ASTHMA

 Asthma means ‘laboured breathing’ in Greek.

 It is a broad term used to refer to a disorder of the respiratory system that
leads to episodic difficulty in breathing.
 Around 300 million people worldwide have asthma.
 India has 10% of World's asthma patients.
 Asthma is the most common chronic disorder in children in India.
 Higher occurrence of asthma in boys than girls and in children whose parents
have an allergic disorder.
 Between 30% and 70% of children will become symptom free by adulthood.
 Asthma is considered to be one of the consequences of Western civilisation.
 Asthma appears to be related to a number of environmental factors.
 Air pollution resulting from industrial sources and transport may be
interacting with smoking, dietary and other factors to increase the incidence
of asthma.
 Market data says the sale of anti-asthma medicines in the country went up to
almost 50% over the past four years.
 Thirteen of the world’s 20 most polluted cities are in India.
DEFINITION
 Asthma is defined as a chronic inflammatory
disorder of the airways.
 Inflammatory symptoms are associated with
airflow obstruction and an increase in airway
response to a variety of stimuli.
 Obstruction is often reversible either with
treatment or spontaneously.
ETIOLOGY
Trigger Examples
Allergens Pollens, moulds, house dust mites,
excreta of animals
Industrial Chemicals Isocyanate containing paints, eposy
resins, aluminium, hair spray
Drugs Aspirin, penicillins, ibuprofen, β-
blockers
Foods Nuts, fish, seafood, dairy products,
food coloring (tartrazine, benzoic
acid)
Other industrial triggers Wood or grain dust, cotton dust,
cigarette smoke, sulphur dioxide
Miscellaneous Cold air, exercise, emotion, stress,
viral respiratory tract infections
CLINICAL PRESENTATION (SIGNS
& SYMPTOMS)
 Persistent cough
 Recurrent episodes of dyspnoea (difficulty in
breathing)
 Wheezing (a high pitched whistling sound in
bronchi when breathing)
 Chest tightness
DIAGNOSIS
 The decrease in the following lung function tests are the basis to diagnose
asthma with the help of Spirometer:
 Forced expiratory volume in 1 second (FEV 1): is a measure of the forced
expiratory volume in the first second of exhalation. Normal value of FEV 1
is 0.75-5.5 L.
 Forced vital capacity (FVC): is the maximum volume of air exhaled with
maximum effort after maximum inspiration. Normal value of FVC is 3-5 L.
 FEV1 is usually expressed as a percentage of total volume of air exhaled
and is reported as FEV1/FVC ratio (index of airways obstruction). Normal
individual can exhale at least 70% of their total capacity in 1 second.
 Expiratory peak flow rate (EPFR): is the maximum speed of expiration.
Normal value of EPFR is 400-800L/min for men and 200-600 L/min for
women whereas 50-100L/min represents severe obstruction.
 The diagnosis of asthma can be confirmed by measuring the response to a
bronchodilator or by examining a patient's day-to-day variation in PEF
readings. A diurnal variability of more than 20% is highly suggestive of
asthma.
PATHOPHYSIOLOGY
 Extrinsic or allergic or eosinophilic asthma is common in
children, associated with a genetic predisposition and precipitated
by known allergens.
 Intrinsic or non-eosinophilic asthma develops in adulthood with
symptoms triggered by non-allergic factors such as viral
infections, irritants, emotional upset.
 Mast cells, eosinophils, epithelial cells, macrophages and
activated T-lymphocytes are main components of inflammation in
asthma.
 These cells act on the airways to cause inflammation either
directly or through neural mechanisms. These cell derived
mediators cause marked hypertrophy and hyperplasia of bronchial
smooth muscle, mucus gland hypertrophy leading to excessive
mucus production and airway plugging, airway edema, acute
bronchoconstriction and impaired mucociliary clearance.
 Mast cells components (histamine, leukotrienes,
prostaglandins, bradykinin) are released as a result of an
IgE antibody mediated reaction on the surface of the cell.
 These mast cell components attract eosinophils and
neutrophils.
 Macrophages release prostaglandins, platelet activating
factor (PAF), thromboxane.
 PAF sustain bronchial hyperactivity and causes plasma
leakage of respiratory capillary resulting into increase in
mucosal edema. It also facilitates the accumulation of
eosinophils within airways.
