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Asthma

  • Author: Michael J Morris, MD, FACP, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Jun 16, 2016
 

Practice Essentials

Asthma is a common chronic disease worldwide and affects approximately 26 million persons in the United States. It is the most common chronic disease in childhood, affecting an estimated 7 million children. The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. See the image below.

Pathogenesis of asthma. Antigen presentation by th Pathogenesis of asthma. Antigen presentation by the dendritic cell with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.

Signs and symptoms

Signs and symptoms of asthma include the following:

  • Wheezing
  • Coughing
  • Shortness of breath
  • Chest tightness/pain

Other nonspecific symptoms in infants or young children may be a history of recurrent bronchitis, bronchiolitis, or pneumonia; a persistent cough with colds; and/or recurrent croup or chest rattling.

See Clinical Presentation for more detail.

Diagnosis

Updated guidelines from the National Asthma Education and Prevention Program (NAEPP) highlight the importance of correctly diagnosing asthma, by establishing the following[1] :

  • Episodic symptoms of airflow obstruction are present
  • Airflow obstruction or symptoms are at least partially reversible
  • Exclusion of alternative diagnoses

Spirometry with postbronchodilator response should be obtained as the primary test to establish the asthma diagnosis. Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. The chest radiograph remains the initial imaging evaluation in most individuals with symptoms of asthma, but in most patients with asthma, chest radiography findings are normal or may indicate hyperinflation. Exercise spirometry is the standard method for assessing patients with exercise-induced bronchoconstriction.

See Workup for more detail.

Management

For all but the most severely affected patients, the ultimate goal is to prevent symptoms, minimize morbidity from acute episodes, and prevent functional and psychological morbidity to provide a healthy (or near healthy) lifestyle appropriate to the age of child.

Pharmacologic treatment

Pharmacologic management includes the use of relief and control agents. Control agents include inhaled corticosteroids, long-acting bronchodilators (beta-agonists and anticholinergics), theophylline (Theo-24, Theochron, Uniphyl), leukotriene modifiers, anti-IgE antibodies, and IL-5 antibodies. Relief medications include short-acting bronchodilators, systemic corticosteroids, and ipratropium (Atrovent).

The pharmacologic treatment of asthma is based on stepwise therapy. Asthma medications should be added or deleted as the frequency and severity of the patient's symptoms change.

Allergen avoidance

Environmental exposures and irritants can play a strong role in symptom exacerbations. The use of skin testing or in vitro testing to assess sensitivity to perennial indoor allergens is important. Once the offending allergens are identified, counsel patients on how to avoid them. Efforts should focus on the home, where specific triggers include dust mites, animals, cockroaches, mold, and pollen.

See Treatment and Medication for more detail.

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Background

Asthma is a common chronic disease worldwide and affects approximately 26 million persons in the United States. It is the most common chronic disease in childhood, affecting an estimated 7 million children, and it is a common cause of hospitalization for children in the United States.

The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present.[2, 3]

Airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

Spirometry with postbronchodilator response should be obtained as the primary test to establish the asthma diagnosis. Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. The chest radiograph remains the initial imaging evaluation in most individuals with symptoms of asthma, but in most patients with asthma, chest radiography findings are normal or may indicate hyperinflation. Exercise spirometry is the standard method for assessing patients with exercise-induced bronchospasm.

Physical findings vary with the severity of the asthma and with the absence or presence of an acute episode and its severity. The severity of asthma is classified as intermittent, mild persistent, moderate persistent, or severe persistent. Patients with asthma of any level of severity may have mild, moderate, or severe exacerbations.

Pharmacologic management includes the use of relief and control agents. Control agents include inhaled corticosteroids, long-acting bronchodilators (beta-agonists and anticholinergics), theophylline (Theo-24, Theochron, Uniphyl), leukotriene modifiers, anti-IgE antibodies, and anti-IL-5 antibodies. Relief medications include short-acting bronchodilators, systemic corticosteroids, and ipratropium (Atrovent). With severe exacerbations, indications for hospitalization are based on findings after the patient receives 3 doses of an inhaled bronchodilator. In general, patients should be assessed every 1-6 months for asthma control.

