Bronchial Asthma &

Approach to SOB
Badr Alsayed, MBBS MPH
 Dyspnea (SOB)
• A term used to characterize a subjective
experience of breathing discomfort that is
comprised of qualitatively distinct sensations
that vary in intensity. The experience derives
from interactions among multiple
physiological, psychological, social, and
environmental factors, and it may induce
secondary physiological and behavioral
responses
Mechanisms of Dyspnea
Mechanisms of Dyspnea
DYSPNEA IN HPI
“QUESTIONS”
DIFFERENTIAL DIAGNOSIS OF
DYSPNEA
 Non-cardiorespiratory
• Anemia
• Metabolic acidosis
• Obesity
• Psychogenic
• Neurogenic
 Cardiac
• LVF
• Mitral valve disease
• Cardiomyopathy
• Constrictive pericarditis
• Pericardial effusion
 Respiratory
Airways
– Laryngeal tumor – Lung cancer
– Foreign body – Bronchiolitis
– Asthma – Cystic fibrosis
– COPD
– Bronchiectasis
 Respiratory
Parenchyma
• Pulmonary fibrosis • Tumor (Metastatic,
• Alveolitis lymphangitis)
• Sarcoidosis • Diffuse infections (PCP)
• TB
• Pneumonia
 Respiratory
Pulmonary circulation
• PE
• Pulmonary vasculitis
• Primary pulmonary arterial hypertension
 Respiratory
others
• Pleural:
– Pneumothorax
– Effusion
– Fibrosis
• Chest wall:
– Kyphoscoliosis
– Ankylosing spondylitis
• Neuromuscular:
– MG
– Neuropathies
– GBS
BRONCHIAL ASTHMA
 Definition
• Chronic reversible inflammatory airway
disease characterized by airway remodeling
and hyperresponsiveness lead to recurrent
attacks of breathlessness and wheezing
• Greek verb (aazein), that means “panting” or
“gasping”
 Bronchial asthma
• “A chronic inflammatory disorder of the airways
in which many cells and cellular elements play a
role. The chronic inflammation is associated with
airway responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest
tightness, and coughing, particularly at night or in
the early morning. These episodes are usually
associated with widespread, but variable, airflow
obstruction within the lung that is often reversible
either spontaneously or with treatment”
GINA 2015
 Airway Remodeling
• Structural alteration of the airway with
characteristic changes in the nature, content,
and distribution of airway elements
 Challenges
• No feature is unique to asthma
• No feature is universal in ALL asthmatic
• No gold standard diagnostic test for asthma!

GINA 2015
 Bronchial
Asthma

Bronchial
Asthma
Pulmonary Pneumonitis
Fibrosis

Cardiac
COPD
OSA

BE

Unfortunately, many patients present with SOB labelled as BA

without any further work-up!!
 Prevalence
• It decreases with increasing age
• There are important racial and gender
differences in the prevalence and morbidity of
asthma
 Prevalence
• One of the most common chronic diseases
• Affects 235 million people by April 2017
• 383 000 deaths due to asthma in 2015
• ~10–12% of adults
• ~15% of children
• Less in developing countries
 Epidemiology
• In children: 8-25% (Overall Prevalence)
• In adults: prevalence of asthma is UNKNOWN
• Affecting almost 2 millions Saudi
• Increasing prevalence

Al Frayh AR et al, Ann Allergy Asthma Immunol 2001

Rabe KF et al, J Allergy Clin Immunol 2004
Abudahish A et al, Saudi Med J 2006
Al-Ghamdi BR et al, East Mediterr Health J 2008
 National Data
• Despite all advances in BA management, only
39% of primary care physicians met the
standards of the national guidelines

Al-Kabbaa AF et al, J Family Community Med 2002

Al-Jahdali HH et al, Saudi Med J 2008

Bronchial Asthma Control

31

64

Controlled Partial Contrlled

Challenges to Achieve Control in Saudi
Arabia
• Socioeconomic status
• Number of siblings!
• Knowledge of caregivers
• Smoking
• Animal exposure
• Social stigma!!
• Myth of “Inhalers Addiction”
SINA 2016
 ISAAC
• The prevalence of asthma varied widely
between countries, ranging from 2.1% to 4.4%
in Albania, China, Greece, and Indonesia to
29.1% to 32.2% in Australia, New Zealand, and
the United Kingdom.

