CURRENT

MANAGEMENT OF
ASTHMA
Dr V.O.Abah
Consultant Family Physician
U.B.T.H
INTRODUCTION
 Asthma is a highly prevalent condition with
significant morbidity and negative impact on
quality of life of patients.
 It carries a risk of mortality.
 Fortunately current knowledge promises
good control of the disease and
improvement in quality of life.
 Every doctor should know this and every
patient should benefit from it.
INTRO

 Current approach to care represents a

paradigm shift from old concepts.
 1. pathology
 2 treatment
 3. control
DEFINITION
 Asthma is a chronic inflammatory disease of
the airways characterised by airway
hyperesponsiveness and airflow limitation
that is reversible either spontaneously or on
treatment.
KEY COMPONENTS
 1.Inflammation
 2.hyperresponsiveness
 3.airflow limitation.
EPIDEMIOLOGY
 Affects about300 million people worlwide
10% of population in developed world
 250,00 deaths yearly
 Estimated additional 100 million people by
2025
 Most common chronic ds of childood and
commonest cause of school absenteeism
 DALYs ~ 15MILLION /YEAR
RISK FACTORS
 Males > females in early onset asthma but
revered in adult asthma
 Genetics :atopy
 Exposure to air pollution
 age
PATHOLOGY
 The airway epithelium is made of cilliated
columnar epithelium with associated resident
immune mediatory cells and infiltrating
immune cells during inflammation.
 The airway epithelium is a target and major
contributor to the inflammatory process
 The cells thought to play important parts in
the inflammatory response:
 mast cells, eosinophils, neutrophils
lymphocytes, and airway epithelial cells.
 Exposure to allergens triggers immune response
resulting in airway hyper responsiveness
manifesting mainly as:
 Broncho constriction (smooth muscle spasm)
 Airway oedema
 Mucus hyper secretion
 Airway remodelling: Increased deposition of
collagen in the epithelium, increased
vascularization, hypertrophy of smooth
muscle and mucus secretory glands and
denudation of epithelium :
 consequence: permanent obstruction and
reduction in lung function mimicking COPD
 Inflammation affects the bronchi first but
progresses to the smaller airways as disease
progresses.

 There is chronic on going sub acute

inflammation even in the absence of
symptoms.

 Acute episodes represent inflammatory

events triggered by exposure to precipitants
and could last hours to days even after
remission of the cardinal symptom of
bronchospasms
 Mediators
 Cells Histamine Effects
 Mast cells Leukotrienes Bronchoconstricti
Prostaglandins on
 Macrophages
Thromboxane Plasma exudation
 Eosinophils PAF Mucus
 T lymphocytes Bradykinin hypersecretion
Tachykinins AHR
 Epithelial cells Reactive oxygen Structural
 Fibroblasts species changes
Adenosine (fibrosis, sm
 Neurons
Anaphylatoxins hyperplasia,
 Neutrophils Endothelins angiogenesis,
 Platelets? Nitric oxide mucus
Cytokines hyperplasia
 Basophils? Growth factors
INFLAMMATORY CASCADE
 Allergens….. Denritc cells …… LN ….. T&B
Lymphocytes….. T cell differentiation,B cell
production of IgE.
 IgE Attach to mast cells(Sensitization)……
subsequent exposure….. Degranulation …
release of inflammatory mediators…
recruitment of other inflammatory cells and
massive release of mediators…… acute
attack.
INFLAMMATORY RESPONSE TO
ASTHMA
ASTHMA TRIGGERS
 Allergens
 Infection
 Pollutants: dust and fumes
 Cigarrete smoking
 Drugs
 Industrial sensitizers
 Cold
 Exercise
 GERD
 Obesity
 Psychological factors
CLINICAL FEATURES
 Major symptoms: cough, breathlessnes,
wheeze
 Signs: Dyspnea and Rhonchi (expiratory)
 Presentation varies from mild acute to
severe acute.
 Intermittent or persistent
 Symptom profile determines diagnostic label
and treatment plan
CLASSIFICATION BY SYMPTOM
PROFILE
 Type day time sym. Night time
sym
 Intermittent: <2/wk
<2/mnth
 Mild persistent >2/wk <1/day >2/mnth
 Mod persistent daily >1/wk
 Severe persistent continual frequent
 difficult to treat continual continual