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Anatomy

The airways of the lungs consist of the cartilaginous bronchi, membranous bronchi, and gas-exchanging bronchi termed the respiratory bronchioles and alveolar ducts. While the first 2 types function mostly as anatomic dead space, they also contribute to airway resistance. The smallest non-gas-exchanging airways, the terminal bronchioles, are approximately 0.5 mm in diameter; airways are considered small if they are less than 2 mm in diameter.[4]

Airway structure consists of the following:

  • Mucosa, which is composed of epithelial cells that are capable of specialized mucous production and a transport apparatus
  • Basement membrane
  • A smooth-muscle matrix extending to the alveolar entrances
  • Predominantly fibrocartilaginous or fibroelastic-supporting connective tissue.

Cellular elements include mast cells, which are involved in the complex control of releasing histamine and other mediators. Basophils, eosinophils, neutrophils, and macrophages also are responsible for extensive mediator release in the early and late stages of bronchial asthma. Stretch and irritant receptors reside in the airways, as do cholinergic motor nerves, which innervate the smooth muscle and glandular units. In bronchial asthma, smooth muscle contraction in an airway is greater than that expected for its size if it were functioning normally, and this contraction varies in its distribution.

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Pathophysiology

The 2007 Expert Panel Report 3 (EPR-3) of the National Asthma Education and Prevention Program (NAEPP) noted several key changes in the understanding of the pathophysiology of asthma[1] :

  • The critical role of inflammation has been further substantiated, but evidence is emerging for considerable variability in the pattern of inflammation, thus indicating phenotypic differences that may influence treatment responses
  • Of the environmental factors, allergic reactions remain important. Evidence also suggests a key and expanding role for viral respiratory infections in these processes
  • The onset of asthma for most patients begins early in life, with the pattern of disease persistence determined by early, recognizable risk factors including atopic disease, recurrent wheezing, and a parental history of asthma
  • Current asthma treatment with anti-inflammatory therapy does not appear to prevent progression of the underlying disease severity

The pathophysiology of asthma is complex and involves the following components:

  • Airway inflammation
  • Intermittent airflow obstruction
  • Bronchial hyperresponsiveness

Airway inflammation

The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present.[2] See the image below.

Pathogenesis of asthma. Antigen presentation by th Pathogenesis of asthma. Antigen presentation by the dendritic cell with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.

Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.

The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.

A study by Balzar et al reported changes in airway resident mast cell populations from a large group of subjects with asthma and normal control subjects.[5] A greater proportion of chymase-positive mast cells in the airways and increased prostaglandin D2 levels were identified as important predictors of severe asthma as compared with other steroid-treated subjects with asthma.

Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise. In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease.

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 interleukin (IL)-2 and IFN-α, which are critical in cellular defense mechanisms in response to infection. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation. A study by Gauvreau et al found that IL-13 has a role in allergen-induced airway responses.[6]

The current "hygiene hypothesis" of asthma illustrates how this cytokine imbalance may explain some of the dramatic increases in asthma prevalence in westernized countries.[7] This hypothesis is based on the concept that the immune system of the newborn is skewed toward Th2 cytokine generation (mediators of allergic inflammation). Following birth, environmental stimuli such as infections activate Th1 responses and bring the Th1/Th2 relationship to an appropriate balance.  However, unequivocal support for the "hypgiene hypothesis" has not been demonstrated.[8]

Airflow obstruction

Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve. Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction.[9]

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.

Bronchial hyperresponsiveness

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 intra-alveolar pressure due to hyperinflation all lead to ventilation-perfusion mismatch. Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. Vasoconstriction is also considered an adaptive response to ventilation/perfusion mismatch.

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, patients with asthma 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 occurs. 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 acidosis due to retention of carbon dioxide as alveolar ventilation decreases.