The International Study of Asthma and Allergies in Childhood (ISAAC)

 A complex inflammatory disease
• Neutrophils
• Basophils
• Eosinophils
• Mast cells
• Macrophages
• structural cells
 Mediators
• Cytokines
• Chemokines
• Histamine
• Leukotrienes
• Thromboxane
• Reactive oxygen species
 Pathophysiology
• Multifactorial
• Genetic and Environmental
• IgE production (Mast cell)
• Inflammatory mediators
• Early reaction
• Late reaction
 Pathophysiology
• The airway mucosa is infiltrated with activated
eosinophils and T lymphocytes
• Thickening of the basement membrane due to
sub-epithelial collagen deposition
• The epithelium is often shed or friable, increased
numbers of epithelial cells in the lumen

(The degree of inflammation is poorly related to

disease severity)
 Pathophysiology
• Airway inflammation
• Angiogenesis
• Airway hyper-responsiveness
• Airflow limitation: mucosal and smooth
muscle hypertrophy, fibrosis
• Airway remodeling
Pathophysiology
IS BRONCHIAL ASTHMA ONE DISEASE
OR SPECTRUM OF PHENOTYPES?!
phenotypes
 Triggers
• Allergens
• Upper respiratory tract viral infections
• Exercise
• Hyperventilation
• Cold air
• Sulfur dioxide
 Risk Factors
• “Hygiene Theory”
• Infections
• Obesity
• Exposure to allergens such as house dust
mites and mold
• Tobacco smoke
Hygiene Hypothesis
 Infections
• Respiratory syncytial virus (RSV):
– the most common cause of bronchiolitis and
is associated with an increased risk of
developing subsequent wheezing or asthma
• Chlamydophila pneumoniae
• Mycoplasma pneumoniae
 Obesity
• Adipokines such as leptin, adiponectin,
plasminogen activator inhibitor-1 (PAI-1),
and resistin
• Low levels of adiponectin, a potent anti-
inflammatory hormone secreted by
adipose tissue
• Increased leptin levels, which may be
associated with increased inflammation in
the airways of obese asthmatics
 How Much Weight Obese Asthmatic
Must Lose to See an Effect?
• Behavioral Weight Loss and Physical Activity
Intervention in Obese Adults with Asthma. A
Randomized Trial
• 330 obese uncontrolled asthmatic
• 12-month intervention
• Weight loss of 10% or more is required to
produce clinically meaningful improvement in
asthma

