Asthma 2018 new

ASTHMA
Dr.Rishi Kumar Saini.
Asst. Prof.
Deptt. Of Respiratory medicine

G
IN
A
lobal
itiative for
sthma
© Global Initiative for Asthma

GINA 2018 / GINA 2017
Asthma is a heterogeneous disease, usually characterized by chronic airway
inflammation.
It is defined by the history of respiratory symptoms such as wheeze, shortness of
breath, chest tightness and cough that vary over time and in intensity, together
with variable expiratory airflow limitation.
(Indian Guideline )
“Asthma is defined as a chronic inflammatory disorder of the airways which
manifests itself as recurrent episodes of wheezing, breathlessness, chest
tightness and cough.
It is characterized by bronchial hyper-responsiveness and variable airflow
obstruction, that is often reversible either spontaneously or with treatment.

Asthma is usually associated with airway hyper responsiveness to direct or
indirect stimuli, and with chronic airway inflammation. These features
usually persist, even when symptoms are absent or lung function is
normal, but may normalize with treatment.

ASTHMA PHENOTYPES
Allergic asthma:
Non-allergic asthma:
Late-onset asthma
Asthma with fixed airflow limitation:
Asthma with obesity

SOME ALLERGENS WHICH MAY CAUSE ASTHMA
House-dust mites which live in
carpets, mattresses and
upholstered furniture
Spittle, excrements,
hair and fur
of domestic
animals
Plant pollen
Pharmacological
agents (enzymes,
antibiotics,
vaccines, serums)
Food
components
(stabilizers,
genetically modified
products)
Dust of
book
depo-
sitories

ASTHMA TRIGGERS
©2010
Some
Triggers

I. Non-modifiable risk factors
i. Age and gender:
In India, the prevalence of asthma increased with advancing age. Female gender has
consistently been associated with higher prevalence of asthma in adults. In children,
slight male predominance has been reported.
ii. Atopy:
Atopy is production of abnormal amounts of IgE antibodies in response to common
environmental allergens. A history of atopy is the strongest risk factor for development of
asthma
iii. Family history of asthma and/or atopy:
A family history of atopy and/or asthma is strongly associated with development of
asthma.
asthma in those with family history of asthma was 6.1 (95% CI, 5.4-6.9) and 8.8 (95% CI,
8.1-9.6), respectively.
iv. Genetic risk factors:
Genome-wide association studies have identified a locus on chromosome 17q12-21 as a
risk factor for childhood-onset asthma, but not for atopy or adult-onset asthma.Studies
from India have described polymorphism in different genes such as GSTM 1, GSTT 1,
MBL2 and others to be associated with asthma.
RISK
FACTORS :

II. Modifiable risk factors
i. Tobacco smoke:
Several studies from India, both in children and adults, have consistently reported higher
prevalence of asthma in those exposed to tobacco smoke. Dose–response relationship
has been reported for both active and passive/environmental (ETS) tobacco smoke
exposure.
In fact, tertiary smoking defined as fetus exposed to tobacco smoke as a consequence
of mother being exposed to ETS has also been reported to increase the risk of
development of asthma.
Tobacco smoke exposure not only increases risk of asthma but also affects the course
of asthma, for example, by increasing the risk of acute exacerbations.
ii. Biomass exposure:
Indoor air pollution due to combustion of solid fuels for cooking and heating has been
shown to significantly increase the risk of asthma. (1.3-1.6. %)
iii. Infections:
Respiratory viral infections early in life, especially those due to respiratory syncytial virus

iv. Occupational exposures:
More than 300 substances have been reported to predispose to occupational
asthma. prevalence reported in industrial workers is slightly higher than that in general
population.
v. Formula feed and cow milk in infancy:
Duration of exclusive breast-feeding is inversely associated with incidence of
wheezing in childhood and atopic asthma in later life. On the contrary, infants fed
with formula feed (cow milk or soy protein) have been reported to have a higher
incidence of wheezing illnesses in early childhood.
vi. Diet:
A history of perceived worsening of asthma in relation to dietary items is fairly
common among Indian asthmatics ranging from 60% to 90%. However, the skin
prick test (SPT)-proven sensitization is seen in only a small fraction ranging from
1.7% for black gram to 6.2% for rice.
vii. Obesity:
Asthma is more common in obese individuals especially those with body mass
index (BMI) >30 kg/m2.
Obese patients also have multiple co-morbidities making treatment of asthma

PATHOPHYSIOLOGY
Cells
Mediators
Inflammation
Symptoms
Triggers
Bronchial
Hyper-responsive

The diagnosis of asthma should be based
on:
A history of characteristic symptom patterns
Evidence of variable airflow limitation, from bronchodilator
reversibility testing or other tests
Document evidence for the diagnosis in the patient’s notes, preferably before starting
controller treatment
It is often more difficult to confirm the diagnosis after treatment has been started
Asthma is usually characterized by airway inflammation and airway hyper
responsiveness, but these are not necessary or sufficient to make the diagnosis of
asthma.

