BY DR MAHMOOD
• Background: Asthma is a common disorder that
primarily involves the airways. Traditionally,
asthma has been considered a disorder of
airway smooth muscle mediators and anatomic
elements of the airway mucosa. Although the
causes of asthma are separated into allergic and
nonallergic ones, considerable crossover is
observed in the features of both types of
asthma, and treatment varies little between them
• Airway inflammation is associated with airway
hyperreactivity or bronchial hyperresponsiveness (BHR),
which is defined as the inherent tendency of the airways
to narrow in response to a variety of stimuli (eg,
environmental allergens and irritants).
• Approximately 500,000 annual hospitalizations (34.6% in
persons <18 y) are because of asthma. The cost of
illness related to asthma is around $6.2 billion. Each
year, an estimated 1.81 million people (47.8% £18 y)
require treatment in the emergency department. Among
children and adolescents aged 5-17 years, asthma
accounts for a loss of 10 million school days and costs
caretakers $726.1 million because of work absence.
• Interactions between environmental and genetic factors
result in airway inflammation, which limits airflow and
leads to functional and structural changes in the airways
in the form of bronchospasm, mucosal edema, and
• Airway obstruction causes increased resistance to
airflow and decreased expiratory flow rates. These
changes lead to a decreased ability to expel air and may
result in hyperinflation. The resulting overdistention helps
maintain airway patency, thereby improving expiratory
flow; however, it also alters pulmonary mechanics and
increases the work of breathing.
• Hyperinflation compensates for the airflow
obstruction, but this compensation is limited
when the tidal volume approaches the volume of
the pulmonary dead space; the result is alveolar
hypoventilation. Uneven changes in airflow
resistance, the resulting uneven distribution of
air, and alterations in circulation from increased
intraalveolar pressure due to hyperinflation all
lead to ventilation-perfusion mismatch. Hypoxic
vasoconstriction also contributes to this
• In the early stages, when ventilation-perfusion mismatch results in
hypoxia, hypercarbia is prevented by the ready diffusion of carbon
dioxide across alveolar capillary membranes. Thus, asthmatic
patients who are in the early stages of an acute episode have
hypoxemia in the absence of carbon dioxide retention.
Hyperventilation triggered by the hypoxic drive also causes a
decrease in PaCO2.
• An increase in alveolar ventilation in the early stages of an acute
exacerbation prevents hypercarbia. With worsening obstruction and
increasing ventilation-perfusion mismatch, carbon dioxide retention
• In the early stages of an acute episode, respiratory alkalosis results
from hyperventilation. Later, the increased work of breathing,
increased oxygen consumption, and increased cardiac output result
in metabolic acidosis. Respiratory failure leads to respiratory
• New insights in the pathogenesis of asthma
suggest the role of lymphocytes. Airway
inflammation in asthma may represent a loss of
normal balance between two "opposing"
populations of Th lymphocytes. Two types of Th
lymphocytes have been characterized: Th1 and
Th2. Th1 cells produce IL-2 and IFN-a, which
are critical in cellular defense mechanisms in
response to infection. Th2, in contrast,
generates a family of cytokines (IL-4, -5, -6, -9,
and -13) that can mediate allergic inflammation.
• Evidence exists that the prevalence of
asthma is reduced in association with
certain infections (Mycobacterium
tuberculosis, measles, or hepatitis A);
exposure to other children (eg, presence
of older siblings and early enrollment in
childcare); and less frequent use of
antibiotics. Furthermore, the absence of
these lifestyle events is associated with
the persistence of a Th2 cytokine pattern.
• Under these conditions, the genetic background of the child, with a
cytokine imbalance toward Th2, will set the stage to promote the
production of IgE antibody to key environmental antigens (eg, dust
mites, cockroaches, Alternaria, and possibly cats).
• Therefore, a gene-by-environment interaction occurs in which the
susceptible host is exposed to environmental factors that are
capable of generating IgE, and sensitization occurs.
• A reciprocal interaction seems to exist between the two
subpopulations in which Th1 cytokines can inhibit Th2 generation
and vice versa.