Jun Ma1,2, Peg Strub et al, Annals of the American Thoracic Society, 2015
 Genetics
• Polygenic inheritance
• Poorly defined
• Atopic: runs in families
• Non-atopic: intrinsic or late asthma
• Severity of asthma: genetically determined
• Response to therapy: genetically
determined
 Tobacco Use and Environmental
Exposure
• An increased risk of abnormal lung
function
• Wheezing illnesses in childhood, an effect
that persists into adulthood
• Population-based studies demonstrate
that environmental tobacco exposure in
childhood also results in an increased risk
of asthma
 Coexisting Disorders and Conditions
• GERD
• Sleep disorders
• Beta-blockers induced
• NSAIDs (including ASA) allergies
• Allergic Rhinitis
 Clinical Features
• Wheezing
• Dyspnea
• Coughing
• Difficulty in filling their lungs with air
• May worse at night
• Increased mucus production
• The pattern of symptoms
 Investigations
• Spirometry
• Serial peak expiratory flow rate (PEFR)
• Bronchoprovocation testing is paned in SA
• Trial of inhaled steroids or bronchodilator
Peak Flow Meter
Morning dipping
Pathophysiology
Flow-Volume Loop in early and late
asthma
Skin Testing
 Clinical Assessment
• Assess asthma control
• Document current treatment (side effects,
adherence, and inhaler technique)
• Written asthma action plan
• Assess comorbidities such as rhinosinusitis,
GERD, obesity, obstructive sleep apnea, and
anxiety (You may refer)
• Close monitoring for patients with severe
asthma (You may refer)
 Asthma Control Test
• Controlled: an ACT score of ≥20
• Partially controlled: an ACT score of 16–19
• Uncontrolled: an ACT score of <16.
 Controlled
All of the following:
1) No daytime symptoms or <1x/wk
2) Limitations of activities: none
3) Nocturnal awakening: none
4) Need for reliever (rescue) medication: <2x/wk
5) FEV1 or peak flow: normal
6) Exacerbations: none
 Partly controlled
Any measure present, in any week:
1) Symptoms >2x/wk
2) Limitations of activities: any
3) Nocturnal awakening: any
4) Need for reliever (rescue) medication: >2x /wk
5) FEV1 or peak flow: <80% predicted or of personal
best (if known)
6) Exacerbations: one or more a year
 Uncontrolled
• Three or more features of partly controlled
asthma
• Present in any week
• An exacerbation in any 1 week makes a poorly
controlled asthma week
 Severity Classification
• Mild asthma: Controlled asthma at step 1 or 2 (as
needed
reliever treatment, monotherapy of low-dose ICS, or
leukotriene receptor antagonist [LTRA])
• Moderate asthma: Controlled asthma at step 3 (on
combination of ICS/long-acting beta 2 agonist [LABA] or
other alternative options at steps 3)
• Severe asthma: Asthma that requires treatment step 4
or 5
(on combination of high-dose ICS/LABA with or without
add-on treatment).
 Serious Complications
• Pneumothorax
• Coma
• Respiratory failure/arrest
 Classification
• Mild-intermittent
• Mild-persistent
• Moderate-persistent
• Severe
• Very sever (life-threatening)
Clinical classification of severity[

Use of short-
acting beta2-
Severity in
Symptom Nighttime %FEV1 of agonist for
patients ≥ 12 FEV1Variability
frequency symptoms predicted symptom control
years of age [9]
(not for
prevention of EIB)

Intermittent ≤2 per week ≤2 per month ≥80% <20% ≤2 days per week

>2 per week >2 days/week

Mild persistent 3-4 per month ≥80% 20–30%
but not daily but not daily

Moderate >1 per week but

Daily 60–80% >30% Daily
persistent not nightly

Throughout the Frequent (often Several times per

Severe persistent <60% >30%
day 7x/week) day
 Aims of Asthma Therapy
• Minimal (ideally no) chronic symptoms, including
nocturnal
• 2- Minimal (infrequent) exacerbations No
emergency visits
• 3- Minimal (ideally no) use of B-agonist
• 4- No limitations on activities, including exercise
• 5- PEF circadian variation <20%, (Near) normal
PEF
• 6- Minimal (or no) adverse effects from medicine
 Treatment
• β2-Agonists
• Inhaled Corticosteroids
• Leukotriene Modifiers
• Phosphodiesterase 4 Inhibitors (Theophylline)
• Anti-Immunoglobulin E Treatment
(omalizumab, a monoclonal antibody to IgE)
• Nonpharmacologic Treatment (Bronchial
thermoplasty)
 Additional essential Management
Strategies
• Control of Triggers
• Medication Adjustment Based on Asthma
Control
 Clinician-Patient Partnership
• For chronic asthma, treatment should balance
the best symptom control with the lowest
possible dosage of medication
 Clinician-Patient Partnership
• Crucial components of self-management plans
include education, self-monitoring with
symptoms and/or peak flow, regular review,
and patient directed self-management using a
written action plan
Nonpharmacological Management
• Physician-patient partnership
• Asthma Education
• Written action plan
• Identify and reduce exposure to risk factors

SINA 2016
Nonpharmacological Management
• Indoor allergens and air pollutants
• Outdoor allergens
• Occupational exposures
• Food and drugs
• Influenza vaccination

SINA 2016
 Take Home Message
• Educate your patients: Triggers
• Importance of maintenance therapy
• No “addiction” to inhalers
• Do not underestimate asthma attack
• If not certain about the diagnosis, “?”
• Use referral system wisely
• Encourage family support
THANKS