 Eosinophils release inflammatory mediators such as
leukotriene C4 (LTC4) and PAF.
 Epithelial damage and thick viscous mucus
cause further deterioration in lung function.
 The increase in size of bronchial glands and
goblet cells produces more mucus.
 The airways is blocked by thick mucus along
with epithelial and inflammatory cell debris.
 Mucociliary clearance is also decreased due to
inflammation of epithelial cells.
GOALS OF TREATMENT FOR
CHRONIC ASTHMA
 Prevent chronic and troublesome symptoms
(coughing, breathlessness)
 Prevent recurrent exacerbation
 Minimize the need for hospitalization
 Prevent loss of lung functions
 Maintain normal pulmonary functions
 Reduce frequent use of inhaled short acting β–
agonist for quick relief of symptoms
 Maintain normal activity levels (exercise, work)
 Minimum or no adverse effects of therapy
TREATMENT OF CHRONIC
ASTHMA
 Nonpharmacologic Therapy:
 Patient
education and teaching of self
management skills
 Avoidance of known triggers
 Smoking cessation for smokers
PHARMACOTHERAPY
 The pharmacological management of asthma depends upon
the frequency and severity of symptoms.
 Infrequent attacks can be managed by treating each attack
when it occurs, but with more frequent attacks preventive
therapy is used.
 Inhalation is the preferred route of administration of drugs in
asthma due to direct delivery of drugs to airways in smaller
doses with faster onset of action and fewer side effects than
systemic routes.
 Treatment is usually given in a stepwise progression according
to severity of symptoms and response to current treatment.
 At each stage, the patient’s inhaler technique should be
assessed and inhalation device should be changed if necessary
to increase patient compliance.
 Relievers are the agents that give immediate relief
of symptoms i.e. bronchodilators. Examples: short
acting β–agonists, anticholinergics,
methylxanthines and long acting β–agonists.
 Controllers or Preventers or Protectors are the
agents that reduce inflammation or give long term
bronchodilation. Examples: Anti-inflammatory
agents [corticosteroids, mast cell stabilizers
(cromones), leukotriene antagonists, anti-IgE
monoclonal antibodies], and steroids sparing
agents.
BRONCHODILATORS
 β-Agonists:
 β-Agonists are mainstay of asthma management.
 These agents cause bronchodilation through β receptor stimulation ↑
cAMP formation in bronchial muscle cell relaxation.
 Salbutamol and terbutaline are selective short acting β2-agonists with
side effects of cardiotoxicity, tachycardia and palpitation.
 Inhaled β2-agonists are the first line treatment for asthma for
symptomatic relief of breathlessness and wheezing. Example:
Salbutamol 200 µg.
 Only treatment for infrequent symptoms with no advantage to regular
administration.
 Oral β2-agonists as tablets can be added in asthma with persistent
poor control (step 4) for additional symptom control.
 High dose β2-agonists are only required if conventional dose does not
achieve adequate symptom control.
ADDITIONAL BRONCHODILATORS
 These agents may be required if β-agonists are unable to
control symptoms adequately.
 Inhaled anticholinergic agents:
 They block muscarinic receptors in bronchial smooth muscle
and cause bronchodilation but are not as potent as β2-agonists.
 They have a slower onset of action but a longer duration of
action than β2-agonists.
 Helpful specially in elderly having complicated asthma with
obstructive airways disease.
 Dosage: 20-40 µg 3-4 times daily for ipratropium bromide.
 Dry mouth, precipitation of acute glaucoma, urinary retention
and constipation are the side effects.
 Examples: Ipratropium bromide, tiotropium bromide.
 Methylxanthines:
 Oral theophylline as slow release form can be added as add on
therapy (step 3) for additional symptom control.
 Theophylline and oral β2-agonists slow release are especially
helpful in a single night time dose for troublesome nocturnal
symptoms.
 These oral bronchodilators (theophylline + oral β2-agonists) are also
helpful in patients who are unable to use inhaler effectively but with
more pronounced side effects compared to inhaler therapy.
 Dose: Starting dose of theophylline is 400-500 mg/day in adults
and increased to 800-1000 mg/day if required. Higher dose for
children based on age of the child.
 The common side effects are nausea and vomiting at low dose
while tachycardia and seizure at high dose.
