Asthma Bronchiale

Handoko MD

Department of Internal Medicine

Pulmonology and Respiratory Medicine Division
dr. Ramelan Navy Hospital Surabaya
 World asthma prevalence

Estimated 300 million affected individuals worldwide

The global prevalence of asthma in children and adults
ranges from 1-18% of the population
INDONESIA ?in different countries
- UPFThe percentage
Paru RSUD Dr. of children
Sutomo reported
(1993) :
to Prevalensi
have had asthma
di Jawaincreased significantly
Timur 7,7% (13-70 th)
The increases
- SKRT (1995) prevalence
: Prevalensi in
asma 1,3%
Africa, Latin America and Asia
- Yunus, F (2001)
indicate that :global
Prevalensi
burdendi of
Jakarta
asthma8,9%
is continuing to rise
Annual worldwide deaths from asthma
have been estimated at 250,000
Definition (GINA, 2012)

Chronic inflammatory disorder of the airways in which many cells

and cellular elements play a role.

The chronic inflammation causes an

associated increase in airway hyperresponsiveness that
leads to recurrent episodes of wheezing, breathlessness, chest
thightness, and coughing, particularly at night or in the early
morning.

These episodes are usually associated with widespread but

variable airflow obstruction that is often reversible either
spontaneously or with treatment.
Asthma, the definition (GINA, 2013)
Chronic inflammatory disorder of the airways in which
many cells and cellular elements play a role.
The chronic inflammation causes an associated increase in
airway hyperresponsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest thightness,
and coughing, particularly at night or in the early morning.
These episodes are usually associated with widespread
but variable airflow obstruction that is often reversible
either spontaneously or with treatment.
 Factors the development & expression of asthma (GINA, 2013)
Genetic Genes pre-disposing to atopy
Genes pre-disposing to airway
Host factors hyperresponsiveness
Obesity
Sex
Indoor:
Domestic mites, furred animals (dog,
Allergens cats, mice), cockroach allergen, fungi,
molds, yeasts
Outdoor:
Environmental Pollens, fungi, molds, yeasts
factors
Infections (predominantly viral)
Occupational sensitizers
Tobacco smoke (passive & active smoking)
Outdoor/indoor air pollution
Diet
House dust mite and pollen (Allergy, 2002)
Inflammatory cells
Mediators
Mast cells
Eosinophils Histamines
Th2 cells Leukotrienes
Prostanoids Effects
Basophyls
Neutrophils PAF Bronchospasm
Platelets Kinins Plasma exudation
Adenosine Mucus secretion
Structural cells
Endothelins AHR
Epithelial cells Nitric oxide Structural changes
Smooth muscle cells Cytokines
Endothelial cells Chemokines
Fibroblasts Growth factors
Nerves

Many cells and mediators are involved in asthma and

have several effects in the airways
(Barnes, 2004)
The Pathophysiology of asthma (Barnes, 2004)
 The Pathophysiology of asthma (Barnes, 2004)

The participation of several interacting inflammatory cells

results in acute and chronic inflammatory effects in the airway
 Allergens Inflammation in the airway of
Sensitizer asthmatic patients leads to
Viruses airway hyperresponsiveness and
Air pollutants symptoms
(Barnes, 2004)

INFLAMMATION AIRWAY
Chronic eosinophilic
bronchitis HYPERRESPONSIVENESS

TRIGGERS
SYMPTOMS Allergens
Cough Exercise
Wheeze Cold air
Chest tightness SO2
Dyspnea
Particulates
 Asthma Management and
Prevention Program

1. Develop Patient-Doctor Partnership

2. Identify and Reduce Exposure to Risk Factors
3. Assess, Treat, and Monitor Asthma
4. Manage Asthma Exacerbations
5. Special Considerations
 Challenges in Asthma Management

• Over dependence on “rescue medication”

• Sub-optimal control1
• Low compliance on “maintenance therapy”
• Lack of clinical evidence on the benefit of
ICS dose addition when asthma progress
• The complexity of current therapy
• Lack of education and patients understanding
on asthma therapy

FitzGerald JM, et al. Can Resp J 2006; 13:253-9

Harrison TW, et al. Lancet 2004 ;363:271–5
 SEVERITY OF ASTHMA EXACERBATIONS (GINA 2013)

