Asthma

Osomfuo Prof. Sir J.W. Acheampong

Asthma is a disorder that causes the airways
of the lungs to swell and narrow leading to
wheezing, shortness of breath chest
tightness and coughing.
Asthma is a chronic inflammatory disease of
the airways that is characterized by increased
responsiveness of the tracheobronchial tree to
a multiplicity of stimuli. It is manifested by a
widespread narrowing of the air passages
which may be relieved spontaneously or as a
result of therapy and clinically by paroxyms of
dyspnea, cough, wheezing and chest
tightness.
Inflammation of Bronchial wall involve
1. Eosinophils
2. Mast cells
3. Lymphocytes
4. Cytokines & inflammatory products of
these cells
5.Neutrophils & macrophages are less well
defined
Associated with
Oedema
Smooth muscle hypertrophy and hyperplasia
Thickening of basement membrane
Mucous plugging and
Epithelial damage
Triggers of the asthmatic response
Organic materials
Pollen
Mite containing house dust
Feathers
Animal dander
Fungal spores
Ingested allergens
Fish
Egss
Milk reach Bronchi via
Yeast the blood stream
wheat
Non specific
Cold air
Tobacco smoke
Dust
Acid fumes
Respiratory viral infection
Emotional stress
Strenuous exertion (exercise – induced
asthma)
Prescription Drugs
Use of β-adrenoceptor antagonist
Aspirin
NSAID
 Classification of Asthma

Early onset Late onset Asthma

or
(Extrinsic Atopic) (non-atopic)
Early-onset Asthma (Atopic)
1. Begins in childhood
2. Occurs in individuals who readily form 1gE
antibodies to commonly encounted allegens
3. Can be identified by
a. Skin hypersensitivity test which produce
positive reactions to a wide range of common
allergens
4. Allegic rhinitis and
5. Eczema are often present
6. Positive family history
 Previous exposure to allergen

formation of 1gE

Specific allergen

Anaphylactic antigen antibody reaction in the

bronchi may follow further exposure to specific
allergen
Causes the release from mast cell in the
bronchial wall
Asthmatic broncho constrictors response
and often a secondary late reaction of
allergic type in the bronchial wall.
Inhalled allergen
through 1gE dependent mechanism

Interacted with surface mast cell

Mast cells – release mediators such as histamine

which then act on receptors on smooth muscle cells
and lead to bronchoconstriction
Other cells involved in chronic Asthma
1. Eosinophils – activated eosinophils
 Release bioactive lipid mediators and
oxygen radicals
 Eosinophilcationic protein
 Eosinophil neurotoxins
 Eosinophil peroxidase
 T-lyphocytes are activated
Late-onset Asthma (non-atopic)
Patients are adults
No evidence of external allergens
Intrinsic or idiosyncratic asthma
No family history of allergy
negative skin tests
normal serum levels of IgE
Symptom complex on contracting URTI
Paroxysms of wheezing and dyspnoea
Clinical features of Asthma
1. Episodic or chronic or overlap
2. Atopic - episodic
3. Non atopic – chronic asthma
Episodic Asthma
1. Patient has no respiratory symptoms or
signs between episodes
2. Wheeze & dyspnoea may occur anytime
and can be of sudden onset
3. Can be triggered by allergens exercise or
viral infection (common cold)
4. May be mild or severe and may last for hrs,
days or even week.
Severe acute Asthma (Previously status
asthmaticus)
Features of severity
Pulse rate > 110 per min
Pulsus paradoxus
Unable to speak in sentences
PEF < 50% of expected