 Theophylline has narrow therapeutic index hence proper
 Long acting β-agonists:
 When low dose inhaled steroids fail to control
asthma symptoms adequately as add on therapy
(step 3), long acting β2-agonists should be
added instead of increasing the steroid dose.
 These agents are in addition to short acting
agents.
 Unsuitable to acute symptom relief due to
slower onset of action.
 Examples: Salmeterol, formoterol.
CONTROLLER MEDICATION
 Inhaled anti-inflammatory agents:
 Regular anti-inflammatory treatment should be used for patients with
recent exacerbations, nocturnal asthma, impaired lung function or using
inhaled bronchodilator more than once a day.
 Corticosteroids:
 Corticosteroids suppress the chronic airway inflammation associated with
asthma.
 Dosage: Beclometasone or budesonide 400 µg per day in divided doses.
 Consider steroids for patients with any of the following:
 Exacerbation of asthma in last 2 years
 Using inhaled β2 agonists three times a week or more
 Symptoms three times a week or more, or waking one night a week.
 If symptoms persist, the steroid dose is increased stepwise accordingly.
 The dose of inhaled corticosteroid should be reduced once symptoms
improve and stabilize.
 A maximum dose of 1.5-2 mg per day can be used.
 Oropharyngeal candidiasis is common side effect.
 Use of large volume spacer device, rinsing the mouth with water
or brushing teeth after inhalation minimize oropharyngeal
candidiasis.
 Mast cell stabilizers (Cromones):
 Inhaled cromones are less effective than corticosteroids in asthma.
 Can be used in conjunction for patients not responding completely
to inhaled β2-agonists.
 As alternative to corticosteroids in case of tolerance problem.
 The common side effects are coughing, transient bronchospasm
and throat irritation.
 Examples: Cromolyn sodium (sodium cromoglycate), nedocromil
sodium.
 Leukotriene antagonists:
 They are oral leukotriene receptor antagonists that
reduce the proinflammatory (airway edema) and
bronchoconstriction effects of leukotriene D4.
 They are less effective than corticosteroids in controlling
asthma but are effective in combination with steroids.
 Mainly effective in aspirin induced asthma.
 If no improvement in control within 4-6 weeks then it
should be stopped.
 The common side effects are abdominal pain, diarrhoea,
headache, dizziness.
 Examples: Zafirlukast, montelukast.
 Anti-IgE monoclonal antibodies:
 Omalizumab is approved for the treatment of
allergic asthma not well controlled by inhaled
or oral corticosteroids.
 Beneficial specially in patients with severe
persistent allergic asthma.
 High cost drug.
 Steroid sparing agents:
 Reduce the steroid dose in patients dependent
on systemic steroids.
 The side effects are potentially toxic hence
close monitoring is required.
 Examples: Methotrexate, cyclosporin and gold.
ACUTE SEVERE ASTHMA
 Uncontrolled asthma can progress to an acute state
where inflammation, airway edema, excessive mucus
accumulation, and severe bronchospasm result in
profound airway narrowing that is poorly responsive
to usual bronchodilator therapy.
 Patients may be anxious in acute distress and
complain of severe dyspnea, shortness of breath,
chest tightness, or burning.
 If an acute attack becomes persistent and difficult to
treat, it is known as acute severe asthma.
 Peak expiratory flow (PEF) and FEV1 are less than
50% of normal predicted value.
GOALS OF TREATMENT FOR
ACUTE SEVERE ASTHMA
 Correction of significant hypoxemia (low
blood oxygen)
 Rapid reversal of airways obstruction (within
minutes)
 Reduction of the likelihood of recurrence of
severe airflow obstruction
 Hasten recovery
 Development of action plan in case of future
exacerbation
TREATMENT OF ACUTE ASTHMA
 Nonpharmacologic Therapy:
 Patient education and teaching of self
management skills
 Avoidance of known triggers
 Smoking cessation for smokers
 Supplemental oxygen therapy to maintain
arterial oxygen saturation above 90% (above
95% in pregnant women and patients with
heart disease)
 Correction of significant dehydration
PHARMACOTHERAPY
 The management of acute asthma depends on
the following factors:
 The severity of the attack and its response to
treatment
 Present treatment
 Patient’s past history
PREVENTION OF ACUTE ATTACK
 The ideal way of treating an acute attack is to educate
patients to recognize when their condition is deteriorating
so that they can initiate treatment to prevent the attack
becoming severe. This can be achieved with an
individualized self-management plan.