asthma
DIAGNOSIS
 Usually clinical.
 Cardinal symptoms: cough usually non productive
worse at night
 wheeze
 Chest tightness and
 Symptoms are reversible or variable over time and
obviously precipitated by triggers.
 Sign: dyspnea and Rhonchi
 Therapeutic response to asthma therapy
INVESTIGATIONS
 Spirometry
 FEV1/FVC<70%
 Reversibility test: >12% or 200ml increase in FEV1
following use of SABA
 Peak Expiratory Flow:>20% or 60l/min increase
after SABA

 Methacholine challenge test: PC20

 20% fall in the FEV1 or PEF following inhalation of
methacholine.
 Test of hyper responsiveness. Carries a risk of
severe attack or even anaphylaxis.
PEF
 Serial PEF monitoring measures diurnal variation in
airway limitation indicated by : early morning dip
in PEF recordings.
 PEF: Record best of 3 attempts
 A reduction in PEF to 50-79% of patient’s personal
best indicates deterioration and change in tx plan
 Monitoring response in acte exacerbations
 In diagnosis of occupational asthma
 Note : Lung function is normal in the absence of
symptoms especially for intermittent asthmatics.
INVESTIGATIONS
 CXR
 Pulse oximetry and blood gas analysis
 E/U/Cr
DIAGNOSTIC CHALLENGES
 1. Nucturnal asthma:
 2. asthma in the elderly: Co existing asthma
and COPD
 Occupational Asthma
 Asthma in children < 5yrs
 Cough variant asthma
 Atopic cough
 Exercise induced bronchoconstriction
GOALS OF TREATMENT
 To achieve and maintain control of symptoms
for long periods of time with few or no
exacerbations.
 To enable the patient live quality active
lives unhindered by the condition.
 Good control is indicated by: control of
symptoms
 Control of exacerbations
 Prevention of decline in lung function
 Reduce side effects of drugs
COMPONENTS OF ASTHMA CONTROL
 1 Doctor Patient partnership:
 good Dr/Pt relashionship
 Develop personal action plans
 Educate Patient :Disease facts

Disease is very controllable.

Quality of life can be maintained
Inhaler Technique
 Medication use:
 Appropriate inhaler technique
 control vs reliever medication
 Compliance.
 Assesment of effect of asthma on patient life
style.
2.IDENTIFY AND REDUCE EXPOSURE TO
RISK FACTORS:

 Smoking cessation
 Home hygiene
 Remove allergens: pets, furnishings.
 Avoid aerosol irritants
 Manage asthma exacerbations.
3. ASSESS, TREAT AND MONITOR ASTHMA

 Accurate diagnosis and appropriate

treatment plan
 Monitoring and Signs of decompensation:
symptom profile can change
 Compliance.
 Monitoring using the PEF,
 ACT
4.MANAGE EXACERBATION
 Identify patients at risk:
 Pt wit Phx ofsevere asthma req. intensive
care
 Been hospitalised for asthma in the last year
 Non compliant.
 Recently stopped using oral steroids
 Not using ICS or over dependent on B@
agonists
 Has psychiatric or other social problems that
may adversly affect compliance
 Patients should go to hospital if SABA use
does not produce sustained relief for up to
3hrs
 There is no relief after 4-6hrs of oral CS use
DRUGS USED IN ASTHMA
 Relief of broncho constriction: B2 agonists: SABA
&LABA
 Theophyllines
 Ipratropium bromide or oxitropium bromide

