ASTHMA: DIAGNOSIS AND
MANAGEMENT
Asthma Clinical Quality Team
NMCSD
2004
Burden of Disease
General
• 26 million adults and children in the USA have received a
diagnosis of asthma sometime during their lifetime
– 8.6 million were under 18 years of age
• 10.6 million individuals experienced an asthmatic episode
during the previous 12 months
– 3.8 million were children
• Hospitalizations increased 6.7% between
1988 and 1997
National Center for Health Statistics. Raw Data from the National Health Interview Survey, US,
1997-1998. (Analysis by the American Lung Association Best Practices Division, Using SPSS
and SUDAAN software)
Burden of Disease
Death Rate, 1979 to 1997
1.8
1.6
Deaths
per
100,000
Population
Female
Male + Female
Male
1.4
1.2
1
0.8
'79 '80 '81 '82 '83 '84 '85 '86 '87 '88 '89 '90 '91 '92 '93 '94 '95 '96 '97
Year
National Center for Health Statistics. Raw Data from the National Health Interview Survey, US,
1997-1998. (Analysis by the American Lung Association Best Practices Division, Using SPSS and
SUDAAN software)
Asthma definition
• Inflammatory airways disorder involving mast
cells, eosinophils, PMN’s, epithelial cells,
macrophages and T cells.
• This inflammation leads to clinical sequelae of
episodic bronchospasm (wheezing),
breathlessness, chest tightness and cough
• Episodes are usually associated with variable
airflow obstruction that is reversible
Pathophysiology (inflammation)
• Allergens (or other inciting agents) in the
airway trigger local inflammation which exists
chronically (multiple cell types)
• Leads to airway hyperresponsiveness to
various precipitants (cold air, exercise).
• In addition to smooth muscle spasm, see
mucosal edema and mucus hypersecretion of
the airways
Clinical presentation
• Episodic wheezing, shortness of breath,
coughing paroxysms
• Often related to specific triggers (cold air,
exercise, post-viral URI)
• Patients will sometimes relate a history of
frequent “bronchitis” as a child
• Often have a personal or family history of
atopic disorders (AR, asthma,eczema)
Diagnosing asthma
• Asthma is a clinical diagnosis. Historical and
objective data must be combined to arrive at
the diagnosis.
• History: Cough, recurrent wheeze, SOB.
Symptoms worsen with triggers such as
allergen exposure, exercise, pollutants. Sx
occur or worsen at night, resulting in
awakening.
• Physical exam: wheezing is not always
asthma; asthma pts don’t always wheeze.
Diagnosis
• Objective lung studies: To document clinically
suspected reversible airways obstruction,
spirometry is used. There are 3 ways to
document reversible obstruction.
• (1) Spirometry, pre- and post- inhaled
bronchodilator therapy (eg, albuterol)
• (2) Spirometry before and after a course of
sytemic or inhaled steroids.
• (3) Bronchoprovocation studies
Spirometry diagnosis
• Classically, see a low FEV1 (amount of air
expired in one second with maximal effort)
with a decreased FEV1/FVC ratio (FVC is a
rough measure of lung capacity) in an
asthmatic with active disease.
• To document asthma, must see a greater
than or equal to 12% increase in FEV1 post
bronchodilator or after a course of steroids.
• Failure to see 12% increase or greater does
not mean asthma excluded
Bronchoprovocation
• Bronchoprovocation studies include cold air
challenge, histamine challenge, exercise
challenge, and methacholine challenge.
• All of these studies attempt to demonstrate the
airway hyperresponsiveness seen in asthma.
Useful in individuals where the diagnosis of
asthma is uncertain.
• Methacholine challenge done by inhaling
increasing doses of the agent, then performing
spirometry. Asthmatics will have a decline in
their FEV1 and FEV1/FVC ratio after this
challenge.
Methacholine challenge
• Looking for a drop of 20% or greater in FEV1
from baseline as a positive test. The dose
that causes this drop is called the PD20.
• The lower the PD20 dose, the more
supportive the result is of asthma diagnosis.
Generally, a PD20 of 8 mg/ml or less is
considered positive. A higher PD20 could
represent a false positive.
• A negative full dose challenge is strongly
suggestive that the patient is not asthmatic.
Positive methacholine challenge
at 5mg/ml dose
Precipitating/sustaining factors
for asthma
•
•
•
•
•
Allergen exposure
Exercise
Viral URI’s
Rhinosinusitis
GERD
Viral respiratory infections
• The vast majority (~80%) of acute asthma
exacerbations are secondary to viruses
• Most common agent is rhinovirus
• Mechanism is poorly understood. Most
plausible is that existing airway
inflammation is up-regulated.