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Etiology

Factors that can contribute to asthma or airway hyperreactivity may include any of the following:

  • Environmental allergens (eg, house dust mites; animal allergens, especially cat and dog; cockroach allergens; and fungi)
  • Viral respiratory tract infections
  • Exercise, hyperventilation
  • Gastroesophageal reflux disease
  • Chronic sinusitis or rhinitis
  • Aspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivity
  • Use of beta-adrenergic receptor blockers (including ophthalmic preparations)
  • Obesity [10]
  • Environmental pollutants, tobacco smoke
  • Occupational exposure
  • Irritants (eg, household sprays, paint fumes)
  • Various high- and low-molecular-weight compounds (eg, insects, plants, latex, gums, diisocyanates, anhydrides, wood dust, and fluxes; associated with occupational asthma)
  • Emotional factors or stress
  • Perinatal factors (prematurity and increased maternal age; maternal smoking and prenatal exposure to tobacco smoke; breastfeeding has not been definitely shown to be protective)

Aspirin-induced asthma

The triad of asthma, aspirin sensitivity, and nasal polyps affects 5-10% of patients with asthma. Most patients experience symptoms during the third to fourth decade. A single dose can provoke an acute asthma exacerbation, accompanied by rhinorrhea, conjunctival irritation, and flushing of the head and neck. It can also occur with other nonsteroidal anti-inflammatory drugs and is caused by an increase in eosinophils and cysteinyl leukotrienes after exposure.[11]

A study by Beasley et al demonstrated some epidemiological evidence that exposure to acetaminophen is associated with an increased risk of asthma.[12] However, no clinical studies have directly linked asthma symptoms with acetaminophen use.

Primary treatment is avoidance of these medications, but leukotriene antagonists have shown promise in treatment, allowing these patients to take daily aspirin for cardiac or rheumatic disease.  Aspirin desensitization has also been reported to decrease sinus symptoms, allowing daily dosing of aspirin.[13]

Gastroesophageal reflux disease

The presence of acid in the distal esophagus, mediated via vagal or other neural reflexes, can significantly increase airway resistance and airway reactivity. Patients with asthma are 3 times more likely to also have GERD.[14] Some people with asthma have significant gastroesophageal reflux without esophageal symptoms. Gastroesophageal reflux was found to be a definite asthma-causing factor (defined by a favorable asthma response to medical antireflux therapy) in 64% of patients; clinically silent reflux was present in 24% of all patients.[14]

Work-related asthma

Occupational factors are associated with 10-15% of adult asthma cases. More than 300 specific occupational agents have been associated with asthma. High-risk jobs include farming, painting, janitorial work, and plastics manufacturing. Given the prevalence of work-related asthma, the American College of Chest Physicians (ACCP) supports consideration of work-related asthma in all patients presenting with new-onset or worsening asthma. An ACCP consensus statement defines work-related asthmas as including occupational asthma (ie, asthma induced by sensitizer or irritant work exposures) and work-exacerbated asthma (ie, preexisting or concurrent asthma worsened by work factors).[15]

Two types of occupational asthma are recognized: immune-related and non-immune-related. Immune-mediated asthma has a latency of months to years after exposure. Non-immune-mediated asthma, or irritant-induced asthma (reactive airway dysfunction syndrome), has no latency period and may occur within 24 hours after an accidental exposure to high concentrations of respiratory irritants. Pay careful attention to the patient's occupational history. Those with a history of asthma who report worsening of symptoms during the week and improvement during the weekends should be evaluated for occupational exposure. Peak-flow monitoring during work (optimally, at least 4 times a day) for at least 2 weeks and a similar period away from work is one recommended method to establish the diagnosis.[15]

To see complete information on Allergic and Environmental Asthma, please go to the main article by clicking here.

Viral exposure in children

Evidence suggests that rhinovirus illness during infancy is a significant risk factor for the development of wheezing in preschool children and a frequent trigger of wheezing illnesses in children with asthma.[16] Human rhinovirus C (HRVC) is a newly identified genotype of HRV found in patients with respiratory tract infections. A study of children with acute asthma who presented to the emergency department found HRVC present in the majority of patients. The presence of HRVC was also associated with more severe asthma.[17]

Approximately 80-85% of childhood asthma episodes are associated with prior viral exposure. Prior childhood pneumonia due to infection by respiratory syncytial virus, Mycoplasma pneumoniae, and/or Chlamydia species was found in more than 50% of a small sample of children aged 7-9 years who later had asthma.[18] Treatment with antibiotics appropriate for these organisms improves the clinical signs and symptoms of asthma.