Symptoms :
Increased probability that symptoms are due to asthma if:
• More than one type of symptom (wheeze, shortness of breath, cough, chest
tightness)
• Symptoms often worse at night or in the early morning
• Symptoms vary over time and in intensity
• Symptoms are triggered by viral infections, exercise, allergen exposure, changes
in weather, laughter, irritants such as car exhaust fumes, smoke, or strong smells
Decreased probability that symptoms are due to asthma if:
• Isolated cough with no other respiratory symptoms
• Chronic production of sputum
• Shortness of breath associated with dizziness, light-headedness or peripheral
tingling
• Chest pain
• Exercise-induced dyspnea with noisy inspiration (stridor)

DIAGNOSIS OF ASTHMA – PHYSICAL EXAMINATION
Physical examination in people with asthma
 Often normal
 The most frequent finding is wheezing on auscultation, especially on forced expiration
Wheezing is also found in other conditions, for example:
 Respiratory infections
 COPD
 Upper airway dysfunction
 Endobronchial obstruction
 Inhaled foreign body
Wheezing may be absent during severe asthma exacerbations (‘silent chest’)
GINA 2017

Investigations :
ESSENTIAL: NON-ESSENTIAL:
1.Peak flow recording/simple spirometry 1.Blood test : CBC- eosinophillia
IgE – (atopy)positive skin prick tests
to common allergens(associated with rhinits and eczema
2.Bronchodilator reversibilty testing 2.CXR
3.Skin tests
4.methacholine/histamine
challenge
BHR,PC20- causing 20%fall in FEV1
asthma is suggested if PC20<8mg/ml(normal
pc>16mg/ml)
5.bronchial provocation tests
6.sputum analysis – sputum
eosinophillia
7.laryngoscopy/ent examination
8.bronchoscopy
9.lung biopsy
10.biomarker :sputum differential
cytology, exhaled breath pH and nitric oxide, exhaled breath proteins (like IL-6, IL-8),
and serum proteins (like eosinophilic cationic protein, adiponectin, and periostin)

Peak flow recording/simple spirometry
Diagnosis is highly likely if:
1.20% of diurnal PEF variation on >3days/week
2.FEV1 >15% decrease after 6min exercise
3.FEV1 >15%(and 200ml) increase after 2 week trial of oral steroid(30mg
prednisolone od)
Bronchodilator reversibilty testing
FEV1 >15%(and 200ml) increase after single dose of a short acting beta 2-
agonist therapy or 200mg bd of inhaled beclometasone or equivalent for 6-
8weeks.
400ml improvement is strongly suggestive of asthma.smaller improvement are
less sensitive and need careful interpretation.

DIAGNOSIS OF ASTHMA – VARIABLE AIRFLOW
LIMITATION
Confirm presence of airflow limitation
 Document that FEV1/FVC is reduced (at least once, when FEV1 is low)
 FEV1/ FVC ratio is normally >0.75 – 0.80 in healthy adults, and
>0.90 in children.
Confirm variation in lung function is greater than in healthy
individuals
 The greater the variation, or the more times variation is seen, the greater probability
that the diagnosis is asthma
 Excessive bronchodilator reversibility (adults: increase in FEV1 >12% and >200mL;
children: increase >12% predicted)
 Excessive diurnal variability from 1-2 weeks’ twice-daily PEF monitoring (daily
amplitude x 100/daily mean, averaged)
 Significant increase in FEV1 or PEF after 4 weeks of controller treatment
 If initial testing is negative:
 Repeat when patient is symptomatic, or after withholding bronchodilators
 Refer for additional tests (especially children ≤5 years, or the elderly)
GINA 2017, Box 1-2