• Frequent handwashing and routine
influenza vaccination can prevent viralinduced asthma exacerbations.
Allergen exposure
• Estimated that 50% or so of asthmatics are
atopic. In these individuals, allergens are
believed to be a major driving factor in chronic
inflammation.
• Most significant are indoor allergens dust mite
and cat. Also important in some environments is
cockroach. Outdoor aller-gens can also sustain
airway inflammation.
• Elimination of indoor allergens mentioned above
can result in disease improvement.
Exercise-induced bronchospasm
• Probably not a distinct disease entity, but
rather a subset of asthma.
• Those with symptoms exclusively during
exercise are probably mild asthmatics who
only get symptoms at the extremes of
exertion.
• Classically, see worst symptoms and airway
obstruction 5 to 10 minutes after exercise.
• Possibly due to cool,dry air inspiration that
results in drying/irritation of bronchial mucosa
GERD and asthma
• GERD has been proposed by many authors as a
chronic and acute driving factor for asthma, likely via
a vagal reflex.
• Role is controversial, but evidence mounting:
perfusion of acid into the esophagus leads to an
increase in cough response and increased airways
hyperresponsivess.
• Studies show medical treatment with PPI can
improve asthma symptom control, but not objective
lung studies (PEF,FEV1). Some studies suggest a
70% improvement in symptoms.
• Fundoplication may provide even better results than
medical management.
GERD and asthma
• Spivak et al (1999) looked at 39 pts who had
fundoplication for GERD aggravating asthma.
Sx improved overall, and 7 of 9 steroid
dependent asthmatics able to d/c steroids
• GERD is probably worth investigating in
asthmatic who is on multiple meds, poorly
controlled, and has no other driving factors.
• Certainly, significant asthmatic with reflux
symptoms should be started on empiric
therapy
Rhinosinusitis and asthma
• NIH guidelines recognize an association
between asthma and rhinosinsitis that was
first noted hundreds of yrs ago
• By unkown mechanism (neural?),
inflammation of nose and sinuses appears to
drive or worsen asthma in some individuals
• Most marked in those with opacified/ infected
sinuses. Curing the sinus/nasal disease
often markedly improves the asthma.
Rhinosinusitis and asthma
• Rhinitis/asthma link supported by studies which show
lower airway dynamics (FEV1, methacholine
challenge) are affected by nasal allergen challenge.
Also, exhaled lower airway NO (a marker of lower
airway inflammation) is decreased by nasal steroid
use.
• 2002 Harvard Pilgrim study (Adams et al) of all
asthmatics in a managed care organization over a 5
year period. Regular use of nasal steroids reduced
ED visits for asthma by 30-50%, depending on rate
of use.
Asthma classification
• NIH guidelines classify asthmatics into 4
groups based on severity
• Classification is important for physician
communication and so appropriate therapy
can be used based on published guidelines.
• NHLBI/NIH guidelines for the diagnosis and
management of asthma available online:
www.nhlbi.nih.gov/guidelines/asthma
Classification of Asthma Severity:
Clinical Features Before Treatment
Step 4
Days With
Symptoms
Continuous
Nights With
Symptoms
Frequent
PEF or
FEV1
60%
PEF
Variability
30%
Severe
Persistent
Step 3
Daily
5/month
60%-<80%
30%
Moderate
Persistent
Step 2
3-6/week
3-4/month
80%
20-30%
Mild
Persistent
Step 1
2/week
2/month
80%
Mild
Intermittent
Footnote: The patient’s step is determined by the most severe feature.
20%
Stepwise Approach to Therapy for
Adults and Children >Age 5:
Maintaining Control
STEP 4
Multiple long-term-control
medications, include
oral corticosteroids
STEP 3
> 1 Long-term-control
medications
STEP 2
1 Long-term-control medication:
anti-inflammatory
STEP 1
Quick-relief medication: PRN
Step down if
possible

Step up if
necessary
 Patient education
and
environmental
control at every
step
 Recommend
referral to
specialist at
Step 4; consider
referral at Step 3

Asthma therapy
• One goal of asthma therapy is to prevent
symptoms that limit activity and/or result in
missed school/work days
• Avoid hospitalizations/ER visits
• Avoid asthma deaths (3,000 - 5,000/year)
• Another goal: Prevent “unchecked”
inflammation that may lead to airway
remodeling and irreversible damage
Asthma therapy
• Obvious triggers, drivers of the airway
inflammation should be treated and/or
avoided if possible.
