BRONCHIAL ASTHMA John Bendrix T.

Tolentino, MD
1st year Pediatric Resident
BRONCHIAL ASTHMA
 A heterogenous disease, usually
characterized by airway inflammation
 Defined by history of respiratory
symptoms such as wheeze, shortness of
breath, chest tightness and cough that
varies over time and in intensity,
together with variable expiratory
airflow limitation

Source: Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention 2020
BRONCHIAL ASTHMA
 chronic inflammation heightens the
twitchiness of the airways—airways
hyperresponsiveness—to common
provocative exposures (direct or
indirect stimulus)

Source: Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention 2020
BRONCHIAL ASTHMA
The hallmarks of the disease are:
increased airway responsiveness to
a variety of stimuli
resulting in episodic
bronchoconstriction
inflammation of the bronchial
walls and
increased mucus secretion
BRONCHIAL ASTHMA:
ETIOLOGY AND RISK
FACTORS
 RISK FACTORS THAT LEAD TO
ASTHMA DEVELOPMENT
HOST FACTORS ENVIRONMENTAL FACTORS

 Genetic Predisposition  Indoor Allergens

 Atopy  Outdoor Allergens

 Tobacco Smoke
 Airway Hyperresponsiveness
 Air Pollution
 Respiratory Infections
 Parasitic Infections
 Socioeconomic factors
 Family Size
 Obesity
Source: Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention 2020
BRONCHIAL ASTHMA:
ETIOLOGY AND RISK FACTORS
 combination of environmental exposures and
inherent biologic and genetic susceptibilities has
been implicated
 immune responses to common airways exposures
can stimulate prolonged, pathogenic
inflammation and aberrant repair of injured
airways tissues.

 Lung dysfunction (AHR, reduced airflow) and

airway remodeling develop.

Source: Nelson’s Textbook of Pediatrics 21st Edition

BRONCHIAL ASTHMA
Prolonged Pathogenic inflammation and
aberrant repair of injuries

Lung Dysfunction, Airway

Hyperresponsiveness and reduced air
flow

In a growing lung, it adversely affect

airway growth and differentiation

Altered airways at mature ages

Ongoing exposure worsens it
BRONCHIAL ASTHMA:
ETIOLOGY AND RISK FACTORS
ENVIRONMENT
1. VIRUSES
 Injurious viral infections causing pneumonia & bronchiolitis are risk factors for persistent asthma
in childhood
BRONCHIAL ASTHMA:
ETIOLOGY AND RISK FACTORS
ENVIRONMENT
2. Aeroallergens
 Indoor and home allergens – Pollen,
mites, dust etc.
 Environmental tobacco smoke and
air pollutants (ozone, sulfur dioxide)
 Cold dry air & strong odors can
trigger bronchoconstriction when
airways are irritated
 Eliminating of offending allergen
can lead to resolution of symptoms of
asthma.
BRONCHIAL ASTHMA:
ETIOLOGY AND RISK FACTORS
GENETICS
 Asthma is a complex genetic trait in which multiple susceptibility genes interact
with environmental factors to initiate the pathologic reaction
 considerable variability in the expression of these genes and in the combinations of
polymorphisms
 Some genes may influence the development of asthma, while others modify asthma
severity or the patient’s response to therapy.
 chromosome 5q: near the gene cluster encoding the cytokines IL-3, IL-4, IL-5, IL-
9, and IL-13 and the IL-4 receptor. The receptor for LPS (CD14), and the gene for
β2-adrenergic receptor also map here.
 IL-13 gene: Polymorphisms in the IL-13 gene have the strongest and most
consistent associations with asthma or allergic disease.
 FACTORS THAT EXACERBATE
ASTHMA
✔Allergens
✔Air Pollutants
✔Respiratory Infections
✔Exercise and Hyperventillation
✔Weather Changes
✔Sulfur Dioxide
✔Food, Additives, Drugs

