I.
Background
a. Global Strategy for Asthma Management and Prevention, Global Initiative for Asthma
(GINA) definition: usually characterized by chronic airway inflammation; it is defined by
the history of respiratory symptoms (wheeze, shortness of breath, chest tightness and
cough) that vary over time and in intensity, together with variable expiratory airflow
limitation. *asthma symptoms wax/wane through time, COPD chronic
b. obstruction → wheezing, breathlessness, chest tightness, and coughing (particularly at
night and early in the morning)
c. Severity of disease—from mild intermittent symptoms to a severe and disabling disease if
left untreated
i. All are at risk for acute severe disease
ii. Treat underlying airway inflammation
1. Control asthma
2. Reduce asthma-associated risks
II.
Epidemiology
a. 25.2 million persons in the US (7.9% of population; 9.9% of OH population and 10.8% of
MI population)
i. 11.7% of the population at or below the poverty level
ii. Ethnic minorities share the burden of asthma disproportionately
1. African Americans twice as likely to be hospitalized or die from asthma
than whites
2. Individuals from Puerto Rico have highest asthma rate among Latinos
b. 1.8 million ED visits in 2016
c. 188,000 hospitalizations
d. Most common chronic disease among children (7 million)
i. 14.4 million missed school days per year
ii. Most patients are diagnosed by age 5
iii. Disease persists in 30-40% of adults
iv. Predictors for persistent adult asthma
1. Atopy
a. Genetically determined state of hypersensitivity to environmental
allergens
b. Type I allergic reaction is associated with the IgE antibody and
asthma (anaphylaxis rxn, hyperimmune response to allergens)
2. Onset during school age
3. Presence of bronchial hyperresponsiveness (BHR)
v. Severity of asthma in childhood is predictor of severity in adulthood
e. $56 billion in direct and indirect medical costs
f. Death rate: 0.10 per 1,000 persons; 80-90% of deaths are preventable
III.
Etiology
a. Genetic Factors
i. Asthma in parent is a strong risk factor for asthma in a child
ii. Risk increases with family history of atopy
b. Environmental Factors
i. Secondhand smoke exposure (in utero and during infancy) → ↑ risk of childhood
asthma
ii. Outdoor pollutants (i.e. living near a main road): 13% of pediatric asthma cases
due to traffic-related air pollution
iii. Exposure to specific allergens in the workplace → occupational asthma (develop
disease late in life)
c. Obesity
i. In childhood: risk factor for asthma, especially for girls
ii. In adulthood: risk factor for asthma
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d. Adult-Onset Asthma
i. Atopy
ii. Nasal polyps
iii. Aspirin sensitivity
iv. Occupational exposure
v. Recurrence of childhood asthma
IV.
Pathophysiology
a. Overview
i. Inhaled antigens are taken up by antigen presenting cells → T-lymphocytes →
activation of TH2 type response → B-cell production of antigen-specific IgE and
proinflammatory cytokines and chemokines → activation of eosinophils,
neutrophils, and alveolar macrophages
ii. Further exposure to antigen → cross-linking of IgE in mast cells and basophils →
release of histamine, leukotriene C4 and prostaglandins
iii. Early Phase Response
1. Activation and degranulation of mast cells and basophils
2. Acute bronchoconstriction that lasts ~1 hour after exposure
iv. Late Phase Response
1. Activated airway cells release inflammatory cytokines and chemokines→
more inflammatory cells in the lungs
2. Increased airway inflammation and hyperresponsiveness that occurs 4-6
hours after initial allergen challenge
b. Airway inflammation (chronic; although symptoms are intermittent) *always inflammation,
but not always with symptoms of it
i. T-lymphocytes release cytokines which coordinate:
1. Eosinophilic infiltration
2. IgE production by B-lymphocytes
ii. Mast cells infiltrate airway smooth muscle and bronchial epithelium
1. Cause mucous gland hyperplasia
2. Mast cell degranulation → development of proinflammatory mediators →
inflammatory response and contribute to AHR and airway remodeling
c. Airway hyperresponsiveness (AHR) *same as BHR
i. Exaggerated ability of the airways to narrow in response to stimuli
ii. Related to airway inflammation and structural airway changes
d. Airway obstruction
i. Airway Smooth Muscle Constriction
1. Tone maintained by sympathetic, parasympathetic, & non-adrenergic
2. Constriction results from mediators like histamine and prostaglandins
ii. Airway Edema
1. Inflammatory mediators (histamine, leukotriene, bradykinin) will ↑
microvascular permeability → edema
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2. Rigid airways limit air flow
iii. Mucus Hypersecretion — ↑ number and volume of mucous glands
iv. Airway Remodeling
1. Some patients will have fixed obstruction
2. Characterized by epithelial damage, subepithelial fibrosis, airway smooth
muscle hypertrophy, ↑ mucous production, ↑ vascularity of airways
V.
