Asthma

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For other uses, see Asthma (disambiguation).
Asthma
Classification and external resources

Peak flow meters are used to measure one's peak expiratory

flow rate
ICD-10 J45.
ICD-9 493
OMIM 600807
DiseasesDB 1006
MedlinePlus 000141
article/806890 article/796274 article/800119
eMedicine article/137501 article/296301 article/1000997
article/353436 article/88849
MeSH C08.127.108

Asthma, from the Greek Άσθμα (ásthma), meaning gasp, is a common chronic inflammatory
disease of the airways characterized by variable and recurring symptoms, airflow obstruction,
and bronchospasm.[1] Symptoms include wheezing, coughing, chest tightness, and shortness of
breath.[2]

Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as
salbutamol).[3] Symptoms can be prevented by avoiding triggers, such as allergens[4] and irritants,
and by inhaling corticosteroids.[5] Leukotriene antagonists are less effective than corticosteroids
and thus less preferred.[6]
The prevalence of asthma has increased significantly since the 1970s. As of 2009, 300 million
people were affected worldwide.[7] In 2009 asthma caused 250,000 deaths,[7] although generally
with treatment, prognosis is good.

Contents
[hide]

• 1 Classification
o 1.1 Brittle asthma
o 1.2 Asthma attack
o 1.3 Status asthmaticus
• 2 Signs and symptoms
• 3 Cause
o 3.1 Environmental
o 3.2 Genetic
o 3.3 Gene–environment interactions
o 3.4 Exacerbation
• 4 Risk factors
o 4.1 Hygiene hypothesis
o 4.2 Population disparities
o 4.3 Socioeconomic factors
o 4.4 Athletics
o 4.5 Occupation
• 5 Diagnosis
o 5.1 Differential diagnosis
• 6 Prevention
• 7 Management
o 7.1 Lifestyle modification
o 7.2 Medications
o 7.3 Other
o 7.4 Complementary medicine
• 8 Prognosis
• 9 Epidemiology
o 9.1 Increasing frequency
• 10 History
• 11 References

• 12 External links

[edit] Classification
Clinical classification of severity[8]
Symptom Nighttime %FEV1 of FEV1
Severity
frequency symptoms predicted Variability
 Intermittent <1 per week ≤2 per month ≥80% <20%
>1 per week
Mild persistent >2 per month ≥80% 20–30%
but <1 per day
Moderate persistent Daily >1 per week 60–80% >30%
Severe persistent Daily Frequent <60% >30%

Asthma is clinically classified according to the frequency of symptoms, forced expiratory

volume in 1 second (FEV1), and peak expiratory flow rate.[8] Asthma may also be classified as
atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by
allergens (atopic) or not (non-atopic).[9]

While asthma is classified based on severity, at the moment there is no clear method for
classifying different subgroups of asthma beyond this system.[10] Within the classifications
described above, although the cases of asthma respond to the same treatment differs, thus it is
clear that the cases within a classification have significant differences.[10] Finding ways to
identify subgroups that respond well to different types of treatments is a current critical goal of
asthma research.[10]

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic

obstructive pulmonary disease as this term refers specifically to combinations of bronchiectasis,
chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is
usually reversible; however, if left untreated, asthma can result in chronic inflammation of the
lungs and irreversible obstruction.[11] In contrast to emphysema, asthma affects the bronchi, not
the alveoli.[12]

[edit] Brittle asthma

Main article: Brittle asthma

Brittle asthma is a term used to describe two types of asthma, distinguishable by recurrent,
severe attacks.[13] Type 1 brittle asthma refers to disease with wide peak flow variability, despite
intense medication. Type 2 brittle asthma describes background well-controlled asthma, with
sudden severe exacerbations.[13]

[edit] Asthma attack

An acute asthma exacerbation is commonly referred to as an asthma attack. The classic

symptoms are shortness of breath, wheezing, and chest tightness.[14] While these are the primary
symptom of asthma,[15] some people present primarily with coughing, and in severe cases, air
motion may be significantly impaired such that no wheezing is heard.[13]

Signs which occur during an asthma attack include the use of accessory muscles of respiration
(sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse
that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.
[16]
, a blue color of the skin and nails may occur from lack of oxygen.[17]
[edit] Status asthmaticus

Main article: Status asthmaticus

Status asthmaticus is an acute exacerbation of asthma that does not respond to standard
treatments of bronchodilators and steroids.