• Allergic inflammation may be the result of an excessive expression
of Th2 cytokines. Alternately, the possibility that the loss of normal
immune balance arises from a cytokine dysregulation in which Th1
activity in asthma is diminished has been suggested in recent
• In the US: Approximately 17.3 million Americans have asthma. The
prevalence of asthma in the general population is 5%, and it has
increased 40% in the past decade. Asthma accounts for more
school absences and more hospitalizations than any other chronic
illness. In most children's hospitals in the United States, it is the
most common diagnosis at admission.
• Internationally: Worldwide, 130 million people have asthma. The
prevalence is 8-10 times higher in developed countries (eg, United
States, Great Britain, Australia, New Zealand) than in the developing
countries. In developed countries, the prevalence is higher in low
income groups in urban areas and inner cities than in other groups.
• Morbidity and mortality associated with asthma have increased over
the last 2 decades. This increase is attributed to increasing
urbanization. Despite advancements in our understanding of asthma
and the development of new therapeutic strategies, the morbidity
and mortality rates due to asthma definitely increased between 1980
• In the United States, the mortality rate due to asthma has increased
in all age, race, and sex strata.
• In the United States, the mortality rate due to asthma is more than
17 deaths per 1 million people (ie, 5000 deaths per y). From 1975-
1993, the number of deaths nearly doubled in people aged 5-14
years. In the northeastern and midwestern United States, the
highest mortality rate has been among persons aged 5-34 years.
The prevalence of asthma is higher in minority groups (eg,
blacks, Hispanics) than in other groups; however,
findings from one study suggest that much of the recent
increase in the prevalence is attributed to asthma in
About 5-8% of all black children have asthma at some
The prevalence in Hispanic children is reported to be as
high as 15%.
In blacks, the death rate is consistently higher than in
• Before puberty, the prevalence is 3 times
higher in boys than in girls.
• During adolescence, the prevalence is
equal among males and females.
• Adult-onset asthma is more common in
women than in men.
• In most children, asthma develops before
they are aged 5 years, and, in more than
half, asthma develops before they are
aged 3 years.
History: The National Asthma Education and
Prevention Program Expert Panel Report II
(EPR-2), "Guidelines for the Diagnosis and
Management of Asthma," highlights the
importance of correctly diagnosing asthma.
To establish the diagnosis of asthma, the clinician
must establish the following: (a) episodic
symptoms of airflow obstruction are present, (b)
airflow obstruction or symptoms are at least
partially reversible, and (c) alternative diagnoses
• The severity of asthma is classified as mild
intermittent, mild persistent, moderate persistent,
or severe persistent.
• These categories do not always work well in
children. First, lung function is difficult to assess
in younger children. Second, asthma that is
triggered solely by viral infections does not fit
into any category. While the symptoms may be
intermittent, they may be severe enough to
• Patients with mild intermittent disease have symptoms
fewer than 2 times a week, and pulmonary function is normal
between exacerbations. Exacerbations are brief, lasting from a few
hours to a few days. Nighttime symptoms occur less than twice a
month. The variation in peak expiratory flow (PEF) is less than 20%.
• Patients with mild persistent asthma have
symptoms more than 2 times a week but less than once a day.
Exacerbations may affect activity. Nighttime symptoms occur more
than twice a month. Pulmonary function test results (in age-
appropriate patients) demonstrate that the forced expiratory volume
in 1 second (FEV1) or PEF is less than 80% of the predicted value,
and the variation in PEF is 20-30%.
• Patients with moderate persistent asthma have
daily symptoms and use inhaled short-acting beta2-
agonists every day. Acute exacerbations in patients with
moderate persistent asthma may occur more than 2
times a week and last for days. The exacerbations affect
activity. Nocturnal symptoms occur more than once a
week. FEV1 and PEF values are 60-80% of the
predicted values, and PEF varies by more than 30%.
• Patients with severe persistent asthma have
continuous or frequent symptoms, limited physical
activity, and frequent nocturnal symptoms. FEV1 and
PEF values are less than 60% of the predicted values,
and PEF varies by more than 30%.
• Symptoms of asthma may include wheezing,
coughing, and chest tightness.
• A musical, high-pitched, whistling sound produced by airflow
turbulence is one of the most common symptoms.
• In the mildest form, wheezing is only end expiratory. As
severity increases, the wheeze lasts throughout expiration.