Clinical Presentation and Diagnosis
a. General
i. Range: normal pulmonary function with symptoms only during acute
exacerbations to significantly decreased pulmonary function with continuous
symptoms
ii. Important History: FH, SH, precipitating factors, exacerbations, development of
symptoms, and treatments
Symptoms
Signs
Laboratory Tests
Defining feature (varies over
Defining feature: variable expiratory
- tachypnea
time and intensity):
- tachycardia
flow limitation
- wheezing, SOB, chest
- Use of accessory muscles 1) Spirometry
tightness, coughing (usually
- Auscultation → end
- FEV1/FVC < 80% and one of
worse at night)
expiratory wheezes (mild)
the following (after receiving
or wheezing through
bronchodilator):
- Anxious and agitated
inspiration and expiration
a) ↑ in FEV1 of 12% or 200mL
OR
- Mental status changes may → (severe)
respiratory failure
- Bradycardia and absence
b) ↑ 10% in predicted FEV1
-Presence of precipitating
of wheezing (respiratory
- May be normal if patient is not
factors → symptoms
failure)
Symptomatic (don’t memorize a/b
- Usually have a pattern
numbers)
2) ↑ IgE
3) (+) radioallergosorbent test (RAST)
4) Fractional exhaled nitric oxide
(FeNO): use when history, clinical
course, and spirometry are unclear;
not widely available
a) > 50 ppb adults
b) > 35 ppb for 5-12 years
b. Acute asthma
iii. General
1. Rapid (within 3-6 hours); more commonly deterioration over days to
weeks
2. Severity does not correspond with severity of chronic disease
iv. Symptoms—may be unable to communicate in full sentences
v. Signs—pulsus paradoxus (SBP drops >10 mmHg when inhaling), diaphoresis
(sweating), cyanosis (blue skin)
Dyspnea/SOB
Mild
With activity
Moderate
Limits activity
Peak Expiratory
Flow (PEF)
> 70% of personal
best
40-69% of
personal best
Severe
Interferes with
conversation or
occurs at rest
25-40% of
personal best
Life-threatening
Patient not able to
speak
< 25% of personal
best
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c.
Chronic asthma
vi. Initial classification of severity is based on the following:
1. Current disease impairment
a. Frequency and severity of symptoms
b. Use of short acting β2-agonists for quick relief of symptoms
c. Pulmonary function
d. Impact on normal activity and quality of life
2. Future risk
a. Potential for severe exacerbations and asthma-related death
b. Progressive loss of lung function (adults)
c. Reduced lung growth (children)
d. Occurrence of drug-related adverse effects
vii. Intermittent
viii. Persistent
1. Mild
2. Moderate
3. Severe
Figure 1: Classifying Asthma Severity for Patients Who Are NOT Currently Taking Long-Term Control
Medications
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VI.
