BRONCHIAL ASTHMA

Harun eliek
Definition
Asthma is a chronic inflammatory
disease of the airways which develops
under the allergens influence, associates
with bronchial hyperresponsiveness and
reversible obstruction and manifests
with attacks of dyspnea, breathlessness,
cough, wheezing, chest tightness and
sibilant rales more expressed at
breathing-out.
Epidemiology
According to epidemiological studies
asthma affects 1-18% of population of
different countries.
Only in 2006 more than 300 million
patients suffered from asthma all over
the world, 250 thousands of patients die
of asthma. The incidence of asthma is
higher in countries with increased air
pollution.
Etiology
As asthma is a
respiratory allergic
disease, the influence
of allergens
permeated into the
organism through
airways is essential
for the disease
development.
The allergens are
divided into:
communal,
industrial,
occupational,
natural
pharmacological
ommunal allergens are contained in the air of
apartment houses. They are:
house-dust mites which live in carpets,
mattresses and upholstered furniture;
spittle, excrements, desquamated epidermis,
hair and fur of domestic animals;
vital products of domestic insects (e.g.,
cockroach);
mycelial yeast-like fungi (molds);
tobacco smoke during active or passive
smoking;
various communal aerosols and synthetic
detergents.

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
Genetic abnormalities which lead to excessive
production of allergen-specific antibodies (Ig E) is
called atopy -
Trigger-factors, which provoke bronchospasm,
are: a simultaneous penetration of a large quantity of
allergen, viral respiratory infection, hyperventilation,
physical exertion, emotional stress, becoming too cold,
adverse weather conditions, administration of some
medicines
Risk factors: atopik dermatitis allergic rinitis food
allergy pneumonia smoke low birh weight
Pathophysiology
Asthma pathophysiology is quite
difficult and insufficiently studied.
Undoubtedly, in most cases the disease
is based on 1 type hypersensitivity
reaction. The genesis of any allergic
reaction may be divided into immune,
pathochemical and pathophysio-
logic phases.
Immune phase
After involving into the airways allergens
activate immunocompetent cells. As a result B-
lymphocytes produce antibodies of Ig E class. In
case of asthma T-lymphocytes are inhibited, so
the activation of B-lympocytes and Ig E
production are excessive, exceeding normal
needs.
B-cell
Allergens
T-cell
Allergen-specific
IgE
Further these antibodies bind to the surface of
mast cells, basophils and eosinophils of bronchial
mucous. When a new portion of allergen
involves the respiratory system, it interacts with
IgE-antibodies.

This is a first,
immune
phase of
allergic
reaction.
Pathochemical phase
As a result of antigen-antibody reaction the peculiar
explosion occurs. The membranes of mast cells,
basophils and eosinophils of bronchial mucous wreck with
output of biologically active substances (histamine,
serotonin, chemotaxis factors, heparin, proteases,
thromboxane, leukotrienes, prostaglandins),

which induce hyperergic
inflammation, mucous edema,
spasm of smooth myocytes,
glands hypersecretion, viscous
exudate formation in bronchial
lumen.
Airway fill
with
mucus
Muscles
contract
Airways swell
Pathologic anatomy
Macroscopic
changes:
viscous mucous/
mucopurulent phlegm
airway dyskinesia with
zones of spastic
contraction and
paralytic expansion of
bronchi
obstruction of airway
lumen

lung emphysema,
pneumosclerosis
RV and RA hypertrophy and
dilation
Asthma severity
classification
Clinical course,
severity

Daytime asthma
symptoms

Nighttime
awakenings

FEV1, PEF

Intermittent


< 1 /week

2 and <
/month

>80% predicted.
Daily variability <
20%

Mild
persistent

1 /week
but not daily

> 2 /month

>80% predicted.
Daily variability
20-30%

Moderate
persistent

Daily

> 1 /week

> 60 but < 80%
predicted.
Variability>30%.

Severe
persistent

Persistent,
which limit
normal activity

Daily

<60% predicted.
Variability > 30%.

Severe Persistent Asthma
Symptoms
Continual
Limited physical
activity
Frequent
exacerbations
Frequent
nighttime
symptoms
Lung Function
FEV
1
or PEF <
60% of predicted
PEF variability
>30%
Moderate Persistent Asthma
Symptoms
Daily symptoms
Daily use of
inhaled short-
acting
beta
2
agonist
Exacerbations
affect activity; >
2 X/wk; may last
days
Nighttime
symptoms >1
time/wk
Lung Function
FEV
1
or PEF
> 60% - < 80%
predicted
PEF variability
>30%
Mild Persistent Asthma
Symptoms
Symptoms > 2
X/wk but <1
X/day
Exacerbations
may affect activity
Nighttime
symptoms > 2
X/mo
Lung Function
FEV
1
or PEF >
80% predicted
PEF variability
20-30%
Clinical manifestations
Classic signs and symptoms of
asthma are:
attacks of expiratory dyspnea
shortness of breath
cough
chest tightness
wheezing (high-pitched whistling
sounds when breathing out)
sibilant rales
In typical cases in development of asthma
exacerbation there are 3 periods prodromal
period, the height period and the period of
reverse changes.
At the prodromal period:
vasomotoric nasal reaction with profuse watery
discharge,
sneezing, dryness in nasopharynx,
paroxysmal cough with viscous sputum,
emotional lability,
excessive sweating,
skin itch and other symptoms may occur.