[edit] Signs and symptoms

Wheezing

The sound of wheezing as heard with a stethoscope.

Problems listening to this file? See media help.

Common symptoms of asthma include wheezing, shortness of breath, chest tightness and
coughing. Symptoms are often worse at night or in the early morning, or in response to exercise
or cold air.[18] Some people with asthma only rarely experience symptoms, usually in response to
triggers, where as other may have marked persistent airflow obstruction.[19]

[edit] Cause
Asthma is caused by environmental and genetic factors.[20] These factors influence how severe
asthma is and how well it responds to medication.[21] The interaction is complex and not fully
understood.[22]

[edit] Environmental

Many environmental risk factors have been associated with asthma development and morbidity
in children.

Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high
risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[23] Low air
quality, from traffic pollution or high ozone levels,[24] has been repeatedly associated with
increased asthma morbidity and has a suggested association with asthma development that needs
further research.[25][26]

Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and
childhood asthma.[27] This research finds that both the occurrence of the disease and exacerbation
of childhood asthma are affected by outdoor air pollutants.

Viral respiratory infections are not only one of the leading triggers of an exacerbation but may
increase one's risk of developing asthma.[28]
Psychological stress has long been suspected of being an asthma trigger, but only in recent
decades has convincing scientific evidence substantiated this hypothesis. Rather than stress
directly causing the asthma symptoms, it is thought that stress modulates the immune system to
increase the magnitude of the airway inflammatory response to allergens and irritants.[25][29]

Antibiotic use early in life has been linked to development of asthma in several examples; it is
thought that antibiotics make children who are predisposed to atopic immune responses
susceptible to development of asthma because they modify gut flora, and thus the immune
system (as described by the hygiene hypothesis).[30] The hygiene hypothesis (see below) is a
hypothesis about the cause of asthma and other allergic disease, and is supported by
epidemiologic data for asthma.[31] All of these things may negatively affect exposure to beneficial
bacteria and other immune system modulators that are important during development, and thus
may cause an increased risk for asthma and allergy.

Caesarean sections have been associated with asthma, possibly because of modifications to the
immune system (as described by the hygiene hypothesis).[32]

Respiratory infections such as rhinovirus, Chlamydia pneumoniae and Bordetella pertussis are
correlated with asthma exacerbations.[33]

[edit] Genetic

Over 100 genes have been associated with asthma in at least one genetic association study.[34]
However, such studies must be repeated to ensure the findings are not due to chance. Through
the end of 2005, 25 genes had been associated with asthma in six or more separate populations:
[34]

• GSTM1 • LTA • STAT6 • IL4 • HLA-DQB1

• IL10 • GRPA • NOS1 • IL13 • TNF
• CTLA-4 • NOD1 • CCL5 • CD14 • FCER1B
• SPINK5 • CC16 • TBXA2R • ADRB2 (β-2 • IL4R
adrenergic
• LTC4S • GSTP1 • TGFB1 receptor) • ADAM33

• HLA-DRB1

Many of these genes are related to the immune system or to modulating inflammation. However,
even among this list of highly replicated genes associated with asthma, the results have not been
consistent among all of the populations that have been tested.[34] This indicates that these genes
are not associated with asthma under every condition, and that researchers need to do further
investigation to figure out the complex interactions that cause asthma. One theory is that asthma
is a collection of several diseases, and that genes might have a role in only subsets of asthma.
[citation needed]
For example, one group of genetic differences (single nucleotide polymorphisms in
17q21) was associated with asthma that develops in childhood.[35]

[edit] Gene–environment interactions

 CD14-endotoxin interaction based on CD14 SNP C-159T[36]
Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk

Research suggests that some genetic variants may only cause asthma when they are combined
with specific environmental exposures, and otherwise may not be risk factors for asthma.[20]

The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to
endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction
that is associated with asthma. Endotoxin exposure varies from person to person and can come
from several environmental sources, including environmental tobacco smoke, dogs, and farms.
Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-
159T and level of endotoxin exposure.[36]

[edit] Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an
episode of acute asthma. Different asthmatic individuals react differently to various factors.[37]
However, most individuals can develop severe exacerbation of asthma from several triggering
agents.[37][38]