Mild Moderate Severe Resp. arrest

imminent
Breathless Walking Talking At rest
Can lie down Prefers sitting Hunched forward
Talks in Sentence Phrases Words
Alertness May be agitated Usually agitated Usually agitated Drowsy or confused
Respiratory Rate Increased Increased Often >30/min
Accessory muscle & Usually not Usually Usually Paradoxical thoraco-
suprasternal retractions abdominal movement
Wheeze Moderate, often Loud Usually loud Absence of wheeze
only end exp
Pulse/min <100 100-120 >120 Bradycardia
Pulsus paradoxus Absent May be present Often present
<10 mmHg 10-25 mmHg >25 mmHg
PEF after initial >80% ±60-80% <60% predicted or
bronchodilator (% predicted personal best
or personal best) (<100L/min, or
response lasts <2h)
PaO2 and or Normal >60 mmHg <60 mmHg
PaCO2 <45 mmHg <45 mmHg >45 mmHg
SaO2 % >95% 91-95% <90%
 Levels of asthma control (GINA 2013)

Controlled Partly Controlled

Characteristic (All of the (Any measure Un
following) present in controlled
any week)
Daytime symptoms None > 2x/week
(≤ 2x/week)
Limitations of None Any ≥ 3
activities features
of partly
Nocturnal symptoms/ None Any controlled
awakening asthma
Need for reliever/ None > 2/week
rescue treatment (≤ 2x/week)
Lung function Normal < 80% predicted
(PEF or FEV1) or personal best

Quality of life
 Jackie Joyner-Kersee
Jakie Joyner-Kersee was
born with asthma and won
five medals during her life
as an olympic competitor.
She won two gold medals in
the 1988 and 1992 for the
heptathlon, one gold for the
long jump in 1988, one silver
for heptathlon in 1984, and
two bronze medals for the
long jump in 1992 and 1996.
David Beckham
Jackie Joyner-Kersee Amy Van Dyken Paula Radcliffe

Dennis Rodman Justin Henin Pete Vanderkaay

 Amy Van Dyken
is an American swimmer who
has 6 career Olympic gold medals.
Four of these gold medals came in
the 1996 Summer Olympics,
making her the first American
woman to accomplish such a feat.
She won gold in the 50 meter
free, 100 meter butterfly, 4 x
100 meter freestyle relay, and
the 4 x 100 meter medley relay.
Van Dyken is an asthmatic
who suffered from severe asthma
throughout her childhood and
into adulthood.
She began swimming
on the advice of a doctor
as a way to strengthen her lungs
to cope with her condition and
prevent future asthma attacks.
 Overall Asthma Control

achieving

Current clinical Future risk

control
Instability/worsening
Symptoms Exacerbations
Reliever use Lung function loss
Limitation of Medication
activities adverse effects
Lung function
The goals for successful management of asthma are to:

1. Achieve and maintain control of symptoms

2. Maintain normal activity levels, including exercise
3. Maintain pulmonary function as close to normal
as possible
4. Prevent asthma exacerbations
5. Avoid adverse effects from asthma medications
6. Prevent asthma mortality
Level of control Treatment of action

REDUCE
Controlled Maintain and find
lowest controlling step
Partly controlled Consider stepping up
to gain control

INCREASE
Uncontrolled Step up until controlled
Exacerbation Treat as exacerbation

Reduce TREATMENT STEPS Increase

STEP 1 STEP 2 STEP 3 STEP 4 STEP 5

 Reduce Increase

Step 1 Step 2 Step 3 Step 4 Step 5

Asthma education
Environment control
As needed As needed SABA
SABA
Select one Select one To Step 3 Tx To Step 4 Tx
Select one/more Add either
Low-dose Low-dose ICS + Medium/high- Oral
ICS LABA dose ICS + LABA glucocorticoid
(lowest dose)
Controller
options Medium/high-dose Leukotriene
Leuko ICS modifier Anti-IgE
triene Low dose ICS + Theophylline SR treatment
modifier leukotriene
modifier
Low-dose ICS +
Theophylline SR
 Adenylyl cyclase Phosphodiesterase
2 agonist Xanthine
ATP  c AMP  5 AMP

