Asthma

Dr. Dejen G.
2020
Dire Dawa
 Definition
• A chronic inflammatory disease of the airways,
characterized by increased reactivity of the
tracheobronchial tree to various stimuli
– Airflow obstruction that varies markedly, both
spontaneously and with treatment
• Manifests physiologically by widespread
narrowing of the air passages
• Manifests clinically by paroxysms of dyspnea,
cough, chest tightness, and wheezing
• Most attacks are short-lived, lasting minutes
to hours, and can be managed relatively
easily.
– Less often, patients develop persistent disease
necessitating aggressive therapy.
• Status asthmaticus is the most severe form of
asthma
– Severe obstruction persists for days or weeks
– Can be life threatening
 Epidemiology…
• Ethnic distribution
– More prevalent in minorities and inner-city African-American
and Hispanic populations
• Age
– All ages affected, but more prevalent in early life
– Peak age: 3 years
– ~50% of cases develop before 10 years of age
– Another one-third of cases occur before 40 years of age
• Sex
– 2:1 male-to-female ratio in childhood
– Sex ratio equalizes by 30 years of age
 Etiology
• Multifactorial and depends on the interactions among
multiple susceptibility genes and environmental
factors
1) Indigenous factors
A)Susceptibility genes
– Are genes thought to stimulate airway smooth muscle and
fibroblast proliferation or regulate cytokine production
– Polygenic-
• Polymorphisms of genes on chromosome 5q, including the T H2
cells IL-4, IL-5, IL-9, and IL-13, which are associated with atopy
• ADAM-33, DPP-10, and GPRA
• Increased risk of-
– Familial association
– High degree of concordance in identical twins
– Severity of asthma is also genetically determined
B) Atopy
• Is due to the genetically determined production of specific IgE
Ab, with many patients showing a family Hx of allergic diseases
– Allergic rhinitis ( in over 80% of asthmatic patients), and
– Atopic dermatitis (eczema)
• Is the major risk factor for asthma
– Nonatopic individuals have a very low risk
• Intrinsic Asthma(nonatopic)-
– A minority of asthmatic patients ~10%
– Have negative skin tests to common inhalant allergens
and normal serum concentrations of IgE
– Usually show later onset of disease (adult-onset asthma)
– Commonly have concomitant nasal polyps, and may be
aspirin-sensitive
– They usually have more severe, persistent asthma
– Little is understood about mechanism
• Increased local production of IgE in the airways
• Infections-
– Respiratory syncytial virus infection in infancy?
– Atypical bacteria such as Mycoplasma and
Chlamydophila?
2) Environmental Factors-
• Diet-
– The role of dietary factors is controversial
– Diets low in antioxidants such as vit. C & A, Mg⁺⁺, selenium,
and ω-3 polyunsaturated fats (fish oil) or high in Na⁺ and ω-6
polyunsaturates are associated with an ↑ed risk of asthma
– Vit. D deficiency may also predispose to the development of
asthma
– Studies with supplementary diets have not supported an
important role for these dietary factors
– Obesity is also an independent risk factor for asthma,
particularly in women, but the mechanisms are thus far
unknown
• Air Pollution-
– Air pollutants such as sulfur dioxide, ozone, and
diesel particulates, may trigger asthma symptoms
– Indoor air pollution may be more important with
exposure to nitrogen oxides from cooking stoves
and exposure to passive cigarette smoke
– There is some evidence that maternal smoking is a
risk factor for asthma
• Allergens
– Inhaled allergens are common triggers of asthma
symptoms and have also been implicated in
allergic sensitization
– Exposure to house dust mites in early childhood is
a risk factor for allergic sensitization and asthma
– Domestic pets, particularly cats, have also been
associated with allergic sensitization, but early
exposure to cats in the home may be protective
through the induction of tolerance
• Occupational Exposure
– Affect up to 10% of young adults
– Chemicals such as toluene diisocyanate and
trimellitic anhydride, may lead to sensitization
independent of atopy
– Small animal allergens in laboratory workers and
fungal amylase in wheat flour in bakers
– Occupational asthma may be suspected when
symptoms improve during weekends and holidays
• Other risk factors
– lower maternal age, duration of breast-feeding,
prematurity and low birthweight, and inactivity
– Acetaminophen (paracetamol) consumption in
childhood
 Common triggers…
• Upper respiratory tract viral infections
– Rhinovirus, respiratory syncytial virus, and coronavirus
– Most common triggers of acute severe exacerbations
• Exercise and hyperventilation
• Cold air
• Air pollution
– Sulfur dioxide and irritant gases
– Ozone
– Nitrogen oxides
• Drugs (beta blockers, aspirin)