Home factors that can lead to exacerbation include dust, house mites, animal dander (especially
cat and dog hair), cockroach allergens and molds at any given home.[37] Perfumes are a common
cause of acute attacks in females and children. Both virus and bacterial infections of the upper
respiratory tract infection can worsen asthma.[37]

[edit] Risk factors

Studying the prevalence of asthma and related diseases such as eczema and hay fever have
yielded important clues about some key risk factors.[39] The strongest risk factor for developing
asthma is a history of atopic disease;[28] this increases one's risk of hay fever by up to 5x and the
risk of asthma by 3-4x.[40] In children between the ages of 3-14, a positive skin test for allergies
and an increase in immunoglobulin E increases the chance of having asthma.[41] In adults, the
more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[42]

Because much allergic asthma is associated with sensitivity to indoor allergens and because
Western styles of housing favor greater exposure to indoor allergens, much attention has focused
on increased exposure to these allergens in infancy and early childhood as a primary cause of the
rise in asthma.[43][44] Primary prevention studies aimed at the aggressive reduction of airborne
allergens in a home with infants have shown mixed findings. Strict reduction of dust mite
allergens, for example, reduces the risk of allergic sensitization to dust mites, and modestly
reduces the risk of developing asthma up until the age of 8 years old.[45][46][47][48] However, studies
also showed that the effects of exposure to cat and dog allergens worked in the converse fashion;
exposure during the first year of life was found to reduce the risk of allergic sensitization and of
developing asthma later in life.[49][50][51]

The inconsistency of this data has inspired research into other facets of Western society and their
impact upon the prevalence of asthma. One subject that appears to show a strong correlation is
the development of asthma and obesity. In the United Kingdom and United States, the rise in
asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity.[52][53][54][55] In
Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each
20% increase in body-mass index.[56]

Asthma has been associated with Churg–Strauss syndrome, and individuals with
immunologically mediated urticaria may also experience systemic symptoms with generalized
urticaria, rhino-conjunctivitis, orolaryngeal and gastrointestinal symptoms, asthma, and, at worst,
anaphylaxis.[57] Additionally, adult-onset asthma has been associated with periocular
xanthogranulomas.[58]

[edit] Hygiene hypothesis

Main article: Hygiene hypothesis

One theory for the cause of the increase in asthma prevalence worldwide is the so-called
"hygiene hypothesis"—that the rise in the prevalence of allergies and asthma is a direct and
unintended result of the success of modern hygienic practices in preventing childhood infections.
[59]
Children living in less hygienic environments (East Germany vs. West Germany,[60] families
with many children,[61][62][63] day care environments[64]) tend to have lower incidences of asthma
and allergic diseases. This seems to run counter to the logic that viruses are often causative
agents in exacerbation of asthma.[65][66][67] Additionally, other studies have shown that viral
infections of the lower airway may in some cases induce asthma, as a history of bronchiolitis or
croup in early childhood is a predictor of asthma risk in later life.[68] Studies which show that
upper respiratory tract infections are protective against asthma risk also tend to show that lower
respiratory tract infections conversely tend to increase the risk of asthma.[69]

[edit] Population disparities

Asthma prevalence in the US is higher than in most other countries in the world, but varies
drastically between diverse US populations.[25] In the US, asthma prevalence is highest in Puerto
Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in
Mexicans and Koreans.[70][71][72] Mortality rates follow similar trends, and response to Salbutamol
is lower in Puerto Ricans than in African Americans or Mexicans.[73][74] As with worldwide
asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may
be explained by differences in genetic, social and environmental risk factors.

Asthma prevalence also differs between populations of the same ethnicity who are born and live
in different places.[75] US-born Mexican populations, for example, have higher asthma rates than
non-US born Mexican populations that are living in the US.[76]
There is no correlation between asthma and gender in children, but more adult women are
diagnosed with asthma than adult men.[77]

[edit] Socioeconomic factors

The incidence of asthma is highest among low-income populations both nationally[specify] and
worldwide. Asthma deaths are most common in low and middle income countries,[78] and in the
Western world, it is found in those low-income neighborhoods whose populations consist of
large percentages of ethnic minorities[79].Additionally, asthma has been strongly associated with
the presence of cockroaches in living quarters; these insects are more likely to be found in those
same neighborhoods.[80]