• In a more severe asthmatic episode, wheezing is also
present during inspiration. During a most severe episode,
wheezing may be absent because of the severe limitation of
airflow associated with airway narrowing and respiratory
– Coughing: Cough may be the only symptom of
asthma, especially in cases of exercise-induced or
nocturnal asthma. Usually, the cough is
nonproductive and nonparoxysmal. Also, coughing
may be present with wheezing.
– Children with nocturnal asthma tend to cough after
midnight, during the early hours of morning.
– Chest tightness: A history of tightness or pain in the
chest may be present with or without other symptoms
of asthma, especially in exercise-induced or nocturnal
• Other nonspecific symptoms: Infants or young
children may have history of recurrent bronchitis,
bronchiolitis, or pneumonia; a persistent cough
with colds; and/or recurrent croup or chest
• Most children with chronic or recurrent
bronchitis have asthma. Asthma is the most
common underlying diagnosis in children with
• Older children may have a history of chest
tightness and/or recurrent chest congestion.
• During an acute episode, symptoms vary according to
– Symptoms during a mild episode: Patients may be breathless
after physical activity such as walking. They can talk in
sentences and lie down, and they may be agitated.
– Symptoms during a moderate severe episode: Patients are
breathless while talking. Infants have feeding difficulties and a
softer, shorter cry.
– Symptoms during a severe episode: Patients are breathless
during rest, are not interested in feeding, sit upright, talk in words
(not sentences), and are usually agitated.
– Symptoms with imminent respiratory arrest : The child is drowsy
and confused. However, adolescents may not have these
symptoms until they are in frank respiratory failure.
• Physical: Physical examination in the absence of an acute episode
(eg, during an outpatient visit between acute episodes)
– During an outpatient visit, it is not uncommon for a patient with mild
asthma to have normal findings at physical examination. Patients with
more severe asthma are likely to have signs of chronic respiratory
distress and chronic hyperinflation.
– Signs of atopy or allergic rhinitis, such as conjunctival congestion and
inflammation, ocular shiners, a transverse crease on the nose due to
constant rubbing associated with allergic rhinitis, and pale violaceous
nasal mucosa due to allergic rhinitis, may be present.
– The anteroposterior diameter of the chest may be increased because of
hyperinflation. Hyperinflation may also cause an abdominal breathing
– Lung examination may reveal prolongation of the expiratory phase,
expiratory wheezing, coarse crackles, or unequal breath sounds.
• Physical: Physical examination during an acute episode
may reveal different findings in mild, moderately severe,
and severe episodes and in status asthmaticus with
imminent respiratory arrest.
– Mild episode: The respiratory rate is increased. Accessory
muscles of respiration are not used. The heart rate is less than
100 beats per minute. Pulsus paradoxus is not present.
Auscultation of chest reveals moderate wheezing, which is often
end expiratory. Oxyhemoglobin saturation with room air is
greater than 95%.
– Moderately severe episode: The respiratory rate is increased.
Typically, accessory muscles of respiration are used, and
suprasternal retractions are present. The heart rate is 100-120
beats per minute. Loud expiratory wheezing can be heard.
Pulsus paradoxus may be present (10-20 mm Hg).
Oxyhemoglobin saturation with room air is 91-95%.
• Physical: Severe episode: The respiratory rate is often
greater than 30 breaths per minute. Accessory muscles
of respiration are usually used, and suprasternal
retractions are commonly present. The heart rate is more
than 120 beats per minute. Loud biphasic (expiratory
and inspiratory) wheezing can be heard. Pulsus
paradoxus is often present (20-40 mm Hg).
Oxyhemoglobin saturation with room air is less than
– Status asthmaticus with imminent respiratory arrest: Paradoxical
thoracoabdominal movement occurs. Wheezing may be absent
(associated with most severe airway obstruction). Severe
hypoxemia may manifest as bradycardia. Pulsus paradoxus
noted earlier may be absent; this finding suggests respiratory
In most cases of asthma in children,
multiple triggers or precipitants exist, and
the patterns of reactivity may change with
Treatment can also change the pattern.
Certain viral infections, such as respiratory
syncytial virus (RSV) bronchiolitis in
infancy, predispose the child to asthma.
• Respiratory infections: Most commonly, these
are viral infections.