• Stress
• Irritants (household sprays, paint fumes)
 Clinical manifestations
• Classic symptom triad
– Wheezing
– Dyspnea
– Cough
• Less typically, the patient may have
intermittent episodes of nonproductive cough
or exertional dyspnea
• Typical acute attack
– Often occurs at night
• Occupational asthma, attacks may occur at work or after work
– Patients experience a sense of constriction in the chest, often
with a nonproductive cough
– Respiration becomes audibly harsh
– Wheezing is first noted during expiration and then with
inspiration as well
– Expiration becomes prolonged( I:E =/>1:3)
– If attack is severe or prolonged
• loss of adventitial breath sounds
• Wheezing becomes very high pitched
• In extreme situations, mucus plugging and
impending suffocation are signaled by:
– Lessening or disappearance of wheezing
– Cough may become weak and ineffective
– Accessory muscles become visibly active, and a
paradoxical pulse often develops
• The end of an episode is frequently marked by
a cough that produces thick, stringy mucus
• Patients with allergic asthma
– Exposure to antigen typically produces an immediate
response
– Airway obstruction develops in minutes and then
resolves
– 30–50% of patients have a second wave of
bronchoconstriction, a "late reaction," 6–10 hours later
• Patients with idiosyncratic asthma
– Bronchospasm typically follows an upper respiratory
infection
• Other physical findings
– Respiratory rate
• Increases with severity
– Heart rate
• Increases with severity
• Relative bradycardia may develop with impending
respiratory failure
– Use of accessory respiratory muscles
• Increases with severity
• Paradoxical thoracoabdominal movement with impending
respiratory failure
 Diagnosis
• History -
• Course of previous attacks (e.g., need for hospitalization,
corticosteroid treatment)
– Previous ICU admission or intubation: marker of severe disease and
high-risk patient
• Response to medications
• If occupational exposure is suspected
– Ask about workplace and work history in detail
– Specific contaminants?
– Availability and use of protective devices?
– Do coworkers have similar complaints?
– Ask about every job; short-term exposures may be significant
• P/E-
• Presence of exiratory wheezing
– Absence of wheezing may signify poor airflow and
impending respiratory failure
• Assessment of severity of airflow obstruction
– Increased RR, tachycardia, use of accessory
muscles for breathing, and an elevated pulsus
paradoxus are all helpful indicators of severity
• Pulmonary function tests
• Spirometry test-
– The most useful measures are peak flow and FEV1
– These can be obtained quickly and easily at the
bedside
• Support the clinical diagnosis by demonstrating
reversible airway obstruction
• Helpful in judging severity of airway obstruction
and for following response to treatment
• CBC
– Usually not helpful
– May show eosinophilia
• Serum IgE level
– Elevated in allergic asthma
– Normal in idiosyncratic asthma
– Marked elevations may suggest allergic
bronchopulmonary aspergillosis
• Specific IgE to inhaled allergens [radioallergosorbent
test (RAST)] may be measured in some patients
• Sputum examination (rarely performed unless
infection is suspected)
– Eosinophilia may be present and may signify
increased inflammation and severity of
exacerbation
– Curschmann’s spirals (casts of small airways)
– Charcot–Leyden crystals (probably represent
disintegrated eosinophils)
– Presence of large numbers of neutrophils suggests
bronchial infection
• Chest radiography
– Not always necessary
– Important when complicating infection or
pneumothorax is a consideration
– May show hyperinflation or patchy infiltrates due
to atelectasis behind plugged airways
• Exercise testing – For exercise-induced asthma
• Allergen challenge is rarely necessary
 Treatment
• Aims of therapy
– Minimal (ideally no) chronic symptoms, including
nocturnal
– Minimal (infrequent) exacerbations
– No emergency department visits
– Minimal (ideally no) use of a required β2-agonist
– No limitations on activities, including exercise
– Peak expiratory flow circadian variation < 20%
– (Near) normal peak expiratory flow rate (PEFR)
– Minimal (or no) adverse effects from medicine
• The main drugs for asthma
– Bronchodilators, which give rapid relief of
symptoms mainly through relaxation of airway
smooth muscle
– Controllers, which inhibit the underlying
inflammatory process
• Emergencies
• Identify life-threatening airway obstruction.
Signs of life-threatening exacerbation include:
– Altered mental status
– Paradoxical chest or abdominal movement
– Silent chest
– Paradoxical pulse
– Use of accessory muscles
– Marked hyperinflation of the thorax
 Management of acute severe asthma emergencies

