Asthma and Wheeze Associated with Viral Episode (WAVE) Flashcards
What is the epidemiology of asthma?
1:12 adults and 1:11 children receiving treatment in the UK
60% report significant persistent symptoms
Pre puberty – boys>girls; post puberty – boys
What is suspected aetiology of asthma?
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
What is atopy?
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
What is the hygiene hypothesis?
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
What is the pathology of non-atopic intrinsic asthma?
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
What is the pathology of aspirin induced asthma?
Unknown
Possibly increases leukotrienes and decreases prostaglandins (due to COX inhibition) = airway irritation
Also why dont give NSAIDs in asthma
What is the pathology of occupational asthma?
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
What is the pathology of atopic asthma?
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
What are the effects of cold air and exercise on asthmatic lungs?
Both dry out the mucosa - lining becomes hyperosmolar - leads to mast cell degranulation and inflammation
What are the effects of bronchoconstriction and inflammation on lung function?
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
How does asthma present?
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
How do you differentiate between a severe and a life threatening asthma attack according to BTS guidelines?
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
What lung function tests do you use to investigate asthma?
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%
What other tests might be helpful in investigating asthma?
Atopy and allergy:
Skin prick test - for allergens
Radioallergosorbent test (RAST) - blood test for specific IgE antibodies
Bloods - high eosinophil count
What is some non-pharmacological management of asthma?
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
What is the first step on the ladder of asthma management?
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
What is the second step on the ladder of asthma management?
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
What is the third step on the treatment ladder for asthma?
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)
What are some alternative step 3 managements on the treatment ladder for asthma when LABA is unsuccessful?
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))
What is the fourth step in the management of asthma?
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
What is the fifth step in the management of asthma?
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
What is important with taking ICS and relievers?
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
What are some of the reasons for inadequate response?
(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
What are the long term effects of ICS?
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
How do you mange an acute asthma attack in hospital?
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
What is the mnemonic for acute asthma attack ?
O-H SHIT MA
Oxygen - High flow Salbutamol - NEB or IV (severity depending) Hydrocortisone - IV Ipratropium - IV Theophylline - IV MgSO4 - IV Aminophylline - IV