• In some patients, fungi (eg, allergic
bronchopulmonary aspergillosis), bacteria (eg,
mycoplasmata, pertussis), or parasites may be
• Most infants and young children who continue to
have a persistent wheeze and asthma have high
immunoglobulin E (IgE) production and
eosinophilic immune responses (in the airways
and in circulation) at the time of the first viral
• Allergens: In patients with asthma, 2 types of
bronchoconstrictor responses to allergens exist.
– Early asthmatic responses occur via IgE-induced
mediator release from mast cells within minutes of
exposure and last for 20-30 minutes.
– Late asthmatic responses occur 4-12 hours after
antigen exposure and result in more severe
symptoms that can last for hours and contribute to the
duration and severity of the disease.
– Allergens can be foods, household inhalants (eg,
animal allergens, molds, fungi, roach allergens, dust
mites), or seasonal outdoor allergens (eg, mold
spores, pollens, grass, trees).
• Irritants: Tobacco smoke, cold air,
chemicals, perfumes, paint odors, hair
sprays, air pollutants, and ozone can
initiate BHR by inducing inflammation.
• Weather changes: Asthma attacks can be
related to changes in atmospheric
temperature, barometric pressure, and the
quality of air (eg, humidity, allergen and
• Exercise: Exercise can trigger an early
asthmatic response. Heat and water loss from
the airways can increase the osmolarity of the
fluid lining the airways and result in mediator
release. Cooling of the airways results in
congestion and dilatation of bronchial vessels.
• During the rewarming phase after exercise, the
changes are magnified because the ambient air
breathed during recovery is warm rather than
• Gastroesophageal reflux (GER): The
presence of acid in the distal esophagus,
mediated via vagal or other neural reflexes, can
significantly increase airway resistance and
• Allergic rhinitis, sinusitis, and chronic URTI:
Inflammatory conditions of the upper airways
(eg, allergic rhinitis, sinusitis, or chronic and
persistent infections) must be treated before
asthmatic symptoms can be completely
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• Lab Studies:
• Pulmonary function test (PFT) results are not reliable in
patients younger than 5 years. In young children (3-6 y)
and older children who can't perform the conventional
spirometry maneuver, newer techniques, such as
measurement of airway resistance using impulse
oscillometry system, are being tried. Measurement of
airway resistance before and after a dose of inhaled
bronchodilator may help to diagnose bronchodilator
responsive airway obstruction.
• Spirometry: In a typical case, an obstructive defect is
present in the form of normal forced vital capacity (FVC),
reduced FEV1, and reduced forced expiratory flow over
25-75% of the FVC (FEF 25-75). The flow-volume loop
can be concave. Documentation of reversibility of airway
obstruction after bronchodilator therapy is central to the
definition of asthma. FEF 25-75 is a sensitive indicator of
obstruction and may be the only abnormality in a child
with mild disease. In an outpatient or office setting,
measurement of the peak flow rate by using a peak flow
meter can provide useful information about obstruction in
the large airways. Take care to ensure maximum patient
effort. However, a normal peak flow rate does not
necessarily mean a lack of airway obstruction.
• Plethysmography: Patients with chronic
persistent asthma may have
hyperinflation, as evidenced by an
increased total lung capacity (TLC) at
plethysmography. Increased residual
volume (RV) and functional residual
capacity (FRC) with normal TLC suggests
air trapping. Airway resistance is
increased when significant obstruction is
• Bronchial provocation tests: Bronchial
provocation tests may be performed to
diagnose BHR. These tests are performed
in specialized laboratories by specially
trained personnel to document airway
hyperresponsiveness to substances (eg,
methacholine, histamine). Increasing
doses of provocation agents are given,
and FEV1 is measured. The endpoint is a
20% decrease in FEV1 (PD20).
• Exercise challenge: In a patient with a history of exercise-induced
symptoms (eg, cough, wheeze, chest tightness or pain), the
diagnosis of asthma can be confirmed with the exercise challenge.
In a patient of appropriate age (usually >6 y), the procedure involves
baseline spirometry followed by exercise on a treadmill or bicycle to
a heart rate greater than 60% of the predicted maximum, with
monitoring of the electrocardiogram and oxyhemoglobin saturation.