• A high concentration of oxygen should be given by

face mask to achieve oxygen saturation of >90%.
– Aerosolized β2-agonists are the primary therapy for acute
episodes.
– 3 doses given every 20 minutes by handheld nebulizer,
then a single dose every 2 hours until the attack subsides
– Continuous nebulized β2-agonists may be more effective
than intermittent treatment, especially in severe acute
exacerbations.
• Used in doses of 5-10 mg of albuterol per hour
• Systemic glucocorticoids
– Prednisone (1 mg/kg PO once daily) or Hydrocortisone (100
mg IV every 6 hours)
– No difference between oral and intravenous administration in
moderate exacerbations
– Intravenous therapy is preferred in severe exacerbations.
• Magnesium (as magnesium sulfate)
– A smooth muscle–cell relaxant; may also reduce inflammatory
bronchoconstriction through actions on mast cells
– Especially useful if the response to inhaled β2-agonist in
appropriate
 Chronic stable asthma treatment

• Goals-
• General:
– A stable, asymptomatic state with the best pulmonary function
possible using the least medication
• Specific
– Minimal or absent chronic symptoms or exacerbations
– No limitation on activities
– No absences from school or work
– Maintenance of normal or near-normal pulmonary functions
– Minimal use of SABAs (less than once daily, < 1 canister/month)
– Minimal or absent adverse effects from medications
• A primary step is educating patients
– Asthma triggers should be avoided
• Assess severity of the illness and monitor with
objective measures of lung function
– Disappearance of subjective symptoms or
wheezing in an acute attack should not be used as
the end point for therapy
• Plan for both long-term management and
treatment of exacerbations
Stepwise Therapy
 Bronchodilator therapies

• β2-Adrenergic agonists
• Effects of β2-adrenergic agonists on airways
– Relaxation of airway smooth muscle (proximal and
distal airways)
– Inhibition of mast cell mediator release
– Inhibition of plasma exudation and airway edema
– Increased mucociliary clearance
– Increased mucus secretion
– Decreased cough
– No effect on chronic inflammation
 Controller therapies

• Inhaled glucocorticoids
– Drugs of choice in the long-term control of asthma; most
effective controllers
• Clinical use-
– Beneficial in treating asthma of any severity and age
– Given as first-line therapy for patients with persistent asthma
• If they do not control symptoms at low doses, it is usual to add a
LABA as the next step
– Beclomethasone: 42 μg/puff , Budesonide: 200 μg/dose,
Fluticasone are examples
– Inhaled corticosteroids can take ≥ 1 week to produce
improvements
– In rapidly deteriorating situations, prescribe oral preparations
and initiate inhaled drugs as the dose of the former is reduced
• Systemic glucocorticoids
– The most potent and most effective anti-inflammatory
medications available
– Clinical use
In acute illness, when severe airway obstruction is not resolving
or is worsening despite intense optimal bronchodilator therapy
– In chronic disease, when there has been failure of a previously
optimal regimen and frequent recurrences of symptoms of
increasing severity
– Prevent relapse after acute exacerbations when given for a 5- to
10-day "burst" at 30–45 mg/d PO of prednisone or its equivalent
• Tapering the dose is not necessary!!!
– Examples-
– Prednisolone 40–60 mg/d PO as a single dose or 2
divided doses for 3–10 days
– Prednisone 40–60 mg/d PO
– Hydrocortisone IV
 Monitoring
• Assess asthma control and symptoms at every visit:
– Presence of nocturnal symptoms
– Use (amount and frequency) of SABAs for symptom relief
– Need for urgent medical care
– Peak flow readings at home
– Ability to do physical activity
• Once control is reached and sustained for several weeks,
a step-down reduction in therapy should be undertaken
• Review treatment every 1–2 months
• Monitor S/E of medications
 Complications
• Spontaneous pneumothorax and/or
pneumomediastinum occur rarely
• Status asthmaticus
• Respiratory failure
 Prognosis
• Particularly good prognosis for those whose
disease is mild and develops in childhood
• Even when untreated, persons with asthma do
not continuously move from mild to severe
disease with time.
• Spontaneous remissions occur in ~20% of those
who develop the disease as adults.
– Approximately 40% can be expected to experience
improvement, with less frequent and severe attacks,
as they grow older
• There is no known primary prevention for
asthma.
• In patients with known disease
– Asthma triggers, including tobacco smoke and
other precipitants, should be avoided or
controlled
– Plans should be made for both long-term
management and treatment of exacerbations.
– Regular follow-up care is mandatory.
THANK YOU!!!