Treatment of Asthma
a. Desired outcomes / goals
Chronic Asthma
Prevent chronic and troublesome symptoms
Maintain normal or near normal pulmonary
function
Meet patient’s expectations of satisfaction with
asthma care
Acute Asthma
Correct significant hypoxemia
Reverse airflow obstruction rapidly
Reduce the likelihood of exacerbation relapse or
recurrence of severe airflow obstruction in the
future
Prevent progressive loss of lung function
Require infrequent use (<2 days/wk) of SABA
Maintain normal activity levels
Prevent exacerbations of asthma and the need for
ED visits and hospitalizations
Provide optimal pharmacotherapy with minimal or
no adverse effects
a. Nonpharmacologic Therapy – Focused on patient education
i. Modifiable Risk Factors
1. Avoid exposure to tobacco smoke
2. Avoid known allergies:
a. Rarely related but severe
b. Have injectable epinephrine available if necessary
3. Weight: 5-10% weight reduction in obese patients, BMI >30
ii. Strategies and Interventions
1. Smoking Cessation
a. Encourage cessation at every visit
b. Advise caregivers to avoid smoking near children with asthma
2. Physical Activity: Engage in regular activity
3. Occupational Asthma: Identify and remove occupational triggers
4. Severe Asthma: Refer to a specialist
iii. Be aware of triggers
1. Do not avoid: Exercise, Laughter
2. Hard to avoid: Viral infection, Stress
Indoor and
Outdoor Mold
Strong
odors/Spray
Tobacco Smoke
Medications
Cockroaches
Pollen
Occupational
Substances
Cooking Sources
Animal Dander
Dust Mites
iv. Assess NSAID/Aspirin sensitivity prior to prescribing
1. Aspirin-exacerbated respiratory disease (AERD)
a. Presentation:
i. Nasal congestion and anosmia that progresses to
rhinosinusitis with nasal polyps
ii. Hypersensitivity to aspirin
iii. Asthma attack
b. Acute asthma attack occurs within minutes to 1-2 hours of
receiving aspirin or NSAID product
2. When an NSAID is indicated, acetaminophen may be considered with
observation for at least 2 hours after administration – may still cause an
adverse reaction
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v. Non-selective beta-blockers (carvedilol, labetalol, nadolol, pindolol, propranolol,
timolol)
1. May worsen asthma control
2. Avoid unless benefit outweighs the risk
3. B1 selective agents are best (metoprolol, atenolol, nebivolol)
a. Selectivity is dose-related
vi. Vaccination – encourage patients to keep up to date on all vaccinations
1. Pneumococcal – additional PPSV23 prior to age 65
2. Annual influenza
3. COVID-19 vaccine
b. Counseling
i. Smoking Cessation
ii. Medication Counseling
1. Differentiate between maintenance and as-needed inhalers
2. Assess technique and cleaning regularly
iii. Asthma Action Plan
1. Symptom based
2. PEF-Based (adults only)
c.
Pharmacologic therapy
i. Drug delivery devices
1. Generate particles with aerodynamic diameters from 0.5 to 35 μm
a. > 10 μm: deposit in the oropharynx
b. 5-10 μm: deposit in the trachea and large bronchi
c. 1-5 μm: reach the lower airways (target for delivery in asthma)
d. < 1 μm: act as a gas and are exhaled
2. Particles are deposited in the airways by:
a. Inertial impaction
b. Gravitational sedimentation
3. Appropriate device technique is essential to achieve optimal drug
delivery and therapeutic effect
4.
ii. Corticosteroids
1. Most potent anti-inflammatory agents for asthma
2. Inhaled, oral, injectable
3. Improve response to β2-agonists
4. Inhaled corticosteroids (ICS)
a. Preferred therapy for ALL forms of persistent asthma in ALL age
groups
b. More effective than LTRA in improving lung function and
preventing ED visits and hospitalizations due to asthma
exacerbations
c. Advantage over systemic forms: targeted drug therapy to the
lungs → decrease systemic effects
d. Product selection based on preference for dosage form, delivery
device, and cost
e. Equally effective if given in equipotent doses
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f.
Flat dose-response curve; doubling the dose has limited
additional effect on asthma control
g. More effective when given twice (rather than once daily) except
fluticasone furoate which is only QD
h. Cigarette smoking
i. Decreases response to ICS
ii. Smokers require higher doses than nonsmokers
i. Beneficial effect
i. May be seen within 12 hours of administration
ii. 2 weeks necessary to see significant clinical effects
j. With most devices, majority of drug is deposited in mouth and
throat and swallowed
i. Reduce ADRs by:
1. Using a VHC (valve holding chamber)
2. Rinsing the mouth with water
3. Expectorating after using the ICS
4. Decreasing dose → ↓ in hoarseness
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k.