The patient should be breathing cold, dry air during the exercise to
increase the yield of the study. Spirographic findings and the PEF
rate (PEFR) are determined immediately after the exercise period
and at 3, 5, 10, 15, and 20 minutes after the first measurement. The
maximal decrease in lung function is calculated by using the lowest
postexercise and highest preexercise values. The reversibility of
airway obstruction can be assessed by administering aerosolized
• Blood testing: Eosinophil counts and IgE levels
may help when allergic factors are suspected.
• Recent evidence suggests the usefulness of
measuring the fraction of exhaled nitric oxide
(FeNO) as a noninvasive marker of airway
inflammation, in order to adjust the dose of
inhaled corticosteroids treatment. Currently
FeNO measurement, due to high cost of
equipment, is used primarily as a research tool.
• Chest radiography: Include chest radiography in the
initial workup if the asthma does not respond to therapy
as expected. In addition to typical findings of
hyperinflation and increased bronchial markings, a chest
radiograph may reveal evidence of parenchymal
disease, atelectasis, pneumonia, congenital anomaly, or
a foreign body. In a patient with an acute asthmatic
episode that responds poorly to therapy, a chest
radiograph helps in the diagnosis of complications such
as pneumothorax or pneumomediastinum.
• Paranasal sinus radiography or CT scanning:
Consider using these to rule out sinusitis.
• Asthma is an inflammatory disease characterized by the
recruitment of inflammatory cells, vascular congestion,
increased vascular permeability, increased tissue
volume, and the presence of an exudate. Eosinophilic
infiltration, a universal finding, is considered a major
marker of the inflammatory activity of the disease.
Histologic evaluations of the airways in a typical patient
reveal infiltration with inflammatory cells, narrowing of
airway lumina, bronchial and bronchiolar epithelial
denudation, and mucus plugs. Additionally, a patient with
severe asthma may have a markedly thickened
basement membrane and airway remodeling in the form
of subepithelial fibrosis and smooth muscle hypertrophy
• Medical Care: The goals of asthma therapy are
to prevent chronic and troublesome symptoms,
maintain normal or near-normal pulmonary
function, maintain normal physical activity levels
(including exercise), prevent recurrent
exacerbations of asthma, and minimize the need
for emergency department visits or
hospitalizations, provide optimal
pharmacotherapy with minimal or no adverse
effects, and meet the family's expectations for
• Mild intermittent asthma
• Long-term control: Usually, no daily medication
• Quick relief: Short-acting bronchodilators in the
form of inhaled beta2-agonists should be used
as needed for symptom control. The use of
short-acting inhaled beta2-agonists more than 2
times a week may indicate the need to initiate
long-term control therapy.
• Mild persistent asthma
• Long-term control: Anti-inflammatory treatment in the
form of low-dose inhaled corticosteroids or nonsteroidal
agents (eg, cromolyn, nedocromil) is preferred. Some
evidence suggests that leukotriene antagonists may be
useful as first-line therapy in children. Recently, the use
of montelukast was approved for children aged 2 years
• Quick relief: Short-acting bronchodilators in the form of
inhaled beta2-agonists should be used as needed for
symptom control. Use of short-acting inhaled beta2-
agonists on a daily basis or increasing use indicates the
need for additional long-term therapy.
• Moderate persistent asthma
– Long-term control: Daily anti-inflammatory treatment
in the form of inhaled corticosteroids (medium dose)
is preferred. Otherwise, low- or medium-dose inhaled
corticosteroids combined with a long-acting
bronchodilator or leukotriene antagonist can be used,
especially for the control of nocturnal or exercise-
induced asthmatic symptoms.
– Quick relief: Short-acting bronchodilators in the form
of inhaled beta2-agonists should be used as needed
for symptom control. The use of short-acting inhaled
beta2-agonists on a daily basis or increasing use
indicates the need for additional long-term therapy.
• Severe persistent asthma
• Long-term control
– Daily anti-inflammatory treatment in the form of
inhaled corticosteroids (high dose) is preferred. Other
medications, such as a long-acting bronchodilator
leukotriene antagonist or theophylline, can be added.
– Quick relief: Short-acting bronchodilators in the form
of inhaled beta2-agonists should be used as needed
for symptom control. The use of short-acting inhaled
beta2-agonists on a daily basis or increasing use
indicates the need for additional long-term therapy.
