoms <2x/wk; normal PEF between attacks; FEV1 >80% predicted

Question 17

What is the second step on the ladder of asthma management?

Answer 17

Add an Inhaled Corticosteroid (ICS)

Beclomethasone, Budesonide; Fluticasone (2x as strong as doesnt go through 1st pass metabolism so can use half the dose)

200-400 micrograms INH OD

SE: runny nose, sore throat, myalgia

Brown inhaler/preventer

Given when symptoms >2x/wk but FEV1 still >80% of predicted

Question 18

What is the third step on the treatment ladder for asthma?

Answer 18

Add a Long Acting Beta-2 Agonist (LABA) if >5yrs (LRTA if <5yrs or >17]
yrs)

Seritide, Symbicort

Both are combination LABA + ICS as need to be taken together

(LABA only = salmeterol, formoterol)

OD INH

Given when symptoms are severe - >2x exacerbations/wk which may last days; FEV1 50-80% of predicted

If benefit but still not proper control: increase ICS dose to 400micrograms (if not already on)

Question 19

What are some alternative step 3 managements on the treatment ladder for asthma when LABA is unsuccessful?

Answer 19

For severe symptoms not controlled by core step 3 management

If no response to LABA, stop and increase ICS to 400micrograms
If some benefit from LABA but suboptimal, keep on and increase ICS to 400mcg

If still no response, trial other therapies:

Leukotriene receptor antagonist e.g. monteleukast (4wk trial before long term treatment)

Theophylline

(Omalizumab (anti IgE - for severe atopic asthma))

Question 20

What is the fourth step in the management of asthma?

Answer 20

Increase ICS up to 800micrograms OD

Stop any add ons not contributing to improvement

Refer to specialist management

With continual symptoms + frequent night symptoms + limited activity; FEV1 <60% predicted

Question 21

What is the fifth step in the management of asthma?

Answer 21

Start daily PO steroid in lowest dose providing adequate control

Maintain ICS at 800micrograms

Protection/monitoring for those on long term steroids (e.g. >3m, or 3-4x courses/yr):
BP
BG - DM may occur
BMD - may need bisphosphonates if starts to drop
Growth and cataract checking

Question 22

What is important with taking ICS and relievers?

Answer 22

Always use lowest effective dose (not as critical with relievers)
Proper inhaler technique to minimise oral and GI deposition
Age appropriate devices and education on how to use them - spacers are essential

Question 23

What are some of the reasons for inadequate response?

Answer 23

(ABCDE)

Adherence = number 1 reason for treatment failure

Diagnosis - correct?

Environmental factors - allergens, smokers

Choice of drugs/devices - need escalating or spacer changing?

Bad disease

Question 24

What are the long term effects of ICS?

Answer 24

Slows short/medium term growth - even in mild asthma - but does not have an effect on final adult height

No evidence of increased fracture risk secondary to osteoporotic effects - though poorly controlled may reduce ability to take part in weight bearing exercise which does impact on bone density

Question 25

How do you mange an acute asthma attack in hospital?

Answer 25

Oxygen:
If sats <94% or severe attack
Start on 100% O2 w/non-rebreathe mask or nasal cannula with patient sat upright
Titration to get sats 94-98%

SABA: 1st line
2-10 puffs inhaler through large volumatic spacer; one puff:5 tidal breaths - relief should last 4hrs, if not - need hospital if not already there
Discontinue LABA (if on) if SABA required >4hrly

NEB:
Salbutamol 2.5-5mg at 6L/min flow rate on oxygen driven neb
Can be given every 20-30mins or if giving continuously, give over 30-60mins

If inadequate response to 1st dose, add ipratropium bromide (250-500mcg) on second, do not repeat within 4hrs

Once responding, should be weaned

Steroids:
Give early e.g. in ED as can reduce need for admission
Prednisolone PO (30-40mg >5yrs, 40-50mg in adults) = 1st line, usually OD for 3days but may need more (not tapering required unless >14days)
For life threatening who can’t tolerate oral = IM methylpred 160mg OR
Hydrocortisone 100mg IV =
Do not use ICS as an alternative, but keep patients on any existing ICS

Magnesium sulphate:
NEB, for those with rapid onset severe asthma/sats <92% in those already receiving nebs

ABG:
O2 - <8kPa +
CO2 - >5kPa +
pH low =
life threatening attack
Repeat every couple of hours 

CXR:
Not routine but if clinical suspicions of other pathology e.g. pneumothorax

Sats:
Aim for >92%

PEF:
Check trend for improvement

Question 26

What is the mnemonic for acute asthma attack ?

Answer 26

O-H SHIT MA

Oxygen - High flow 
Salbutamol - NEB or IV (severity depending)
Hydrocortisone - IV 
Ipratropium - IV 
Theophylline - IV 
MgSO4 - IV
Aminophylline - IV