Variability in response to ICS
i. Up to 40% of patients do not respond to ICS
ii. May be related to functional glucocorticoid-induced
transcript 1 gene (GLCCI1) variant in some patients
iii. Pharmacogenomics will assist with individualized
asthma treatment plans
5. Systemic corticosteroids
a. Cornerstone of treatment for acute asthma after starting SABA
i. Onset: 4-12 hours; therefore, start EARLY in course of
exacerbation
ii. Oral route is preferred (IV is not more effective)
iii. Continue until PEF is > 70% of personal best AND
asthma symptoms are resolved
iv. Duration: 3-10 days, tapering is not necessary
b. Avoid as long-term controller meds (due to potential for ADRs)
i. Only use if failed other meds (i.e. immunomodulators)
ii. Use daily or every other day
iii. Repeat attempts to ↓ dose or discontinue the med
AEIOU and sometimes H (steroid longterm complications)
Adrenal suppression
Eyes (claucoma/cataracs)
Infection
Osteoperosis
Ulcerations (GI)
HTN, hyperglycemia
Medication
Methylprednisolone
Prednisolone
Prednisone
Dosage Form
2, 4, 6, 8, 16, 32 mg PO
tablets
5 mg PO tablets; 5 mg/5 mL
and 15 mg/5 mL PO liquid
1, 2.5, 5, 10, 20, 50 mg PO
tablets; 5 mg/mL and 5
mg/5 mL PO liquid
0-11 years
40-60 mg/day PO as single
or two divided doses
1-2 mg/kg/day (MAX 60
mg/day)
1-2 mg/kg/day (MAX 60
mg/day)
> 12 years
40-60 mg/day PO as single
or two divided doses
40-60 mg/day PO as single
or two divided doses
40-60 mg/day PO as single
or two divided doses
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10
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iii. β2-adrenergic agonists
1. Better bronchodilator in acute asthma than anticholinergics, therefore,
are DOC
2. Short-acting inhaled β2-agonists (SABA)
a. Most effective agents for reversing acute airway obstruction
caused by bronchoconstriction
b. MDI + spacer is quicker and as effective as nebulization
c. NOT recommended for chronic daily dosing
ii. Key indicator of uncontrolled asthma
iii. ↓s duration of bronchodilation provided by the SABA
d. Albuterol
i. Most commonly used SABA
ii. MDI and solution for nebulization
e. Levalbuterol
i. MDI and solution for nebulization
ii. Similar efficacy to albuterol
iii. No fewer side effects than albuterol
f. Dosing
i. During asthma exacerbation, doses are doubled and
changed from PRN to scheduled
ii. Home setting:
Medication
Albuterol
(ProAirTM HFA, Proventil®
HFA, Ventolin® HFA)
Albuterol
(Proair RespiClick)
Albuterol
(Accuneb®)
Levalbuterol
(Xopenex HFATM)
Levalbuterol
(Xopenex®)
Dosage Form
HFA (MDI) 90 mcg/puff;
200 puffs/canister
0-11 years
1-2 puffs Q 4-6 hours
PRN
> 12 years
2 puffs Q 4-6 hours
PRN
(DPI) 90 mcg/puff;
200 puffs/inhaler
Nebulizer solution 0.63 mg / 3 mL,
1.25 mg / 3 mL, 2.5 mg / 3 mL,
5 mg / mL
HFA (MDI) 45 mcg/puff;
200 puffs/canister
Nebulizer solution 0.31 mg / 3 mL,
0.63 mg / 3 mL, 1.25 mg / 0.5 mL,
1.25 mg / 3 mL
Not indicated
2 puffs Q 4-6 hours
PRN
1.25-5 mg in 3 mL
saline Q 4-8 hours
PRN
2 puffs Q 4-6 hours
PRN
0.63-1.25 mg in 3 mL
saline Q 6-8 hours
PRN
0.63-5 mg in 3 mL
saline Q 4-6 hours
PRN
2 puffs Q 4-6 hours
PRN (5-11 years)
0.31-1.25 mg in 3 mL
saline Q 6-8 hours
PRN