Most likely due to income and geography, the incidence of and treatment quality for asthma
varies among different racial groups.[81] For example, African Americans are less likely to
receive outpatient treatment for asthma despite their higher prevalence of the disease. They are
much more likely to require an emergency room visit or hospitalization for their asthma
symptoms which is probably a contributing factor to their higher likelihood as a race of dying
from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also
greater in low-income communities than those with better access to treatment.[81][82]

[edit] Athletics

See also: Exercise-induced asthma

Asthma appears to be more prevalent in athletes than in the general population. One survey of
participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15%
had been diagnosed with asthma, and that 10% were on asthma medication.[83]

There appears to be a relatively high incidence of asthma in sports such as cycling, mountain
biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It
is unclear how much of these disparities are from the effects of training in the sport.[83][84]

[edit] Occupation

Main article: Occupational asthma

Asthma as a result of (or worsened by) workplace exposures is a commonly reported

occupational respiratory disease. Still most cases of occupational asthma are not reported or are
not recognized as such. Estimates by the American Thoracic Society (2004) suggest that 15–23%
of new-onset asthma cases in adults are work related.[85] In one study monitoring workplace
asthma by occupation, the highest percentage of cases occurred among operators, fabricators,
and laborers (32.9%), followed by managerial and professional specialists (20.2%), and in
technical, sales, and administrative support jobs (19.2%). Most cases were associated with the
manufacturing (41.4%) and services (34.2%) industries.[85] Animal proteins, enzymes, flour,
natural rubber latex, and certain reactive chemicals are commonly associated with work-related
asthma. When recognized, these hazards can be mitigated, dropping the risk of disease.[86]
[edit] Diagnosis
Severity of acute asthma exacerbations[13]
Near-fatal asthma
Life threatening asthma
Acute severe asthma
Moderate asthma exacerbation Peak flow > 50% best or predicted
High PaCO2 and/or requiring mechanical ventilation
Any one of the following in a person with severe asthma:-
Clinical signs Measurements
Altered conscious level Peak flow < 33%
Exhaustion Oxygen saturation < 92%
Arrhythmia PaO2 < 8 kPa
Low blood pressure "Normal" PaCO2
Cyanosis
Silent chest
Poor respiratory effort
Any one of:-
Peak flow 33-50%
Respiratory rate ≥ 25 breaths per minute
Heart rate ≥ 110 beats per minute
Unable to complete sentences in one breath
Worsening symptoms
No features of acute severe asthma

There is currently not a precise physiologic, immunologic, or histologic test for diagnosing
asthma. The diagnosis is usually made based on the pattern of symptoms (airways obstruction
and hyperresponsiveness) and/or response to therapy (partial or complete reversibility) over time.
[87]

The British Thoracic Society determines a diagnosis of asthma using a ‘response to therapy’
approach. If the patient responds to treatment, then this is considered to be a confirmation of the
diagnosis of asthma. The response measured is the reversibility of airway obstruction after
treatment. Airflow in the airways is measured with a peak flow meter, and the following
diagnostic criteria are used by the British Thoracic Society:[88]
 • ≥20% difference on at least three days in a week for at least two weeks;
• ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six weeks of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30 mg prednisolone.
• ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).

In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a
‘symptom patterns’ approach.[89] Their guidelines for the diagnosis and management of asthma
state that a diagnosis of asthma begins by assessing if any of the following list of indicators is
present.[89][90] While the indicators are not sufficient to support a diagnosis of asthma, the
presence of multiple key indicators increases the probability of a diagnosis of asthma.[89]
Spirometry is needed to establish a diagnosis of asthma.[89]

• Wheezing—high-pitched whistling sounds when breathing out—especially in children.