At the peack of exacerbation there are:
expiratory dyspnea
forced position with supporting on arms
poorly productive cough
cyanotic skin and mucous tunics
hyperexpansion of thorax with use of all accessory
muscles during breathing
at lung percussion: tympanitis, shifted downward
lung borders
at auscultation: diminished breath sounds, sibilant
rales, prolonged breathing-out, tachycardia.
in severe exacerbations: the signs of right-sided
heart failure (swollen neck veins, hepatomegalia),
overload of right heart chambers on ECG.
At the period of the reverse changes,
which comes spontaneously or under
pharmacologic therapy,
dyspnea and breathlessness relieve or
disappear,
sputum becomes not so viscous,
cough turns to be productive,
patient breathes easier.
Asthma complications
The complications of
asthma exacerbations
are:
pneumothorax
lung atelectasis
pneumonia
acute or subacute cor
pulmonale
asthmatic status.
Persistent asthma causes:
fibrosing bronchitis
small bronchi
deformation and
obliteration
emphysema
pneumosclerosis,
chronic respiratory
failure
chronic cor pulmonale.
Asthma in childhood leads to growth inhibition
and thoracic deformation.

Investigations
Eosinophilia, moderate leukocytosis in
blood count as well as increased serum level of
Ig E can be found in patients with asthma,
especially at asthma exacerbations.
Inflammatory cells, Curschmann's
spirals (viscous mucus which copies small
bronchi) and Charcot-Leyden crystals
(crystallized enzymes of eosinophils and mast
cells) can be observed in sputum.

Lab Data
Chest X-ray reveals:
hyperlucency of lung
fields
low standing and
limited mobility of
diaphragm
expanded intercostal
spaces
horizontal rib position.
ECG
especially in case
of severe,
persistent
asthma, shows
hypertrophy of
right heart
chambers.
Right axis deviation,
Rs type complex in V1 lead,
low amplitude R in V5-V6 leads
Lung function assessment
The diagnosis and severity assessment of
asthma is based mainly on parameters of lung
function. The most important of them are:
forced expiratory volume in 1
second (FEV1) and peak
expiratory flow (PEF), which
are measured
during spirometry
at forced
breathing-out.

FEV1 and PEF
directly depend
on bronchial
lumen size and
elastic
properties of
surrounding
lung tissue.
Expiration
Inspiration
PEF
Volume
FEF
FEF
PIF
Flow
Increase in FEV1 and PEF after inhalation of
bronchodilators (b2-agonists) of 15% and more
is specific for asthma.
PEF also can be measured with the help of
individual devices peak flow meters
Diagnosis
Typical clinical
manifestations
and lung function
assessment are
sufficient for
diagnosis of
asthma.
Differential diagnosis
Asthma is to be differentiated with
-viral bronchiolitis
-aspiration
-vascular rings
-airway stenosis
-enlarged lymph nodes
-mediastinal mass
-cystic fibrosis
-foreign body
-vocal cord dysfunction
-cardiovascular disease
-
In contrast to bronchial, in
case of cardiac asthma
the signs of
severe heart
disease and
pulmonary
congestion
can be found.
Management
includes:
1. Avoiding the contact with allergen. If it is
impossible, the specific hyposensitization with
standard allergens should be performed. It is rather
effective in case of monoallergy, in intermittent and
mild persistent asthma, in remission phase.
2. Elimination of trigger factors (rational job
placement, changing the residence, psychological
and physical adaptation, careful drug using) is the
second condition for successful asthma treatment.
3. Optimally selected medical care is the base of
asthma management.
Monitor using clinician assessment/pt.
self-assessment
Spirometry tests
Initial assessment
Post tx after patients symptoms and PF
stabilize
Minimally Q 1-2 yrs
Written action plan based on:
Signs & symptoms &/or PEF
Patient education:
Recognition need for additional therapy
PF measurements changes
Changed from 2 X daily to morning
If morning <80% of personal best PEF,
more frequent monitoring may be desired
Discussion of inconsistencies in
measurement among PF meters added
Emphasis that all pts. regardless of
severity recognize early deterioration
Drug therapy
Antiinflammatory drugs
(basic)
Bronchodilators
2 drug categories are used:
Are divided into:
hormone-containing
(corticosteroids)
nonhormone-containing
(cromones, leukotriene
receptor antagonists)
3 groups:
anticholinergic drugs
b2-agonists
methylxanthines
Corticosteroids
The working
mechanism lays in:
cell membrane
stabilization
inhibition of
inflammatory mediators
restoring the sensivity
of b2-receptors.
Inhaled corticosteroids
(beclamethazone,
inhacort, budesonide,
flixotid, fluticazone,
asmacort, asthmanex) are
the most effective and
safe and considered to be
the first line drugs for
asthma treatment.
Systemic are used during
short courses, mainly in
case of severe persistent
asthma or asthmatic
status.
Cromones
(cromolyn sodium
intal, and nedocromil
tiled)

stabilize cell membranes,
used mainly in pediatric
practice (in childhood)
in case of intermittent
or mild persistent
asthma.
Leukotriene
receptor
antagonists
(montelukast, zafirlukast)

have the moderate
intiinflammatory activity
used in case of aspirin-
induced asthma and
asthma of physical
exertion.