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3. Long-acting inhaled β2-agonists
a. Useful for patients experiencing nocturnal symptoms
b. Step 1 and 2 (intermittent/mild-persistent)
i. Formoterol ONLY used in combo with as needed lowdose ICS
c. Step 3, 4, and 5
i. LABA indicated with low, medium, and high-dose ICS,
respectively
d. LABA should not be used as monotherapy
i. Increased risk of severe asthma exacerbation and
asthma-related deaths
ii. Black Box against their use without an ICS
e. Available in fixed-ratio combination products containing
fluticasone, budesonide, or mometasone
i. Increase adherence (fewer inhalers and inhalations)
ii. Less flexibility with dose adjustments
f. Vilanterol: only available in fixed-ratio combination products with
fluticasone furoate
Medication
Salmeterol
(Serevent Diskus)
Formoterol
(Foradil Aerolizer)
Fluticasone furoate /
vilanterol (Breo
Ellipta)
Dosage Form
DPI 50 mcg / blister
> 5 years
Contents of one blister Q 12 hours
DPI 12 mcg / capsule
Contents of one capsule Q 12
hours
> 18 years of age ONLY: one
inhalation daily
100 mcg / 25 mcg / actuation
200 mcg / 25 mcg / actuation
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iv. Anticholinergics (Muscarinic antagonists)
1. Bronchodilating effects are not as effective as beta agonists in asthma
2. Ipratropium
a. MDI and solution for nebulization
b. Addition to SABA during moderate to severe exacerbation
improves pulmonary function and decreases hospitalization rates
i. Only indicated in emergency department; works more
centrally to open bronchi allowing albuterol to reach
ii. No evidence during hospitalization or for chronic therapy
3. Tiotropium
a. Respimat (mist inhaler); handihaler for COPD
b. If uncontrolled on ICS + LABA, then add on tiotropium
c. May be used as add-on therapy for adult or adolescent patients
with a history of exacerbations; not indicated < 12 years of age
Medication
Ipratropium
nebulizer
(0.25 mg/mL)
Ipratropium
bromide (18
mcg/puff)
Tiotropium
(1.25 mcg/actuation)
Dose: < 12 years
250 mcg Q 20 min x 3
doses, then Q 2-4 hours
Dose: > 12 years
500 mcg Q 30 min x 3
doses, then Q 2-4 hours
4-8 puffs Q2-4 hours
PRN
8 puffs Q 20 min PRN
for up to 30 hours
-----
2 inhalations once daily
Comments
May mix in same
nebulizer as albuterol;
ONLY add to SABA
-----
Maximum benefits in 4-8
weeks
v. Leukotriene modifiers
1. Improve FEV1 and decrease asthma symptoms, SABA use, and asthma
exacerbations
2. Less effective than low dose ICS
3. Combining with an ICS is not as effective as ICS + LABA
4. Beneficial in patients with:
a. Allergic rhinitis
b. Aspirin sensitivity
5. Black box warning with montelukast: neuropsychiatric events (suicidal
thoughts or actions)
Medication
Montelukast
(Singulair®)
Zafirlukast
(Accolate®)
Zileuton
(Zyflo®)
Dosage Form
4 mg or 5 mg chewable
tablets
4 mg granule packets
10 mg tablet
10 mg or 20 mg tablets
600 mg ER tablet
600 mg tablet
0-11 years
1-5 years: 4mg PO HS
6-11 years: 5 mg PO HS
7-11 years: 10 mg PO
BID
NA
> 12 years
12-14 years: 5 mg PO
HS
> 15 years: 10 mg PO
HS
20 mg PO BID
1200 mg BID after meals
600 mg four times / day
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vi. Immunomodulators ****define hyperresponsiveness
vii.