Source: Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention 2020
PATHOPHYSIOLOGY OF
ASTHMA
PATHOLOGICAL CLASSIFICATION OF ASTHMA
1. ATOPIC ASTHMA
2. NON-ATOPIC ASTHMA
3. DRUG-INDUCED ASTHMA
4. OCCUPATIONAL ASTHMA
PATHOPHYSIOLOGY:
OCCUPATIONAL ASTHMA
 Stimulated by fumes (epoxy resins, plastics), organic and chemical dusts
(wood, cotton, platinum), gases (toluene), and other chemicals
(formaldehyde, penicillin products)

 Minute quantities of chemicals are required to induce the attack  usually

occurs after repeated exposure

 Underlying mechanisms vary according to stimulus & include type I

Hypersensitivity reaction
PATHOPHYSIOLOGY: DRUG-
INDUCED ASTHMA
 Aspirin-sensitive asthma, individuals with recurrent rhinitis and nasal polyps
 exquisitely sensitive to small doses of Aspirin as well as other NSAIDs, and they
experience not only asthmatic attacks but also urticaria

 Mechanism: inhibiting the COX pathway of arachidonic acid metabolism without

affecting the lipoxygenase route, thus tipping the balance toward elaboration of the
bronchoconstrictor leukotrienes
PATHOPHYSIOLOGY: ATOPIC
ASTHMA
3. ATOPIC ASTHMA (EXTRINSIC ASTHMA)
 Most common
 Major etiologic factors in atopic asthma
• Genetic predisposition to type I hypersensitivity “atopy”
• Exposure to environmental triggers

 Inheritance of susceptibility genes makes individuals prone to develop

strong TH2 reactions against environmental antigens(allergens)
PATHOPHYSIOLOGY: ATOPIC
ASTHMA
ATOPIC ASTHMA (EXTRINSIC ASTHMA)
Changes in airway in asthma
 Increase in the no. of mucus-secreting goblet cells
 Hypertrophy of submucosal glands
 Basement membrane underlying the mucosal epithelium is thickened
 Hypertrophy and hyperplasia of smooth muscle cells.
PATHOPHYSIOLOGY: ATOPIC
ASTHMA
4. NON-ATOPIC ASTHMA (INTRINSIC ASTHMA)
 Less common
– No evidence of allergen sensitization
– Skin test results are usually negative
IS IT ASTHMA?
o Recurrent episodes of wheezing
o Troublesome cough at night
o Cough and Wheeze after exercise
o Cough, wheeze or chest tightness after exposure to airborne allergens or pollutants
o Colds take more than 10 days to clear

Source: Global Initiative for Asthma: Global Strategy for Asthma Management and Prevention 2020
 ASTHMA DIAGNOSIS
 History and patterns of symptoms
 Physical examination
 Measurements of lung function
 Measurements of allergic status to identify risk factors
BRONCHIAL ASTHMA: CLINICAL
DIAGNOSIS
Most common chronic symptoms:
Intermittent dry coughing
Expiratory wheezing

Older children: shortness of breath &

chest tightness
Younger children: intermittent, non-
focal chest pain

Source: Nelson’s Textbook of Pediatrics 21st Edition

 BRONCHIAL ASTHMA: CLINICAL
DIAGNOSIS
symptoms worse at night, especially during
prolonged exacerbations
Daytime symptoms linked with physical activities
or play
self-imposed limitation of physical activities
general fatigue (possibly due to sleep disturbance)
difficulty keeping up with peers in physical activities

Source: Nelson’s Textbook of Pediatrics 21st Edition

BRONCHIAL ASTHMA:
LABORATORY FINDINGS
PULMONARY FUNCTION TEST
• To confirm the diagnosis
• To determine disease severity
• Forced expiratory airflow measures are helpful in diagnosing and
monitoring asthma and in assessing efficacy of therapy
– SPIROMETRY
– PEFR