SPIROMETRY
Essential if chronic airways disease is suspected
 Confirms chronic airflow limitation
 More limited value in distinguishing between asthma with fixed airflow limitation, COPD and
asthma-COPD overlap
Measure at the initial visit or subsequent visit
 If possible measure before and after a trial of treatment
 Medications taken before testing may influence results
Peak expiratory flow (PEF)
 Not a substitute for spirometry
 Normal PEF does not rule out asthma or COPD
 Repeated measurement may confirm excessive variability, found in asthma or in some patients
with asthma-COPD overlap
GINA 2017, Box 5-3

STEP 3 - SPIROMETRY
Spirometric variable Asthma COPD Overlap
Normal FEV1/FVC
pre- or post-BD
Compatible with asthma Not compatible with
diagnosis (GOLD)
Not compatible unless
other evidence of chronic
airflow limitation
FEV1 ≥80% predicted Compatible with asthma
(good control, or interval
between symptoms)
Compatible with GOLD
category A or B if post-
BD FEV1/FVC <0.7
Compatible with mild
ACO
Post-BD increase in
FEV1 >12% and 400mL
from baseline
- High probability of
asthma
Unusual in COPD.
Consider ACO
Compatible with
diagnosis of ACO
Post-BD FEV1/FVC <0.7- Indicates airflow
limitation; may improve
Required for diagnosis
by GOLD criteria
Usual in asthma-COPD
overlap (ACO)
Post-BD increase in
FEV1 >12% and 200mL
from baseline (reversible
airflow limitation)
- Usual at some time in
course of asthma; not
always present
Common in COPD and
more likely when FEV1
is low
Common in ACO, and
more likely when FEV1 is
low
FEV1<80% predicted Compatible with asthma.
A risk factor for
exacerbations
Indicates severity of
airflow limitation and risk
of exacerbations and
mortality
Indicates severity of
airflow limitation and risk
of exacerbations and
mortality
GINA 2017, Box 5-3
UPDATED
2017

Time (seconds)
Volume
Note: Each FEV1 represents the highest of
three reproducible measurements
TYPICAL SPIROMETRIC TRACINGS
FEV1
1 2 3 4 5
Normal
Asthma
(after BD)
Asthma
(before BD)
Flow
Volume
Normal
Asthma
(after BD)
Asthma
(before BD)
GINA 2017
6

bronchoprovocative tests:
Excessive narrowing of the airway in response to a physical or chemical
stimulus is called bronchial hyper-responsiveness (BHR). It is common in
asthmatics
transient phenomenon in viral upper respiratory infections or may be persistent
in few conditions like sarcoidosis.
Bronchoprovocative tests can be performed using either direct or indirect stimuli
Pharmacologic agents active on bronchial smooth muscles (e.g., methacholine)
are direct stimulants. On the other hand, indirect stimuli (like exercise) cause
release of biological mediators such as histamine and prostaglandins, which in
turn constrict the airway.
A methacholine challenge test may be helpful in excluding asthma objectively
Clinical asthma is unlikely when methacholine challenge at a dose of 16
mg/mL does not produce a 20% fall in FEV1.

Nitric oxide (NO) exhibits physiological effects of vasodilation, bronchodilation
and immune enhancement at low concentrations, and acts as an inflammatory
agent at higher concentrations.
NO levels are elevated in exhaled breath of asthmatics, more specifically in a
subset of patients with eosinophilic inflammation.
The non-invasive nature of the test and its repeatability has made FENO a
potentially useful investigation in asthma management. However, the test is not
freely available, and a reference value for FENO is difficult to establish owing to
the variations noted with age, gender, smoking status, use of anti-inflammatory
medications and measurement techniques.
In general, FENO <25 parts per billion (ppb) is suggestive of non-eosinophilic
inflammation unlikely to be steroid responsive.
FENO >50 ppb is more suggestive of eosinophilic airway inflammation and
steroid responsiveness.
Also, the number of exacerbations in adults did not differ significantly whether
the treatment was FENO guided or symptom guided. Therefore, measurement
of FENO is not routinely recommended for diagnosis or management of
Nitric oxide test

Asthma has been traditionally classified as atopic and non-atopic. In the last
decade, asthma has also been categorized based on clinical features into
various phenotypes by using statistical approaches and cluster analysis
These phenotypes have varying degrees of association with atopy. Studies in
the pediatric population suggest strong evidence demonstrating the relationship
between asthma severity and atopy. However, in adult asthmatics, atopy
although prevalent need not correlate with disease severity.
Tests for determining allergic status (skin prick tests total and antigen specific
IgE) are not useful for all patients with asthma as the presence of a positive test
neither confirms presence of allergy nor proves causality. Therefore, these tests
may be performed only when specific allergy is suspected such as allergic
aspergillosis,and specific treatment is contemplated
Role of allergy testing in asthma