(Lack of wheezing and a normal chest examination do not exclude asthma.)
• history of any of the following:
o Cough, worse particularly at night
o Recurrent wheeze
o Recurrent difficulty in breathing
o Recurrent chest tightness
• Symptoms occur or worsen in the presence of:
o Exercise
o Viral infection
o Animals with fur or hair
o House-dust mites (in mattresses, pillows, upholstered furniture, carpets)
o Mold
o Smoke (tobacco, wood)
o Pollen
o Changes in weather
o Strong emotional expression (laughing or crying hard)
o Airborne chemicals or dusts
o Menstrual cycles
• Symptoms occur or worsen at night, awakening the patient

The latest guidelines from the U.S. National Asthma Education and Prevention Program
(NAEPP) recommend spirometry at the time of initial diagnosis, after treatment is initiated and
symptoms are stabilized, whenever control of symptoms deteriorates, and every 1 or 2 years on a
regular basis.[91] The NAEPP guidelines do not recommend testing peak expiratory flow as a
regular screening method because it is more variable than spirometry. However, testing peak
flow at rest (or baseline) and after exercise can be helpful, especially in young patients who may
experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for
checking the effects of new medications.[91] Peak flow readings can be charted together with a
record of symptoms or use peak flow charting software. This allows patients to track their peak
flow readings and pass information back to their doctor or nurse.[92]
[edit] Differential diagnosis

Differential diagnoses include:[89]

• Infants and Children

o Upper airway diseases
 Allergic rhinitis and sinusitis
o Obstructions involving large airways
 Foreign body in trachea or bronchus
 Vocal cord dysfunction
 Vascular rings or laryngeal webs
 Laryngotracheomalacia, tracheal stenosis, or bronchostenosis
 Enlarged lymph nodes or tumor
o Obstructions involving small airways
 Viral bronchiolitis or obliterative bronchiolitis
 Cystic fibrosis
 Bronchopulmonary dysplasia
 Heart disease
o Other causes
 Recurrent cough not due to asthma
 Aspiration from swallowing mechanism dysfunction or gastroesophageal
reflux
• Adults
o COPD (e.g., chronic bronchitis or emphysema)
o Congestive heart failure
o Pulmonary embolism
o Mechanical obstruction of the airways (benign and malignant tumors)
o Pulmonary infiltration with eosinophilia
o Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE) inhibitors)
o Vocal cord dysfunction

Before diagnosing asthma, alternative possibilities should be considered such as the use of
known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain anti-
inflammatory agents or beta-blockers). Among elderly people, the presenting symptom may be
fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to Chronic
obstructive pulmonary disease(COPD), congestive heart failure, or simple aging.[93]

Chronic obstructive pulmonary disease closely resembles asthma, is correlated with more
exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator
administration (as measured by spirometry), and decreased likelihood of family history of atopy.
[94][citation needed]

The term "atopy" was coined to describe this triad of atopic eczema, allergic rhinitis and asthma.
[57]
Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to
acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also
indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a
modified barium swallow test. If the aspiration is indirect (from acid reflux), then treatment is
directed at this is indicated.[citation needed]

[edit] Prevention
The evidence for the effectiveness of measures to prevent the development of asthma is weak.[95]
Ones which show some promise include: limiting smoke exposure both in utero and after
delivery, breastfeeding, increased exposure to respiratory infection per the hygiene hypothesis
(such as in those who attend daycare or are from large families).[95]

[edit] Management
A specific, customized plan for proactively monitoring and managing symptoms should be
created. Someone who has asthma should understand the importance of reducing exposure to
allergens, testing to assess the severity of symptoms, and the usage of medications. The
treatment plan should be written down and adjusted according to changes in symptoms.[96]

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or
aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, medical treatment
is recommended. Medical treatments used depends on the severity of illness and the frequency of
symptoms. Specific medications for asthma are broadly classified in to fast acting and long
acting.[97][98]

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional
attacks, no other medication is needed. If mild persistent disease is present (more than two
attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene antagonist
or a mast cell stabilizer is recommended. For those who suffer daily attacks, a higher dose of
inhaled glucocorticoid is used. In a severe asthma exacerbation, oral glucocorticoids are added to
these treatments.[89]

[edit] Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most
common triggers include: allergens, smoke (tobacco and other), air pollution, non selective beta-
blockers, and sulfite-containing foods.[89][99]

[edit] Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications
used to treat acute symptoms; and long-term control medications used to prevent further
exacerbation.[100]
Fast acting

Salbutamol metered dose inhaler commonly used to treat asthma attacks.

• Short acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN)

are the first line treatment for asthma symptoms.[3]
• Anticholinergic medications, such as ipratropium bromide provide addition benefit when
used in combination with SABA in those with moderate or severe symptoms.[3]
• Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar
efficacy to SABAs.[101] They are however not recommended due to concerns regarding
excessive cardiac stimulation.[102]

Long term control

Fluticasone propionate metered dose inhaler commonly used for long term control.