• Acute severe asthmatic episode (status asthmaticus)
• Treatment goals are the following:
– Correction of significant hypoxemia with supplemental oxygen: In
severe cases, alveolar hypoventilation requires mechanically
– Rapid reversal of airflow obstruction by using repeated or
continuous administration of an inhaled beta2-agonist: Early
administration of systemic corticosteroids (eg, oral prednisone or
intravenous methylprednisolone) is suggested in children with
asthma that fails to respond promptly and completely to inhaled
– Reduction in the likelihood of recurrence of severe airflow
obstruction by intensifying therapy: Often, a short course of
systemic corticosteroids is helpful.
• When a patient has major allergies to
dietary products, avoidance of particular
foods may help. In the absence of specific
food allergies, dietary changes are not
necessary. Unless compelling evidence for
a specific allergy exists, milk products do
not have to be avoided.
• Albuterol sulfate (Proventil, Ventolin) -- This beta2-
agonist is the most commonly used bronchodilator.
Albuterol is used as needed, and prolonged use may be
associated with tachyphylaxis due to beta2-receptor
downregulation and receptor hyposensitivity.
• Oral inhaler: 90 mcg per inhalation, 2 inhalations q4-6h;
more inhalations may be used in severe, acute episodes;
more frequent dosing can be used to treat acute
• Nebulizer: 2.5 mg via nebulization of 0.5% solution in 2-
3 mL of sodium chloride solution q4-6h
• Pirbuterol acetate (Maxair) -- Available
as a breath-actuated or ordinary inhaler.
The ease of administration with the breath-
actuated device makes it an attractive
choice in the treatment of acute symptoms
in younger children who otherwise cannot
use an MDI. Strength is 200 mcg per
• Levalbuterol (Xopenex) -- Nonracemic form of
albuterol, levalbuterol (R isomer) is effective in
smaller doses and is reported to have fewer
adverse effects (eg, tachycardia, hyperglycemia,
hypokalemia). The dose may be doubled in
acute severe episodes when even a slight
increase in the bronchodilator response may
make a big difference in the management
strategy (eg, in avoiding patient ventilation). 0.63
mg by nebulizer q8h
• Drug Category: Long-acting beta2-agonist -- Long-
acting bronchodilators are not used for the treatment of
acute bronchospasm. They are used for the preventive
treatment of nocturnal asthma or exercise-induced
• Currently, 2 long-acting beta2-agonists are available in
the United States: salmeterol (Serevent) and
formoterol (Foradil). Salmeterol is discussed below.
Salmeterol is available as a combination of salmeterol
and fluticasone (Advair).
• Pediatric Dose<12 years: Not established
>12 years: 1 inhalation of inhalation powder (50 mcg)
q12h; data in children are limited .
• Drug Category: Methylxanthines --
These agents are Theophylline (Theo-24,
Theolair, Theo-Dur, Slo-bid) -- Available in
short- and long-acting formulations.
Because of the need to monitor the drug
levels , this agent is used infrequently.
• Initial dose: 10 mg/kg PO sustained-
release tablets and capsules; not to
exceed 300 mg/d
First dose adjustment: 13 mg/kg PO; not
to exceed 450 mg/d
Second dose adjustment: 16 mg/kg PO;
not to exceed 600 mg/d
• Drug Category: Mast cell stabilizers -- These
agents are Cromolyn sodium (Intal) and
nedocromil sodium (Tilade) .
• ,These nonsteroidal anti-inflammatory agents
are used primarily in preventive therapy.
• Adult DoseCromolyn: 20 mg in 2 mL nebulizer
Nedocromil: 2-4 inhalations bid/tid; 1.75
• Pediatric DoseCromolyn: Administer as in
Nedocromil: Administer as in adults
Drug Category: Corticosteroids --
Steroids are the most potent anti-
inflammatory agents. Inhaled steroids
include beclomethasone, triamcinolone,
flunisolide, fluticasone, and
• Beclomethasone (Beclovent, Vanceril, QVAR)
-- Inhibits bronchoconstriction mechanisms;
causes direct smooth muscle relaxation; and
may decrease the number and activity of
inflammatory cells, which, in turn, decreases
• Pediatric Dose,Low dose: 84-336 mcg/d (42
mcg/oral inhalation, 2-8 inhalations q24h)
Medium dose: 336-672 mcg/d (42 mcg/oral
inhalations, 8-16 inhalations q24h)
High dose: >672 mcg/d (42 mcg/oral inhalation,
>16 inhalations q24h)
• Fluticasone (Flovent) -- Has extremely potent
vasoconstrictive and anti-inflammatory activity.