1. IgE binding inhibitor—Omalizumab (Xolair)
a. For moderate to severe persistent asthma when asthma is not
controlled by ICS and if positive skin test or in vitro reactivity to
aeroallergens
b. Decreases ICS use, reduces number of exacerbations,
improvement of symptoms and QOL, reduces OCS dose in
those who use OCS
c. After initial dose, subsequent IgE levels are not monitored
d. Adverse Effects
i. Injection site reactions
ii. Anaphylaxis (~0.2%)
1. May occur any time after medication
administration
2. Provide prescription for and education on use of
subQ epinephrine
iii. Monitoring patients:
1. For the first three injections: 2 hours following
administration
2. Thereafter: 30 minutes after administration
2. Interleukin-5 Antagonists / Interleukin-5 Receptor Antagonist
a. For severe eosinophilic asthma that is uncontrolled on Step 4-5
treatment
b. Reduces severe exacerbations, improves quality of life, lung
function, and symptom control
c. Decreases median OCS dose in those using OCS
d. Mepolizumab (Nucala) - [anti-IL5]
e. Reslizumab (Cinqair) - [anti-IL5]
f. Benralizumab (Fasenra) - [anti-IL 5 receptor alpha]
g. Adverse Effects
i. Injection site reactions
ii. Anaphylaxis
3. Interleukin-4 Receptor Antagonist
a. Add-on maintenance treatment for Step 5 eosinophilic phenotype
or those requiring maintenance OCS
b. Reduces severe exacerbations, improves quality of life, lung
function, and symptom control
c. Dupilumab (Dupixent)
d. Adverse Effects
i. Injection site reactions
ii. Transient blood eosinophilia
iii. Rare cases of eosinophilic granulomatosis with
polyangiitis (EGPA)
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Medication
Omalizumab
(Xolair)
Dosage Form
> 6 years
> 12 years
> 18 years
SubQ injection, 150 75-375 mg SubQ Q2-4 150-375 mg SubQ Q2-4
mg/1.2 mL after
weeks depending on
weeks depending on
reconstitution with 1.4 body weight and prebody weight and premL sterile water for
treatment serum IgE
treatment serum IgE
injection
level
level
Mepolizumab 100mg powder;
100 mg subQ once every 100 mg subQ once every
(Nucala)
reconstitute with 1.2 4 weeks into the upper 4 weeks into the upper
mL sterile water for
arm, thigh or abdomen arm, thigh or abdomen
SubQ inj
Benralizumab SubQ injection,
NA
30 mg Q4 weeks x 3
(Fasenra)
30mg/mL solution in
doses, then once Q8
prefilled syringe
weeks
Reslizumab
NA > 12 years
Solution, Intravenous NA
3 mg/kg once every 4
(Cinqair)
100 mg/10 mL (10
weeks (maximum dose
mL)
not established). A
minimum of 4 months of
treatment is suggested to
determine efficacy
Dupilumab
SubQ injection, 200 100-200 mg Q2W
400mg x 1, then 200mg
(Dupixent)
mg/1.14 mL,
Q2 weeks OR 600mg x 1,
300 mg/ 2ml
then 300mg Q 2 weeks
vii. Allergen-specific immunotherapy
1. Adjunct treatment to standard pharmacotherapy
2. For when allergy plays a prominent role in asthma
a. pet dander
b. dust mites
c. grass pollens
3. Involves identification and use of clinically relevant allergens with
administration of extracts in progressively higher doses to induce
desensitization / tolerance
4. Associated with reduction in symptom scores, medication requirements,
and improved airway hyperresponsiveness
5. Subcutaneous immunotherapy (SCIT) may be used for ages > 5 years
6. Guidelines recommend AGAINST the use of sublingual immunotherapy
(SLIT)
d. Treatment of chronic asthma
i. Intensity of therapy is based on disease severity (at time of diagnosis) and level
of control (while on therapy)
ii. The LEAST amount of medication necessary to meet the goals of asthma
therapy is used
iii. The first step in asthma management is evaluating asthma severity (Figure 1
above) and control (Figure 2)
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Figure 2: GINA assessment of asthma control in adults, adolescents, and children 6-11 years excludes
people with only exercise-induced
*Excludes reliever taken before exercise, because many people take this routinely
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i. Pharmacologic treatment is initiated based on the recommendations for stepwise therapy (Figure 3)