• Glucocorticoids are the most effective treatment available for long term control.[103]
Inhaled forms are usually used except in the case of severe persitent disease in which oral
steroids may be needed.[103] The inhaled formulation may be used once or twice daily
depending on the severity of symptoms.[104]
• Long acting beta-adrenoceptor agonists (LABD) have at least a 12-hour effect. They are
however not to be used without a steroid due to an increased risk of severe symptoms.[105]
[106][107]
In December 2008, members of the FDA's drug-safety office recommended
withdrawing approval for these medications in children. Discussion is ongoing about
their use in adults.[108]
• Leukotriene antagonist ( such as zafirlukast) are an alternative to inhaled glucocorticoids,
but are not preferred. They may also be used in addition to inhaled glucocorticoids but
are second line to LABD.[103]
• Mast cell stabilizers ( such as cromolyn sodium) are another none preferred alternative to
glucocorticoids.[103]

Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an

asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the
medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be
used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms
however insufficient evidence is available to determine whether or not a difference exist in those
severe symptomatology.[109]

[edit] Other

When an asthma attack is unresponsive to usual medications, other options available for
emergency management may include:

• Oxygen used to alleviate hypoxia if the saturation is less than 92%.[110]

• Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating
effect when used in addition to other treatment in severe acute asthma attacks.[111][112]
• Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive
cases.[112]
• Intravenous salbutamol is not supported by the evidence and thus only used in extremes.
[110]

• Methylxanthines (such as theophylline) do not add significantly to the effects of inhaled

beta-agonists.[110]
• The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical
ventilation is needed in people who are approaching respiratory arrest however evidence
from trials does not exist.[113]

[edit] Complementary medicine

Many asthma patients, like those who suffer from other chronic disorders, use alternative
treatments; surveys show that roughly 50% of asthma patients use some form of unconventional
therapy.[114][115] There is little data to support the effectiveness of most of these therapies.
Evidence is insufficient to support the usage of Vitamin C.[116] Acupuncture is not recommended
for the treatment as there is insufficient evidence to support its use.[117][118] Air ionisers show no
evidence that they improve asthma symptoms or benefit lung function; this applied equally to
positive and negative ion generators.[119]

Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress
covers and others methods had no effect on asthma symptoms.[120] However, a review of 30
studies found that "bedding encasement might be an effective asthma treatment under some
conditions" (when the patient is highly allergic to dust mite and the intervention reduces the dust
mite exposure level from high levels to low levels).[121]

A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic

and respiratory therapeutic manoeuvres, found there is insufficient evidence to support or refute
their use in treating.[122] The Buteyko breathing technique for controlling hyperventilation may
result in a reduction in medications use however does not have any effect on lung function.[123]
Thus an expert panel felt that evidence was insufficent to support its use.[117]

[edit] Prognosis
The prognosis for asthma is good, especially for children with mild disease.[90][not in citation given] Of
asthma diagnosed during childhood, 54% of cases will no longer carry the diagnosis after a
decade.[citation needed] The extent of permanent lung damage in people with asthma is unclear.
Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial
changes.[124] Although conclusions from studies are mixed, most studies show that early
treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by
several parameters.[125] For those who continue to suffer from mild symptoms, corticosteroids can
help most to live their lives with few disabilities. It is more likely to consider immediate
medication of inhaled corticosteroids as soon as asthma attacks occur. According to studies
conducted, patients with relatively mild asthma who have received inhaled corticosteroids within
12 months of their first asthma symptoms achieved good functional control of asthma after 10
years of individualized therapy as compared to patients who received this medication after 2
years (or more) from their first attacks.[citation needed] Though they (delayed) also had good functional
control of asthma, they were observed to exhibited slightly less optimal disease control and more
signs of airway inflammation.[citation needed]

Asthma mortality has decreased over the last few decades due to better recognition and
improvement in care.[126]

[edit] Epidemiology
Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.[127]
no data <100 100–150 150–200 200–250 250–300 300–350 350–400 400–
450 450–500 500–550 550–600 >600

The prevalence of childhood asthma in the United States has increased since 1980, especially in
younger children.