• Pediatric Dose;
• Low dose: 88-176 mcg/d (44 mcg/oral inhalation, 2-4
• Medium dose: 176-440 mcg/d (110 mcg/oral inhalation,
2-4 inhalations q24h)
• High dose: >440 mcg/d (110 mcg/oral inhalation, >4
inhalations q24h or 220 mcg/oral inhalation, 2 inhalations
• Budesonide (Pulmicort Turbuhaler or
Respules) -- Has extremely potent
vasoconstrictive and anti-inflammatory activity.
• Pediatric Dose:
Low dose: 100-200 mcg/d (1 inhalation q24h)
Medium dose: 200-400 mcg/d (1-2 inhalation
High dose: >400 mcg/d (>2 inhalations q24h)
Nebulizer (inhalation susp): 0.25-0.5 mg bid; not
to exceed 1 mg/d
• Drug Category: Systemic corticosteroids -- These agents are
used for short courses (3-10 d) to gain prompt control of
inadequately controlled acute asthmatic episodes. They are also
used for long-term prevention of symptoms in severe persistent
asthma as well as for suppression, control, and reversal of
inflammation. Frequent and repetitive use of beta2-agonists has
been associated with beta2-receptor subsensitivity and
downregulation; these processes are reversed with corticosteroids.
• Higher-dose corticosteroids have no advantage in severe asthma
exacerbations, and intravenous administration has no advantage
over oral therapy. The usual regimen is to continue frequent multiple
daily dosing until the FEV1 or PEF is 50% of the predicted or
personal best values; then, the dose is changed to twice daily. This
usually occurs within 48 hours.
• Drug Category: Systemic
corticosteroids -- Prednisone
(Deltasone, Orasone) and prednisolone
(Pediapred, Prelone, Orapred) --
Immunosuppressants for the treatment of
autoimmune disorders; may decrease
inflammation by reversing increased
capillary permeability and suppressing
PMN activity. 1-2 mg/kg/d PO for 3-10 d;
not to exceed 60-80 mg/d
Drug Category: Systemic corticosteroids
-- Methylprednisolone (Solu-Medrol) --
May decrease inflammation by reversing
increased capillary permeability and
suppressing PMN activity. 1 mg/kg IV q6h
• Drug Category: Leukotriene modifier --
Knowledge that leukotrienes cause
bronchospasm, increased vascular
permeability, mucosal edema, and
inflammatory cell infiltration leads to the
concept of modifying their action by using
pharmacologic agents. These are either 5-
lipoxygenase inhibitors or leukotriene-
• Drug Category: Leukotriene modifier :
• Zafirlukast (Accolate) -- Selective
competitive inhibitor of LTD4, LTE4
• Pediatric Dose
• 5-11 years: 10 mg PO bid
• >12 years: Administer as in adults
• Montelukast (Singulair) –
• The advantages are that it is chewable, it has a
once-a-day dosing, and it has no significant
• Pediatric Dose
• 12-23 months: 1 packet of 4 mg oral granules
• 2-6 years: 4 mg PO hs
• 6-14 years: 5 mg PO hs
• >14 years: Administer as in adults
• Drug Category: Monoclonal antibody -- These
agents bind selectively to human IgE on the
surface of mast cells and basophils.
Omalizumab (Xolair) -- Recombinant, DNA-
derived, humanized IgG monoclonal antibody
that binds selectively to human IgE on surface of
mast cells and basophils. Reduces mediator
release, which promotes allergic response.
Pediatric Dose<12 years: Not established
>12 years: Administer as in adults
• Further Inpatient Care:
• Admit patients for treatment of acute severe
episodes if they are unresponsive to outpatient
care (eg, they have worsening bronchospasm,
hypoxia, evidence of respiratory failure).