Source: Nelson’s Textbook of Pediatrics 21st Edition

1. Spirometry

2. Peak Expiratory Flow

(PEF) Measurement

3. Bronchodilator
response
SPIROMETRY
 AIRFLOW LIMITATION
 BRONCHODILATOR RESPONSE
 EXERCISE CHALLENGE
SPIROMETRY
 Valid spirometric measures depend on a patient's ability to properly perform a full,
forceful, and prolonged expiratory maneuver, usually feasible in children > 6 yr of
age
 If the FEV1 (forced expiratory volume in 1 sec) is within 5% on 3 attempts, then
the highest FEV1 effort of the 3 is used
 In asthma, airways blockage results in reduced airflow with forced exhalation and
smaller partial-expiratory lung volumes
 Typical Spirometric (FEV11)
Tracings
Volume
Volume

FEV
FEV11

Normal Subject

Asthmatic (After Bronchodilator)

Asthmatic (Before Bronchodilator)

1 2 3 4 5
Time (sec)

Note: Each FEV1 curve represents the highest of three repeat measurements
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
1. TRANSIENT EARLY WHEEZING
 Common in early preschool years
 Recurrent cough/wheeze, primarily triggered by common respiratory viral infections
 Tends to resolve during the preschool years, without increased risk of asthma in the
later life
 Reduced airflow at birth , S/O relatively narrow
airways, improves by school age.
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
2. PERSISTENT ATOPY ASSOCIATED ASTHMA
 Begins in early preschool years
 Associated with atopy in early preschool years
 Clinical: Atopic dermatitis in infancy, allergic rhinitis, food allergy
 Biologic: Early inhalant allergen sensitization, Increased IgE, increased blood eosinophils

 Highest risk for persistence into later childhood and adulthood

 Lung function abnormalities: Those with onset < 3 yr acquire reduced airflow by
school age
Those with later onset of symptoms, or with later onset of allergen sensitization, are less
likely to experience airflow limitation in childhood
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
3. NON-ATOPIC WHEEZING
 Wheezing/coughing beginning in early life, often with respiratory syncytial virus
infection; resolves in later childhood without increased risk of persistent asthma
 Associated with bronchial hyperresponsiveness
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
4. ASTHMA WITH DECLINING FUNCTION
 Children with asthma with progressive increase in airflow limitation
 Associated with hyperinflation in childhood, male gender
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
5. LATE-ONSET ASTHMA IN FEMALES, ASSOCIATED WITH OBESITY AND
EARLY-ONSET PUBERTY
 Onset between 8 and 13 yr of age
 Associated with obesity and early-onset puberty; specific for females
TYPES OF ASTHMA: CLINICAL
CLASSIFICATION
5. OCCUPATIONAL-TYPE ASTHMA IN CHILDREN
 Children with asthma associated with occupational-type exposures known to trigger
asthma in adults in occupational settings
 Example: endotoxin exposure in children raised on farms
ASTHMA SEVERITY
LEVELS OF ASTHMA
CONTROL
CHARACTERISTICS CONTROLLED PARTLY UNCONTROLLED
(All of the ff) CONTROLLED (3 or more features of
(any measure present in partly controlled in any
a week) week)
DAYTIME None (<2x/week) > 2x/ week > 2x/ week or
SYMPTOMS throughout the day
LIMITATION OF None (fully active) Any (may cough, wheeze during exercise,
ACTIVITIES vigorous play, or laughing)
NOCTURNAL None Any (typically coughs during sleep or wakes with
SYMPTOMS/ cough, wheezing, and/ or dyspnea)
AWAKENNG
NEED FOR 2x/ week >2x/ week
RELIEVER/ RESCUE
TREATMENT
Six-Part Asthma Management
Program

1. Educate Patients
2. Assess and Monitor Severity
3. Avoid Exposure to Risk Factors
4. Establish Medication Plans for
Chronic Management: Adults and
Children
5. Establish Plans for Managing
Exacerbations
6. Provide Regular Follow-up Care
 Six-part Asthma Management Program