Bronchodilators
b2-agonists
Anticholinergic
drugs
Smooth
muscle
relaxation
Stimulates
b2-adrenergic
receptors of bronchi
reduce tonus
of vagus
Methylxanthines
inhibit phosphodiesterase
Inhaled b2-agonists are the basic drug
group among bronchodilators.

Short-acting (duration of action 5-6 h) b2-
agonists - salbutamol, fenoterol - are used
for quick relief of asthma symptoms.
Long-acting (> 12 h) b2-agonists -
salmoterol, farmoterol - for prevention of
asthma symptoms occurring.
Anticholinergic drugs (ipratropium bromide,
atrovent, troventol) are used predominantly in
nighttime asthma and in elderly patients
because of the least cardiotoxic effect.

Methylxanthines in comparison with other
bronchodilators have the less bronchodilating
potential. There are long-acting (>12 h) -
(theopec, theolong, theodur, euphilong) as
well as short-acting (aminophylline,
theophylline) drugs in this group.
Combined inhaled drugs (corticosteroids with b2-
agonists) seretid, simbicort with use of delivery
devices (nebulasers, turbuhalers, spasers,
spinhalers, sinchroners) enhance the effectiveness of
asthma therapy.
Infants and Young Children
Diagnosis difficult
If suspected a diagnostic trial of inhaled
bronchodilators and anti-inflammatory
drugs may be helpful
Infants & young children (<5 yrs)
Step 1 - PRN bronchodilators
Step 2 symptomatic tx > 2x/wk start daily
anti-inflammatory therapy
Infants & young children
Trial of cromolyn or nedocromil (low dose
inhaled steroids are alternative)
Monitor response to anti-inflammatory tx
After control established, attempt step down therapy
Step 3 care
Higher dose steroids to establish control - step
down in 2-3 mos. ~ add nedocromil or
theophylline instead of increasing steroid
Emergency Department
Treatment
Start treatment when asthma
exacerbation recognized
While tx is being given:
Take a more detailed history
Complete physical examination
Perform laboratory studies
PEF on presentation, after initial tx. and at
frequent intervals)
Perform laboratory studies
FEV
1
or PEF <50% pred. then assess
oxygenation by pulse oximetry
Lab studies will vary with situation (CBC,
electrolytes, serum theophylline level.
CXR, ECG). These lab studies are NOT
routinely recommended
Treatment:
O
2
(Sa O
2
90-95),
inhaled short-acting bronchodilator for all
pts. (3 tx Q 20 min, continuous therapy
an option)
Consider anti-cholinergics
oral systemic corticosteroids
(unresponsive to initial beta
2
agonist
therapy, moderate-to-severe asthma,
people who are on steroids)
systemic steroids administered when
admitted
methylxanthines are not recommended
Treatment:
Aggressive hydration NOT
recommended for older children and
adults (may be necessary with infants
and sm. children)
Antibiotics NOT recommended unless
infection present (fever, purulent
sputum)
Mucolytics NOT recommended
Sedation NOT recommended
In recommendations of Global Initiative for Asthma
(GINA) asthma is classified on the base of control
assessment and is divided into well-controlled,
partially controlled and uncontrolled.
Asthma control is considered as:
daytime symptoms 2 /week;
ability to engage in normal daily activity;
the absence of nighttime awakenings as a result of
asthma symptoms;
need in bronchodilators administration 2 /week;
the absence of asthma exacerbations;
normal or near normal lung function parameters.
Hospitalization
Decision to hospitalize depends upon:
duration
severity (symptoms & airflow obstruction)
course & severity of previous exacerbations
medication use at time of exacerbation
access (medical care & meds)
home conditions
psychiatric illness
Prognosis
In case of early detection and
adequate treatment the prognosis
for the disease is favourable.
It becomes serious in severe
persistent and poorly controlled
(insensitive for corticosteroids)
asthma.
The examination of
working capacity
The patients with unfavorable for
the disease conditions of work need
the job replacement.
Physical labours with severe
asthma are disable to work.


Prophylaxis
Preservation of the environment,
healthy life-style (smoking
cessation, physical training) are the
basis of primary asthma prophylaxis.
These measures in combination with
adequate drug therapy are effective
for secondary prophylaxis.