As of 2009, 300 million people worldwide were affected by asthma leading to approximately
250,000 deaths per year.[128][105][7][129]

A 1998 there was a great disparity in prevalence worldwide across the world (as high as a 20 to
60-fold difference), with a trend toward more developed and westernized countries having higher
rates of asthma.[130] Westernization however does not explain the entire difference in asthma
prevalence between countries, and the disparities may also be affected by differences in genetic,
social and environmental risk factors.[25] Mortality however is most common in low to middle
income countries,[131] while symptoms were most prevalent (as much as 20%) in the United
Kingdom, Australia, New Zealand, and Republic of Ireland; they were lowest (as low as 2–3%)
in Eastern Europe, Indonesia, Greece, Uzbekistan, India, and Ethiopia.[130][dated info]

While asthma is more common in affluent countries, it is by no means a restricted problem; the
WHO estimate that there are between 15 and 20 million people with asthma in India.[citation needed] In
the U.S., urban residents, Hispanics, and African Americans are affected more than the
population as a whole.[citation needed] Striking increases in asthma prevalence have been observed in
populations migrating from a rural environment to an urban one,[132][dated info] or from a third-world
country to Westernized one.[133][dated info]

It affects 7% of the population of the United States,[134] 5% of British people.[135] Asthma causes
4,000 deaths per year in the United States.[136] In 2005 in the United States asthma affected more
than 22 million people including 6 million children.[137] It accounted for nearly 1/2 million
hospitalizations,[137] and 14 million missed days of school annually.[citation needed] More boys have
asthma than girls, but more women have it than men.[138] Of all children, African Americans and
Latinos who live in cities are more at risk for developing asthma.[citation needed] African American
children in the U.S. are four times more likely to die of asthma and three times more likely to be
hospitalized, compared to their white counterparts.[citation needed] In some Latino neighborhoods, as
many as one in three children has been found to have asthma.[139]

In England, an estimated 261,400 people were newly diagnosed with asthma in 2005; 5.7 million
people had an asthma diagnosis and were prescribed 32.6 million asthma-related prescriptions.
[140]

The frequency of atopic dermatitis, asthma, urticaria and allergic contact dermatitis has been
found to be lower in psoriatic patients.[57]

[edit] Increasing frequency

Rates of asthma have increased significantly between the 1960s and 2008.[141][142] Some 9% of US
children had asthma in 2001, compared with just 3.6% in 1980. The World Health Organization
(WHO) reports that some 10% of the Swiss population suffers from asthma today,[143] compared
with just 2% some 25–30 years ago.

[edit] History
This section requires expansion.

Asthma was first recognized and named by Hippocrates circa 450 BC. During the 1930s–50s,
asthma was considered as being one of the 'holy seven' psychosomatic illnesses. Its aetiology
was considered to be psychological, with treatment often based on psychoanalysis and other
'talking cures'.[144] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed
cry of the child for its mother, so they considered that the treatment of depression was especially
important for individuals with asthma.[144]

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Bibliography

• "Expert Panel Report 3: Guidelines for the Diagnosis and Management of

Asthma" (PDF). National Heart Lung and Blood Institute. 2007.
http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
• "British Guideline on the Management of Asthma" (pdf). British Thoracic
Society. 2009. http://www.brit-thoracic.org.uk/Portals/0/Clinical
%20Information/Asthma/Guidelines/sign101%20revised%20June%2009.pdf.
• "Global Initiative for Asthma". 2009.
http://www.ginasthma.org/Guidelineitem.asp??l1=2&l2=1&intId=1561.

[edit] External links

• World Health Organization site on asthma
• National Heart, Lung, and Blood Institute — Asthma – U.S. NHLBI Information for
Patients and the Public page.
• MedLinePlus: Asthma – a U.S. National Library of Medicine page
• Asthma Management Handbook 2006 National Asthma Council Australia
• Neurogenic mechanisms of asthma
• the Global Initiative for Asthma (GINA)
• NHS Guidance for the management of Asthma
• Types of Asthma by NHS
• Childhood Asthma
 [show]
v•d•e
Pathology of respiratory system (J, 460–519), respiratory diseases

sinuses: Sinusitis

nose: Rhinitis (Vasomotor rhinitis, Atrophic rhinitis, Hay fever) · Nasal polyp ·
HeadRhinorrhea · nasal septum (Nasal septum deviation, Nasal septum perforation, Nasal septal
hematoma)