 Control of Inflammation: corticosteroids: inhaled,

oral and injectables
 Leukotriene modifiers:zafirlukast and montelukast
 Cromoglycates: sodium cromoglycate and
nedocromil sodium,
TREATMENT PLANS
 Intermittent:
 releiver medication used PRN. If no releif
within 30 mins or used more than 3X/day
report to Dr
 Acute exacerbations: req rescue oral
steroids 20-30mg dly for upto 2wks + SABA
etc.
 STEP 1:MILD INTERMITTENT

Low dose inhaled CS daily

 Alt; CMG, LTM
 Acute exacerbations : ditto
 Step 3 Moderate Persistent:
 Daily low to med dose ICS + LABA
 alt LTM or SR theophylline
 acute exacerbation:ditto

 step 4 Severe Persistent:

 Daily high dose ICS+LABA + SR theophylline,
 Acute exacerbation: ditto

 step 5 difficult to treat asthma: add oral CS and IgE

tx to above
 Adjustment of TX regimen
 Use the least dose of medication rqd to achieve
control
 when symptom profile changes for the worse, step
up treatment.
 Maintain at that level for 2-3mnths while correcting
factors like exposure to precipitants ,inhaler
technique ,compliance etc.
 Step down gradually to the least dose reqd.
 Monitor symptoms.
 Controller ICS withdrawal may be considered if
patient is symptom free for up to 6mnths
MONITORING OF SYMPTOMS
 Symptom and exposure diary
 Use of releiver medication
 Serial PEF measurements
 Asthma control tests
ASTHMA CONTROL TEST
parameters Good fair poor

Daytime symptom None <3days/wk >3days /wk

Night time symp. Not woken <1 night /wk > 1night /wk

Physical activity normal normal restricted

exacerbations none Mild ,infrequent Mod-

severe ,frequent

Missed sch/work none none any

Releiver use none <3doses/wk >3doses/wk

FEV1,FEV1/FVC normal >90%personal best <90% personal

best
PEF normal >90% personal <90% personal
best best
MANAGING LOSS OF CONTROL
 Evaluate :
 Compliance
 Exposure to triggers
 Inhaler technique
 Intercurrent infections
 Psychological factors
INDICATION FOR RESCUE STEROID

 Given when there is acute exacerbation and

continued till after control is established.
 Dose : 30-60mg dly single dose .up to 3weeks
 In children 1-2mg /kg used
 Indication:PEF<60% of pt personal best.
 Acute exacerbation requiring nebulisation or IV
aminophylline`
 Other evidence of loss of control as seen in the ACT.
EXCERBATIONS
 mild to moderate asthmatic attack:
 Nebulisaton with salbutamol or terbutaline
 Review with clinical signs or PEF every 30
mins.
 IV hydrocortisone
 Commence oral steroids
 Treat intercurrent infection.
 Step up treatment plan
 Plan short follow up
 Search for precipitating factor :allergen
exposure.poor compliace,poor inhaler
technique
ACUTE SEVERE ASTMA
 Evaluation: pt with asthma symptoms has
the following fx of severity
 Cannot speak in sentences .
 Severely breathless pulse rate >110/min
 PEF <50%
 Pulsus paradoxus may be present
 Cyanosis,*
 Exhaustion* and confusion*
 Silent chest* ,bradycardia*
MGT
 O2 therapy
 Nebulisation with salbutamol 2.5-10mg or
terbutaline.5-10mg.
 repeated after 30mins
 IV hydrocortisone 100-200mg but can be
titrated up to 1gm
 Oral prednisolone20-60mg
 Monitor clinical signs and PEF every 30 mins
 Set up Iv line
 IV aminophylline given dilute and slowly
over 10-15 minutes followed by infusion
 IV Anticholinergics may be added.
 If response not adequate refer for ICU mgt
 Mechanical respiration may be rqd.
CONCLUSION
 Asthma is very controllable.
 Appropriate anti inflammatory medication
makes this very possible .
 Empower your asthma patients to live fully
Thanks for Your