Goals of Long-term Management

 Achieve and maintain control of symptoms
 Prevent asthma episodes or attacks

 Maintain pulmonary function as close to normal

levels as possible
 Maintain normal activity levels, including
exercise
 Avoid adverse effects from asthma medications

 Prevent development of irreversible airflow

limitation
 Prevent asthma mortality
 Six-part Asthma Management Program

Control of Asthma

 Minimal (ideally no) chronic symptoms

 Minimal (infrequent) exacerbations
 No emergency visits
 Minimal (ideally no) need for “as needed” use of
β2-agonist
 No limitations on activities, including exercise
 PEF circadian variation of less than 20 percent
 (Near) normal PEF
 Minimal (or no) adverse effects from medicine
 Six-Part Asthma Management
Program
.
 The most effective management is by
eliminating the causal factors
 Asthma can be effectively controlled in
most patients, although it can not be
cured
 The major factors contributing to asthma
morbidity and mortality are under-
diagnosis and inappropriate treatment
 Part
Part 4:
4: Long-term
Long-term Asthma Management

Pharmacologic Therapy

Reliever Medications:
 Rapid-acting inhaled β2-agonists
 Systemic glucocorticosteroids
 Anticholinergics(ipra and tiotropium)
 Methylxanthines (theophylline
,aminophylline, theobromide caffeine)
 Part
Part 4:
4: Long-term
Long-term Asthma
Asthma Management
Management

Pharmacologic Therapy
Controller Medications:
 Inhaled glucocorticosteroids
 Systemic glucocorticosteroids

 Cromones

 Methylxanthines (theopylline, doxofylline)

 Long-acting inhaled β -agonists

2
 Long-acting oral β2-agonists
 Leukotriene modifiers (zarfilukast
montelukast)
 Anti-IgE (omlaizumab)
 Part
Part 4:
4: Long-term
Long-term Asthma Management
Stepwise Approach to Asthma
Therapy - Adults
Outcome: Asthma Control Outcome: Best
Possible Results

Controller:
 Daily inhaled
corticosteroid
plus
Controller:  Daily long –
 When
Controller: acting inhaled asthma is
 Daily inhaled controlled,
Controller: Daily inhaled corticosteroid β2-agonist reduce
None plus  plus (if needed) therapy
corticosteroid  Daily long- -Theophylline-SR
acting inhaled -Leukotriene
β2-agonist
 Monitor
-Long-acting inhaled
β2- agonist
-Oral corticosteroid

Reliever: Rapid-acting inhaled β2-agonist prn

STEP 1: STEP 2: STEP 3: STEP 4: STEP Down
Intermittent Mild Persistent Moderate Severe
Persistent Persistent

Alternative controller and reliever medications may be considered.

 Stepwise Approach to Asthma Therapy: Adults
Step 1: Intermittent Asthma

Daily Controller Reliever

Medications Medications

None required Rapid-acting inhaled 2-agonist

for symptoms (but < once a week)

Rapid-acting inhaled 2-agonist,

cromone, or leukotriene modifier
before exercise or exposure to
allergen

 Continuously review medication technique, compliance and environmental control

 Review treatment every three months.
 Step up if control is not achieved; step down if control is sustained for at least 3 months
 Preferred treatments are in bold print
 Stepwise Approach to Asthma Therapy: Adults
Step 2: Mild Persistent Asthma

Daily Controller Reliever

Medications Medications
Low-dose inhaled Rapid-acting inhaled 2-agonist
glucocorticosteroid for symptoms (but < 3-4 times/day)

Other options (order by cost): Other options:

 sustained-release theophylline, or  inhaled anticholinergic, or
 Cromone, or  short-acting oral 2-agonist, or
 leukotriene modifier  short-acting theophylline

 Continuously review medication technique, compliance and environmental control.