Figure 3: Suggested initial controller treatment in patients > 12 years of age with asthma
**TOP ROUTE: Alternative to GINA guideline → intermittent (1), mild persistent (2), mod persistent (3), 4 (mod persistent), 5 (severe persistent)
*Must be Symbicort for controller in top track because formoterol is the only LABA with fast onset and it must be used as both rescue and
maintenance inhaler
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Figure 4: Stepwise approach to control symptoms and minimize future
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ii. Therapeutic plans should be individualized
iii. Intermittent Asthma (Step 1)
1. Classification includes patients with exercise-induced bronchospasm
(EIB), seasonal asthma, or asthma symptoms associated with infrequent
trigger exposure
2. Preferred Controller and Reliever: Low-dose ICS-formoterol PRN
3. Other controller option: Low-dose ICS whenever SABA is taken
4. Other reliever option: SABA as needed
5. Patients pre-treat prior to exposure to a known trigger
iv. Persistent chronic asthma
1. Require daily long-term control therapy (scheduled)
2. ICS is DOC at all levels of severity and in all age groups
3. Low-dose ICS-formoterol or SABAs is prescribed for all patients with
chronic asthma for use on a PRN basis
a. Preferred reliever therapy
i. Patient receiving ICS-formoterol maintenance: ICSformoterol PRN
ii. Patient NOT receiving ICS-formoterol maintenance:
SABA PRN
4. NEW to 2021 Guidelines: Add-on azithromycin may be considered
a. Used for persistent symptomatic asthma despite high dose ICSLABA (referred to specialist)
b. Sputum culture evaluation for atypical mycobacteria
c. Check ECG at baseline; ensure QTc is < 450 msec
5. After initiating therapy
a. Monitor patients within 1-3 months to ensure asthma control has
been achieved (Figure 2)
b. Before increasing therapy:
i. Evaluate inhaler technique
ii. Reduce treatment to previous level and use an
alternative treatment if no response
c. Intensification is based on individualized response to therapy
6. Patients with controlled asthma
a. Monitor at 1-6 month intervals to ensure control is maintained
b. Once control has been maintained for 3 months, a gradual
stepdown in long-term controller therapy is attempted
c. Controversy in how to taper long-term controller medication
i. Current data supports decreasing ICS dose before
removing LABA
ii. FDA warnings: use LABA treatment for the shortest time
possible
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e. Treatment of acute asthma (exacerbation)
i. Early and appropriate intensification of therapy is important to resolve the
exacerbation and prevent relapse and future severe airflow obstruction
ii. Early and aggressive treatment is necessary for quick resolution
iii. Optimal treatment depends on the severity of the exacerbation
iv. Patient’s condition deteriorates over several hours, days, or weeks
v. Algorithm for home management (Figure 5)
Figure 5: Algorithm for Home Management
*SABA is alternative reliever*
vi. Based on initial response to SABA therapy, severity of exacerbation is assessed,
and treatment is appropriately intensified
vii. Criteria for proceeding to the ED
1. Deteriorating quickly
2. Not responding to quick relief medications
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viii. Algorithm for ED management (Figure 6)
1. Discharged home
a. Responding to therapy in the ED with sustained response to
SABA
b. Medications: SABA, 3-10 day course of PO corticosteroid, ICS,
other long-term controller medications (continue normal
medications with the additions)
2. Admitted to the hospital
a. Do not respond adequately to intensive therapy within 3-4 hours
b. Medications: oxygen, continuous nebulization of SABA, and
systemic corticosteroid
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Figure 6: Management of Asthma Exacerbations in the Emergency Department
ix. Oxygen
1. Children, pregnant women, patients with coexisting heart disease: give
oxygen to maintain saturation 94-98%
2. All other patients: give oxygen to maintain saturation 93-95%
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f.