• Once the patient is admitted, further
investigations (eg, PFTs, allergy testing, and
investigations to rule out other associated
conditions and complications) can be performed.
• Regular follow-up visits (1-6-mo intervals) are essential
to ensure control and appropriate therapeutic
• Outpatient visits should include the following:
– Interval history of asthmatic complaints, including history of
acute episodes (eg, severity, measures and treatment taken,
response to therapy)
– History of nocturnal symptoms
– History of symptoms with exercise and exercise tolerance
– Review of medications, including use of rescue medications
– Review of home-monitoring data (eg, symptom diary, peak flow
meter readings, daily treatments)
• Patient evaluation should include the following:
– Assessment for signs of bronchospasm and
– Evaluation of associated conditions (eg, allergic
– Pulmonary function testing (in appropriate age group)
• Address issues of treatment adherence and
avoidance of environmental triggers and
• Any patient with a high risk of asthma should be referred
to a specialist. The following may suggest a high risk:
– History of sudden severe exacerbations
– History of prior intubation for asthma
– Admission to an ICU because of asthma
– Two or more hospitalizations for asthma in the past year
– Three or more emergency department visits for asthma in the
– Hospitalization or an emergency department visit for asthma
within the past month
– Use of 2 or more canisters of inhaled short-acting beta2-agonists
• The goal of long-term therapy is to prevent
• The patient should avoid exposure to
environmental allergens and irritants that
are identified during the evaluation.
• Pneumothorax status asthmaticus with
• Fixed (nonreversible) airway obstruction
• Of infants who wheeze with URTIs, 60% are asymptomatic by age 6
years; however, children who have asthma (recurrent symptoms
continuing at age 6 y) have airway reactivity later in childhood.
• Some findings suggest a poor prognosis if asthma develops in
children younger than 3 years, unless it occurs solely in association
with viral infections.
• Individuals who have asthma during childhood have significantly
lower FEV1 and airway reactivity and more persistent
bronchospastic symptoms than those with infection-associated
• Children with mild asthma who are asymptomatic between attacks
are likely to improve and be symptom-free later in life.
• Children with asthma appear to have less severe symptoms as they
enter adolescence, but half of these children continue to have
• Patient and parent education should include instructions on how to use
medications and devices (eg, spacers, nebulizers, MDIs). The patient's MDI
technique should be assessed on every visit.
• Discuss the management plan, which includes instructions about the use of
medications, precautions with drug and/or device usage, monitoring
symptoms and their severity (peak flow meter reading), and identifying
potential adverse effects and necessary actions.
• Write and discuss in detail a rescue plan for an acute episode. This plan
should include instructions for identifying signs of an acute attack, using
rescue medications, monitoring, and contacting the asthma care team.
• Parents should understand that asthma is a chronic disorder with acute
exacerbations; hence, continuity of management with active participation by
the patient and/or parents and interaction with asthma care medical
personnel is important.
• Emphasize the importance of compliance with and adherence to treatment.
• Incorporate the concept of expecting full control of
symptoms, including nocturnal and exercise-induced
symptoms, in the management plans and goals (for all
but the most severely affected patients).
• Avoid unnecessary restrictions in the lifestyle of the child
or family. Expect the child to participate in recreational
activities and sports and to attend school as usual.
• For excellent patient education resources, see
eMedicine's Asthma Center. Also, visit eMedicine's
patient education articles Asthma, Asthma FAQs,
Understanding Asthma Medications, Asthma in Children,
and Asthma in School Children: Educational Slides.
• Medical/Legal Pitfalls:
• Failure to recognize the severity of an acute
severe episode (ie, status asthmaticus) and to
initiate aggressive management (eg, intubation
and ventilation) can lead to fatal complications
such as respiratory failure and even death.
• Failure to diagnose pneumothorax can lead to
• Identification of associated or complicating
conditions (eg, allergic rhinitis or sinusitis) is
important for comprehensive management.
• Special Concerns:
• In children, long-term use of high-dose steroids
(systemic or inhaled) may lead to adverse
effects, including growth failure. Recent data
from the Childhood Asthma Management
Program (CAMP) study and results of the long-
term use of inhaled steroids (budesonide)
suggest that the long-term use of inhaled
steroids has no sustained adverse effect on
growth in children.