GTP  c GMP  5 GMP

Acetylcholine
Guanylyl Anticholinergic
cyclase
SPIROMETER
Metered Dose Inhaler
(MDI)
JET NEBULIZER
ULTRASONIC
NEBULIZER
Management of asthma exacerbations in acute care setting (GINA, 2013)

Initial assessment : History, PE, PEF or FEV1, SaO2, ABG

Initial Tx: O2 to achieve SaO2  90% (95% in children)

Inhaled rapid-acting 2 agonist continuously for 1 hour
Systemic steroids if no immediate response or if pt recently took
oral glucocorticoid, or if episode is severe
Sedation is contraindicated in the treatment of attacks

Reassess after 1 hour

PE, PEF, SaO2, and other tests as needed

Criteria for moderate episode Criteria for severe episode

PEF 60-80% predicted/personal best History of risk factors for NFA.
Moderate symptoms, accessory Severe symptoms at rest, chest
muscle use retraction
Treatment PEF < 60% predicted/personal best
Oxygen No improvement after initial treatment
Inhaled 2 agonist & anti-Ch q 60 min Treatment
Oral glucocorticoids Oxygen
Continue treatment 1-3 hours, Inhaled 2 agonist & anti-Cholinergic
provided there is improvement Systemic glucocorticoids
Magnesium iv
 Re-assess after 1-2 hour

Good response Incomplete response Poor response within

Response sustained within 1-2 hours 1-2 h
60 min after last Risk factors for NFA Risk factors for NFA
treatment, normal PE, PE: Mild-moderate PE: symptoms severe,
no distress signs drowsiness, confusion
PEF > 70% PEF < 60% PEF < 30%
SaO2 > 90% (95%) SaO2 not improving PaCO2 > 45 mmHg
Admit to acute care PaO2 < 60 mmHg
Improved: criteria for setting Admit to ICU
discharge home Oxygen Oxygen
PEF > 60% predicted/ Inhaled 2 agonist ± Inhaled 2 agonist +
personal best + anticholinergic anti-Cholinergic
sustained on oral/ Systemic Glucocorticoids iv
inhaled medications glucocorticoid Consider iv 2 agonist
Continue tx with Magnesium iv Consider iv theophylline
inhaled 2 agonist Monitor PEF, SaO2, PR Possible intubation & MV
Consider, in most cases,
oral glucocorticoids, add
a combination inhaler
Re-assess at intervals Poor or incomplete
Patient education :
response and
Take medcn correctly,
no improvement in 6-12h:
Review action plan, close
Improved admit to ICU
medical follow up
Famous people with asthma
Famous people with asthma
 Highest evidence level for
Symbicort SMART in GINA guidelines
“If a combination inhaler containing
formoterol and budesonide is selected,
it may be used for both rescue and
maintenance. This approach has been shown
to result in reductions in exacerbations and
improvements in asthma control in adults
and adolescents at relatively low dose
treatment”. (Evidence A)
Global Initiative for Asthma 2010, page 64.
www.ginasthma.com
Extrinsic asthma
 Allergic/atopic asthma
 Triggered by allergies
 The attack is clearly linked to the body's
response to something (allergens) inhaled or,
occasionally, ingested
Asthma develops in childhood is likely to be extrinsic
National Institute of Allergy & Infectious Diseases :
> 90% of asthmatic children < 16 yo and
~ 70% of asthmatic ages 16-30 yo have allergy

Symptoms of extrinsic asthma often vary seasonally and

occur intermittently
In more than half the cases of extrinsic asthma, there is
usually a personal or family history of other allergies,
such as hay fever and skin conditions
Intrinsic asthma
 Nonallergic asthma, not allergy related
 Develops in people > 30 yo
 It is related to triggers such as
respiratory infections, exercise, stress,
inhalation of chemical irritants (cleaning fluids
or fresh paint) and air pollution
 It is believe that extrinsic asthma is caused by
an overactive immune system
Allergens & Triggers
Things that set off this immune system overreaction
 Dust
 Mold
 Animal hair and saliva
 Pollen
 Metabisulfite
a preservative found in many food & drinks