 Immediate initiation of further treatment and early
referral is key of management.
 The dose of inhaled β2 agonist should be increased, and
start a short course of oral steroid (40-60 mg prednisolone
every morning for 1 week). Increase the dose of inhaled
corticosteroid if required.
 Hospital admission is necessary in case of further
deterioration of the conditions (PEFR <50%).
IMMEDIATE MANAGEMENT OF
ACUTE SEVERE ASTHMA
 Oxygen is administered at high concentration and at high rate.
 β2 agonist is administered giving prompt bronchodilation lasting
4-6 hours.
 In mild to moderate exacerbation, β2 agonist like salbutamol is
administered by metered dose inhaler with a spacer attachment
(4-6 puffs).
 Nebulizers are used in severe symptoms because of high dose
delivery with no requirement of co-ordination in patients.
 Oral prednisolone (40-50 mg for 5 days) is also given.
 In case of life threatening conditions such as cyanosis,
bradycardia, confusion, exhaustion or unconsciousness, high
dose of bronchodilators are used. Example: Salbutamol 5000 µg
with ipratropium bromide 500µg, repeated after 15 minutes and
regularly if required.
 Intravenous aminophylline can be given with a bolus
dose of 250 mg over 30 minutes, followed by
continuous infusion of 500 µg/kg/h.
 IV magnesium sulphate (1.2-2 g) as a 20 minute
infusion is helpful in some patients showing no good
response to initial treatment.
 Further deterioration in condition require assisted
ventilation in intensive care unit (ICU).
 Regular monitoring of arterial blood gases and oxygen
saturation by Pulse oximetry should be performed to
assess condition.
 Antibiotics are used only in case of bacterial infection.
SUBSEQUENT MANAGEMENT OF
ACUTE SEVERE ASTHMA
 The subsequent management of acute severe asthma depends on
the patient’s clinical response.
 All patients should be monitored throughout treatment for PEFRs
and arterial blood gas concentration to ensure adequate oxygen
supply.
 As the patient responds to treatment, infusion can be stopped.
 As improvement continues, an inhaled β2 agonist is substituted for
the nebulized form and oral corticosteroid stopped or reduced to
maintenance dose if necessary.
 The checking of inhaler technique of patient should be done and
correct any problem or try alternate device before discharge.
 A self management plan should be drawn up and discussed with
each patient.
 Early primary care follow up and referral to a hospital specialist
are recommended.
INHALATION DEVICES
 The choice of a suitable inhalation device is
important in the treatment of asthma.
 The incorrect use of inhaler results into
suboptimum treatment.
 Factors affecting the selection of appropriate
inhalation device are:
 Patient’s age
 Severity of disease
 Co-ordination
 Personal preference
 Manual dexterity
METERED DOSE INHALER (MDI)
 Advantages of MDI:
 Multidose
 Small
 Widely available for most of the drugs used in asthma
 Disadvantages of MDI:
 Correct use requires a good technique (need co-ordination
between inspiration and actuation)
 Only deliver 10% drug to the airways with 80% deposited
in oropharynx
 Irritation in pharynx & bronchi
 Oral candidiasis and dysphonia (impaired voice) due to
corticosteroid administered by MDI
 Difficult to use specially for younger children
MDI TECHNIQUE
 Shake vigorously
 Remove cap
 Hold upright
 Breathe out gently, not fully
 Start breathing in slowly and deeply
 Actuate during inspiration
 Continue slow inhalation
 No aerosol loss is visible
 Hold breath 10 seconds
 Next dose after 1 minute
MDI WITH SPACER EXTENSION
 Increases lung deposition
 Reduces oropharyngeal deposition
 Reduces oral candidiasis and dysphonia from
inhaled corticosteroids
 Useful for people having poor co-ordination
between inspiration and actuation
NEBULIZERS
 Require little co-ordination from the patient as drug is
inhaled through a facemask or mouthpiece using normal
tidal breathing.
 Useful in patients unable to use conventional inhalers.
 Patients receive a higher dose than MDI.
 Helpful in avoiding the need of intravenous drugs in acute
severe asthma attack.
 The safe and correct use of nebulizers requires
counselling.
 Overreliance on nebulizer can result in delay in seeking
medical advice.
 The high doses of bronchodilator increase the incidence of
side effects.
Thanks