tonsil: Tonsillitis · Adenoid hypertrophy · Peritonsillar abscess

pharynx: Laryngopharyngeal reflux (LPR) · Pharyngitis (Strep throat) · Retropharyngeal

abscess

larynx: Croup · Laryngitis · Laryngopharyngeal reflux (LPR) · Laryngospasm

Neck
vocal folds: Laryngopharyngeal reflux (LPR) · Vocal fold nodule

epiglottis: Epiglottitis

trachea: Tracheitis · Tracheal stenosis

acute: Acute bronchitis

chronic: COPD (Chronic bronchitis, Acute exacerbations of chronic bronchitis,

Bronchial/
Acute exacerbation of COPD, Emphysema, Diffuse panbronchiolitis) · Asthma
obstructive
(Status asthmaticus, Aspirin-induced) · Bronchiectasis

unspecified: Bronchitis · Bronchiolitis (Bronchiolitis obliterans)

Pneumoconiosis (Asbestosis, Baritosis, Bauxite fibrosis, Berylliosis,

External
Caplan's syndrome, Chalicosis, Coalworker's pneumoconiosis,
agents/
Siderosis, Silicosis, Talcosis, Byssinosis)
occupational
Hypersensitivity pneumonitis (Bagassosis, Bird fancier's lung, Farmer's
lung disease
lung)
Interstitial/
restrictive
ARDS · Pulmonary edema · Löffler's syndrome/Eosinophilic
(fibrosis)
pneumonia · Respiratory hypersensitivity (Allergic bronchopulmonary
aspergillosis)
Other

Hamman-Rich syndrome · Idiopathic pulmonary fibrosis · Sarcoidosis

ObstructivePneumonia/ By Viral · Bacterial (Pneumococcal, Klebsiella) / Atypical

or pneumonitis
 bacterial (Mycoplasma, Legionnaires' disease,
Chlamydiae) · Fungal (Pneumocystis) · Parasitic ·
pathogen
noninfectious (Chemical/Mendelson's syndrome,
Aspiration/Lipid)

By Community-acquired · Healthcare-associated · Hospital-

vector/routeacquired
restrictive
By
Broncho- · Lobar
distribution

IIP UIP · DIP · BOOP-COP · NSIP · RB

Atelectasis · circulatory (Pulmonary hypertension, Pulmonary

Other
embolism) · Lung abscess

Pleuritis/pleurisy

Pneumothorax/Hemopneumothorax (Tension pneumothorax)

Pleural
disease Pleural effusion: Hemothorax · Hydrothorax · Chylothorax · Empyema/pyothorax ·
Malignant

Fibrothorax

Mediastinal
Mediastinitis · Mediastinal emphysema
disease

M: RES anat(n, x, l, noco(c)/cong/tumr, proc,

c)/phys/devp sysi/epon, injr drug(R1/2/3/5/6/7)
[show]
v•d•e
Immune disorders: hypersensitivity and autoimmune diseases (279.5-6)

Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis ·

Foreign
Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy

Autoimmunenone

Foreign Pernicious anemia · Hemolytic disease of the newborn

Autoimmune Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura

Cytotoxic · Bullous pemphigoid · Pemphigus vulgaris · Rheumatic fever ·
Goodpasture's syndrome
 "Type
5"/recepto Graves' disease · Myasthenia gravis
r

Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis ·

Foreign Rheumatoid arthritis · Farmer's lung · Post-streptococcal glomerulonephritis ·
Serum sickness · Arthus reaction

AutoimmuneSystemic lupus erythematosus · Subacute bacterial endocarditis

Foreign Allergic contact dermatitis · Mantoux test

Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome ·

Autoimmune
Multiple sclerosis · Coeliac disease · Giant cell arteritis

GVHD Transfusion-associated graft versus host disease

Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) ·

Foreign
Transplant rejection · Latex allergy (I+IV)

Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine

Autoimmune
syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease

M: LMC cell/phys/auag/auab imdf/ipig/hyps/tumr proc, drug(L3/4)

Retrieved from "http://en.wikipedia.org/wiki/Asthma"
Categories: Asthma | Chronic lower respiratory diseases
Hidden categories: Articles with hAudio microformats | All articles with unsourced statements |
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