Asthma self-management
i. Written asthma action plans
1. Part of standard of care, although does not decrease mortality
2. Give patients freedom to adjust therapy based on personal assessment
of disease control using a predetermined plan
3. Includes:
a. Instructions on daily management
b. How to recognize and handle worsening asthma
i. May evaluate symptoms or monitor PEF
ii. Early signs of deterioration
1. Increasing nocturnal symptoms
2. Increasing use of SABAs
3. Not responding to increased use of SABA
iii. Patients may be provided with a prescription for oral
corticosteroids to use on a PRN basis
ii. Peak expiratory flow (PEF)
1. Measurement is considered for patients with:
a. Moderate to severe persistent asthma
b. A poor perception of worsening asthma or airflow obstruction
c. Unexplained response to environmental or occupational
exposures
2. Measured daily upon awakening and when asthma symptoms worsen
iii. For PEF-based asthma action plans
1. Patient’s personal best PEF is established over a 2-3 weeks period when
the patient is receiving optimal therapy
2. Subsequent PEF measurements are evaluated in relation to their
variability from the patient’s best PEF measurement
iv. See Figure 6 for asthma action plan templates
PEF = 80-100% of personal best
PEF = 50-79% of personal best
Green Zone
Yellow Zone
PEF = < 50% of personal best
Red Zone
Current therapy is acceptable
Impending exacerbation, intensify therapy with SABA,
possibly add oral corticosteroids, call physician
Medical alert, use SABA immediately, take oral corticosteroid,
go to the ED
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g. Special populations
i. Pregnancy
1. 4-8% of pregnant women are affected by asthma
2. About 1/3 of women will experience worsening asthma during pregnancy
3. Uncontrolled asthma is a greater risk to the fetus than asthma
medication use
4. Asthma exacerbations should be managed aggressively
5. Stepwise approach in pregnancy is similar to general population
6. budesonide: most safety data; preferred ICS; category B
7. Albuterol: DOC for treatment of asthma symptoms and exacerbations
ii. Young children
1. Treatment for 0-4 years of age is extrapolated from studies completed in
adults and older children
2. Albuterol and ICS are treatments of choice
3. Montelukast use is common due to formulation
4. Nebulization is commonly used
5. MDI + VHC becoming more popular due to decreased time of
administration compared to nebulization
6. Budesonide: only corticosteroid available as nebulization and is
approved for this age group
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Patient Care Process for the Management of Asthma
Collect
 Patient characteristics (eg, age, race/ethnicity, sex, pregnant)
 Patient history (eg, past medical, known triggers, psychosocial history, GERD)
 Family history (eg, asthma, allergy, atopic dermatitis)
 Home/work environment (eg, environmental, occupational, tobacco smoke, carpet/bedding, pets)
 Current medications and prior response to controller therapies (eg, ICS+/−LABA; montelukast;
LAMA; biologic therapies)
 Subjective and objective data
o Symptoms (description and frequency)
o Nocturnal awakenings
o Albuterol use frequency for symptom control
o Activity limitation
o Exacerbation frequency
o Peak expiratory flow readings
Assess
 Comorbidities (eg, allergies, rhinosinusitis, obesity, obstructive sleep apnea, GERD, smoking,
diabetes)
 Symptom frequency including exercise tolerance
 Exacerbation history (eg, oral corticosteroid use, emergency department visits, hospitalization)
 Current medications that may contribute to or worsen asthma (eg, NSAID, aspirin)
 Appropriateness and effectiveness of current medications in controlling symptoms and preventing
exacerbations
 Inhaler technique and adherence; potential barriers
 Socioeconomic barriers to obtain medications
 Adherence to nonpharm recommendations (eg, allergen avoidance, environmental control)
Plan
 Tailored environmental modifications (eg, pet removal, carpet removal, pillow and mattress
covers, exercise pretreatment, occupational exposures)
 Medication therapy regimen: dose, route, frequency, duration, and MDI spacer; specify the
continuation and discontinuation of existing therapies
 Monitoring parameters including efficacy (eg, daily symptoms, nocturnal awakenings, albuterol
use, exercise tolerance, peak expiratory flow [in selected patients]), and time frame
 Patient/family education (eg, purpose of treatment, environmental modifications, drug therapies,
inhaler technique)
 Self-monitoring of symptoms, albuterol use, peak expiratory flow (in selected patients)—where
and how to record results
 Referrals to other providers when appropriate (eg, specialist physician)
Implement
 Provide patient/family education regarding all elements of treatment plan
 Use motivational interviewing and coaching strategies to maximize adherence
 Schedule follow-up based on symptoms and medication changes
Follow-up: Monitor and Evaluate
 Determine symptom control and exacerbation outcomes
 Presence of adverse effects
 Patient adherence to treatment plan using multiple sources of information
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