Patient with
respiratory symptoms
Are the symptoms typical of asthma?
Detailed history/examination
for asthma
History/examination supports
asthma diagnosis?
Perform spirometry/PEF
with reversibility test
Results support asthma diagnosis?
Treat for ASTHMA
YES
YES
YES
© Global Initiative for AsthmaGINA 2017, Box 1-1 (1/4)

Patient with
for asthma
asthma diagnosis?
Further history and tests for
alternative diagnoses
Alternative diagnosis confirmed?
Treat for alternative diagnosisTreat for ASTHMA
YES
YES
YES
NO
NO
YES

Patient with
for asthma
asthma diagnosis?
Repeat on another
occasion or arrange
other tests
Confirms asthma diagnosis?
Consider trial of treatment for
most likely diagnosis, or refer
for further investigations
YES
YES
YES NO
NO
NO
NO
YES
YES
NO

Patient with
for asthma
asthma diagnosis?
Empiric treatment with
ICS and prn SABA
Review response
Diagnostic testing
within 1-3 months
Repeat on another
occasion or arrange
other tests
Confirms asthma diagnosis?
Consider trial of treatment for
most likely diagnosis, or refer
for further investigations
Clinical urgency, and
other diagnoses unlikely
YES
YES
YES NO
NO
NO
NO
YES
YES
NO

CLASSIFICATION OF
DRUGS
Bronchodilators – rapid relief, by relaxation of
airway smooth muscle
β2 Agonists
Anticholinergic Agents
Methylxanthines
Controllers – inhibit the inflammatory process
Glucocorticoids
Leukotrienes pathway inhibitors
Cromones
Anti-IgE therapy

Β2 AGONISTS IN
ASTHMA
Potent bronchodilators.(TOC)
Usually given by inhalation route.
 MOA:
Relaxation of airway smooth muscle
Non-bronchodilator effects
 Inhibition of mast cell mediator release
 Reduction in plasma exudation
 Increased mucociliary transport
 Inhibition of sensory nerve activation
Inflammatory cells express β2 receptors but these are rapidly
downregulated.
No effect on airway inflammation and AHR.
S h o r t - A c t i n g β2 A g o n i s t s
Albuterol /salbutamol
Levalbuterol, t h e (R)-
enantiomer ofalbuterol
Metaproterenol
Terbutaline
Pirbuterol
Bambuterol
L o n g - A c t i n g β 2 A g o n i s t s
Salmeterol
Formoterol

CORTICOSTEROIDS –
ASTHMA
Effective drugs for treatment of asthma.
Development of inhaled corticosteroids is a
major advance in asthma therapy.
Used prophylactically as a controller
therapy.
Reduce the need for rescue β2 agonist.
 If asthma not controlled at low dose of
ICS then addition of long acting β2
agonist is more effective than doubling
steroid dose.
I n h a l e d
cor ticoster oids( ICS)
 Beclomethasone
 Budesonide
 Fluticasone
 Triamcinolone
 Flunisolide
 Ciclesonide

TREATMENT-
GINA 2017, Box 3-5, Step 1 (4/8)
PREFERRED
CONTROLLER
CHOICE
Other
controller
options
RELIEVER
STEP 1 STEP 2
STEP 3
STEP 4
STEP 5
Low dose ICS
Consider low
dose ICS
Leukotriene receptor antagonists (LTRA)
Low dose theophylline*
Med/high dose ICS
Low dose ICS+LTRA
(or + theoph*)
As-needed short-acting beta2-agonist (SABA) As-needed SABA or
low dose ICS/formoterol#
Medium dose
ICS/LABA**
Med/high
ICS/LABA
*Not for children <12 years
**For children 6-11 years, the preferred Step 3 treatment is medium dose ICS
#For patients prescribed BDP/formoterol or BUD/ formoterol maintenance and reliever therapy
 Tiotropium by mist inhaler is an add-on treatment for patients ≥12 years with a history of exacerbations
Add tiotropium*
High dose ICS
+ LTRA
(or + theoph*)
Add low
dose OCS
Refer for
add-on
treatment
e.g.
tiotropium,*
anti-IgE,
anti-IL5*

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