NB: Apparent distress and respiratory rate may be

misleading
Patient
Adopts an upright position
Fixing the shoulder girdle to assist the
accessory muscles of respiration.
Chest is held near the position of full
inspiration
Percussion note may be hyper-resonant
Breath sound – obscured by numerous high
pitched polyphonic expiratory and
inpiratory rhonchis, otherwise vesicular in
character with prolonged expiration.
Tachycardia > 110
Pulsus paradoxus and sweating
In very severe asthma
Central cyanosis
Bradycardia
Silent chest (rhonchi are no longer
produced)
Chronic Asthma
Symptoms of chest tightness, wheeze and
breathlessness on exertion, together with
spontaneous cough and wheeze during the
night and early morning may be chronic
unless controlled by appropriate therapy.
Severe Asthma persisting from childhood
may cause “pigeon chest deformity”.
Investigation
1. Compatible history
2. Demonstration of variable airflow
obstruction
 Morning dipping of the peak expiratory
flow (serial recordings of peak expiratory
flow (PEF) – note sharp overnight fall
(morning dip) and subsequent rise
during the day in patient with Asthma.
3. Other tests
An exercise test
Histamine or methacholine bronchial
provocation test
Occupational exposure test
Trial of oral corticosteroids (e.g.
prednisolone 30mg dly for 2 weeks)
Elevated sputum or
Peripheral blood eosinophil count or
increased serum level of total or allergen –
specific IgE (radioallergosorbent test RAST)
may be helpful.
Pulmonary function tests
Measurement of the
FEV1 - forced expiratory vol in 1 second
VC - vital capacity (forced or relaxed)
PEF - Peak Expiratory flow
Radiological Examination
In an acute attack of Asthma – lungs appear
inflation hyper inflated
Between episodes: normal radiograph
Chronic cases – hyperinflations (see
Emphysema)
Lateral view – a pigeon chest deformity
Large Bronchus obstructed – opacity
caused by lobar or segmentd collapse.
Chest x-ray always important
1. To exclude pneumothorax
2. Show mediastinal and subcutaneous
emphysem
Arterial blood gas analysis
Measurement of PaO2 and PaCO2 are
indispensable in the management of patients
with severe and acute Asthma.
Management
1. Avoidance – triggers of the asthmatic
response
2. Hyposensitisation (abandoned in
Britain)
Management of Acute Severe Asthma
1. Give O2 – usually (60% - 100%)
2. High doses of inhaled β2 – adrenoceptor agonists
should be nebulised using O2
 Nebulised using salbutamol 2.5 – 5mg
Terbutaline 5mg – 10mg
 Repeat after 30 minutes if necessary
3. Systemic Corticosteroids
4. Hydrocortison 200mg stat or Oral prednisolone
30 – 60mg dly x 3
Management of acute severe Asthma
Features of severity
Pulse rate > 110 per min
Pulsus paradoxu
Unable to speak in sentences
PEF < 50% of expected
Arterial blood gases in life-threatening asthma
A normal (5 – 6 kPa) or high CO2 tension
Severe hypoxaemia (< 8 kPa) especially if being
treated with oxygen
A low pH or high (H+ )
Management of acute severe Asthma
(cont’d)
If features of severity persist:
Ipratropium bromide 0.5mg should be added to
the nebulised β2 – adrenoceptor agonist
An aminophylline infusion (500 µg/kg/hour)
should be commenced with an initial slow i.v.
injection (5mg/kg over 20 minutes) in patients not
on oral theophyllines. Infusion rates should be
adjusted thereafter according to plasma
theopylline levels. Alternatively, salbutamol or
terbutaline (250 µg i.v. over 10 minutes) can be
given
Continue nebulised β2 – adrenoceptor
agonist treatment every 15- 30 minutes as
necessary. Reduce to 4-hourly once clear
clinical response
Mechanical ventilation
Management of chronic persistent
Treatment steps
Addition of regular oral steroid therapy
High dose inhaled steroids and regular
bronchodilators
High-dose inhaled steroids or low-dose
inhaled steroids plus long-acting
inhaled β2-adrenoceptor agonist
Low-dose inhaled steroids (or other
anti-inflammatory agents)
Occasional use of inhaled short-acting
β2-adrenoceptor agonists
Start high and step down
Occasional temporary step-ups will
be needed to control exacerbations
Consider step-down if good
symptom control for 3 months or
more
Only think of withdrawing anti-
inflammatory treatment if patient
well for at least 6 months
Thank you