 Review treatment every three months
 Step up if control is not achieved; Step down if control is sustained for at least 3 months
 Preferred treatments are in bold print
 Stepwise Approach to Asthma Therapy: Adults
Step 3: Moderate Persistent Asthma

Daily Controller Reliever

Medications Medications
Low- to medium-dose inhaled glucocortico- Rapid-acting inhaled
steroid, plus long-acting inhaled 2-agonist 2-agonist for symptoms
(but < 3 - 4 times/day)
Other options (order by cost):
 Medium-dose inhaled glucocorticosteroid plus Other options:
sustained-release theophylline, or  inhaled anticholinergic or
 Medium-dose inhaled glucocorticosteroid plus long-  short-acting oral
acting inhaled β2- agonist, or 2-agonist or
 High-dose inhaled glucocorticosteroid, or
 short-acting theophylline
 Medium-dose inhaled glucocorticosteroid plus
leukotriene modifier

 Continuously review medication technique, compliance and environmental control.

 Review treatment every three months.
 Step up if control is not achieved; Step down if control is sustained for at least 3 months.
 Preferred treatments are in bold print.
 Stepwise Approach to Asthma Therapy: Adults
Step 4: Severe Persistent Asthma

Daily Controller Reliever

Medications Medications
High-dose inhaled glucocorticosteroid, Rapid-acting inhaled
plus long-acting inhaled β2agonist 2-agonist for symptoms
(but < 3-4 times/day)
plus one or more of the following, if
needed (order by cost): Other options:
 inhaled anticholinergic or
 sustained-release theophylline, or  short-acting oral
 leukotriene modifier or 2-agonist or
 oral glucocorticosteroid  short-acting theophylline

 Continuously review medication technique, compliance and environmental control.

 Review treatment every three months.
 Step up if control is not achieved; Step down if control is sustained for at least 3 months.
 Preferred treatments are in bold print.
 SIX-PART
SIX-PART ASTHMA
ASTHMA MANAGEMENT
MANAGEMENT PROGRAM
PROGRAM
PART 5: ESTABLISH PLANS FOR
MANAGING EXACERBATIONS

Primary therapies for exacerbations:

Repetitive administration of rapid-acting inhaled β2-
agonist
Early introduction of systemic glucocorticosteroids
Oxygen supplementation
Closely monitor response to treatment
with serial measures of lung function
 Emergency Department Management

Acute Asthma
Initial Assessment
History, Physical Examination, PEF or FEV 1

Initial Therapy
Bronchodilators; O2 if needed
Good Response
Incomplete/Poor Response Respiratory Failure

Observe for at Add Systemic Glucocorticosteroids

least 1 hour
Good Response Poor Response
If Stable,
Discharge to Discharge Admit to Hospital Admit to ICU
Home
HOSPITAL MANAGEMENT OF
ACUTE EXACERBATIONS
inhaled bronchodilator, and systemic corticosteroid therapy
Supplemental oxygen is administered
SABAs can be delivered frequently (every 20 min to 1 hr) or continuously (at 5-15
mg/hr).
 Inhaled ipratropium bromide is often added to albuterol every 6 hr if patients do not
show a remarkable improvement
 Short-course systemic corticosteroid therapy is recommended for use in moderate to
severe asthma
corticosteroids administered orally is found to be as effective as intravenous
corticosteroids
 Chest physical therapy, incentive spirometry, and mucolytics are not recommended
during the early acute period of asthma exacerbations as they can trigger severe
bronchoconstriction
 Several therapies, including parenterally administered epinephrine, β-agonists,
methylxanthines, magnesium sulfate (25-75 mg/kg, maximum dose 2.5 g, given
intravenously over 20 min)
Parenteral (subcutaneous, intramuscular, or intravenous) epinephrine or
terbutaline sulfate
Respiratory failure - intubation, and mechanical ventilation.
A follow-up appointment within 1-2 wk of a child’s discharge from the
hospital after resolution of an asthma exacerbation should be used to monitor
clinical improvement.
THANK YOU!