• Treat sinusitis, GERD.
• Full physical activity should not be
discouraged.
• Allergen avoidance may be useful adjunct to
meds (for identified indoor allergens).
Pharmacotherapy
(long-term control meds)
•
•
•
•
Inhaled steroids
Long-acting beta agonists
Anti-leukotriene agents
Theophylline
Mild intermittent
• NIH guidelines dictate that patients may be
treated with prn bronchodilators as long as
symptoms continue to occur two or less
times weekly and spirometry is normal (at
baseline)
Mild persistent
• Most easily remembered as patients with
symptoms more than twice weekly (but not
daily) who have normal baseline
spirometry
• Require anti-inflammatory medication
• Vast majority of experts/clinicians use
inhaled steroids as first line.
• Some advocate use of anti-leukotrienes
Mild persistent
• Concern is that anti-LT drugs only attack one
arm of the inflammatory process, while
inhaled steroids have broader activity. So
steroids preferred.
• Low dose inhaled steroids (e.g., Flovent 44
mcg/puff 2 puffs BID or Azmacort 4 puffs BID)
usually sufficient in this group.
• If not controlled with the above, pt is behaving
more like a moderate persistent patient
Moderate persistent
• Patient with daily symptoms/need for
albuterol, or baseline FEV1 60-80% pred
• Three choices at this point:
• (1) Going from low to medium dose steroids
(eg, Flovent 110 2 puffs bid)
• (2) Add a long-acting bronchodilator
• (3) Add an anti-leukotriene agent (eg,
Singulair)
All are reasonable options. Which is correct?
Moderate persistent
• Studies suggest that if pt not controlled on
this, adding Serevent is the next best option
(Busse et al, 1999: Kelsen et al, 1999). This
is reflected in recently updated NIH
guidelines, where the addition of a longacting B-agonist is recommended prior to
using higher dose inhaled steroids or
leukotriene receptor antagonists.
• Therefore, option 2 is the most correct choice.
Long-acting beta agonists
(Serevent)
• If needed, these agents should only be used
in conjunction with an anti-inflammatory
medication (act synergistically).
• Serevent is available in combination with
Flovent as Advair (100/50, 250/50, or
500/50).
• Therapy with Serevent alone may just be
bronchodilating without any effect on the
underlying inflammation. This can result in
undesirable clinical outcomes.
Severe persistent
• These are pts with contiual sx, baseline FEV1
under 60%, frequent nighttime awakenings,
multiple hospitalizations and intubations.
• Need high dose inhaled steroid,Serevent, and
possibly Singulair as well.
• Theophylline, and finally oral steroid may be
needed to fully control such patients.
• A detailed investigation for causes of difficult
to treat asthma should be undertaken
Monitoring asthma therapy
• Patient self-reporting of asthma symptoms is
variably reliable in assessing control.
• Important sx: exercise tolerance, nighttime
awakenings, prn albuterol use, missed
school/work days
• NIH guidelines suggest that objective monitoring
(periodic peak flow and/or spirometry) should be
performed at regular intervals. This data should
be combined with patient symptoms to direct
therapy.
Monitoring asthma
• Spirometry should be repeated at least every 1 to
2 years to assess the maintenance of airway
function (NIH guidelines).
• Peak flow meter use is recommended for
moderate and severe asthmatics, especially
those who perceive obstruction poorly.
• Patients should be given instructions on how to
proceed depending on peak flow results (asthma
action plan). Written asthma action plans
specifically have been shown to improve
outcomes.
The Effect of a Peak Flow-Base
Action Plan
• 150 asthmatics randomized to 1 of 3 groups
– No action plan
– Symptom-based plan
– Peak flow-based plan
• All received asthma education
No plan
# urgent care visits
#admissions
55
12
PF plan
5
2
Symptom
plan
45
6
Cowie RL, et al. Chest 1997;112:1534-38
Peak Flow & Symptom-Based
Home Action Plan
Managing exacerbations in ED
• Supplemental O2. Repeat albuterol/atrovent nebs (3). The
practice of adding atrovent to albuterol improves outcomes
• If exacerbation initially seems severe, or pt not responding,
systemic steroids are indicated (several hour effect time).
• Magnesium use is controversial – little evidence of effect except
possibly in very severe exacerbations
• If impending or actual respiratory failure occurs, pt may require
intubation first.
• If patient fails to improve (doesn’t reach 70% of predicted or
best PEF as a general guideline), hospitalization needed. High
dose systemic steroids and frequent nebs the usual treatment
course, with slow taper of steroids as an outpatient.