Sinusitis

Of patients with asthma, 50% have concurrent sinus disease. Sinusitis is the most important exacerbating factor for asthma symptoms. Either acute infectious sinus disease or chronic inflammation may contribute to worsening airway symptoms. Treatment of nasal and sinus inflammation reduces airway reactivity. Treatment of acute sinusitis requires at least 10 days of antibiotics to improve asthma symptoms.[19]

Exercise-induced asthma

Exercise-induced asthma (EIA), or exercise-induced bronchoconstriction (EIB), is an asthma variant defined as a condition in which exercise or vigorous physical activity triggers acute bronchoconstriction in persons with heightened airway reactivity. It is observed primarily in persons who have asthma (exercise-induced bronchoconstriction in asthmatic persons) but can also be found in patients with normal resting spirometry findings with atopy, allergic rhinitis, or cystic fibrosis and even in healthy persons, many of whom are elite or cold weather athletes (exercise-induced bronchoconstriction in athletes). Exercise-induced bronchoconstriction is often a neglected diagnosis, and the underlying asthma may be silent in as many as 50% of patients, except during exercise.[20, 21]

The pathogenesis of exercise-induced bronchoconstriction is controversial. The disease may be mediated by water loss from the airway, heat loss from the airway, or a combination of both. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37°C (98.6°F). The nose is unable to condition the increased amount of air required for exercise, particularly in athletes who breathe through their mouths. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction, occurring within minutes of completing exercise. Results from bronchoalveolar lavage studies have not demonstrated an increase in inflammatory mediators. These patients generally develop a refractory period, during which a second exercise challenge does not cause a significant degree of bronchoconstriction.

Factors that contribute to exercise-induced bronchoconstriction symptoms (in both persons with asthma and athletes) include the following:

  • Exposure to cold or dry air
  • Environmental pollutants (eg, sulfur, ozone)
  • level of bronchial hyperreactivity
  • Chronicity of asthma and symptomatic control
  • Duration and intensity of exercise
  • Allergen exposure in atopic individuals
  • Coexisting respiratory infection

The assessment and diagnosis of exercise-induced bronchoconstriction is made more often in children and young adults than in older adults and is related to high levels of physical activity. Exercise-induced bronchoconstriction can be observed in persons of any age based on the level of underlying airway reactivity and the level of physical exertion.

Genetics

Research on genetic mutations casts further light on the synergistic nature of multiple mutations in the pathophysiology of asthma. Polymorphisms in the gene that encodes platelet-activating factor hydrolase, an intrinsic neutralizing agent of platelet-activating factor in most humans, may play a role in susceptibility to asthma and asthma severity.[22]

Evidence suggests that the prevalence of asthma is reduced in association with certain infections (Mycobacterium tuberculosis, measles, or hepatitis A); rural living; 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, sets the stage to promote the production of immunoglobulin E (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 is apparent between the 2 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. Alternatively, recent studies suggest the possibility that the loss of normal immune balance arises from a cytokine dysregulation in which Th1 activity in asthma is diminished.[23]

In addition, some studies highlight the importance of genotypes in children's susceptibility to asthma and response to specific antiasthma medications.[24, 25, 26, 27]

Obesity

A study by Cottrell et al explored the relationship between asthma, obesity, and abnormal lipid and glucose metabolism.[28] The study found that community-based data linked asthma, body mass, and metabolic variables in children. Specifically, these findings described a statistically significant association between asthma and abnormal lipid and glucose metabolism beyond body mass association. Evidence is accumulating that individuals with a high body mass index have worse asthma control and sustained weight loss improves asthma control.[29]

Accelerated weight gain in early infancy is associated with increased risks of asthma symptoms according to one study of preschool children.[30]

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Epidemiology

Asthma affects 5-10% of the population or an estimated 23.4 million persons, including 7 million children.[15] The overall prevalence rate of exercise-induced bronchospasm is 3-10% of the general population if persons who do not have asthma or allergy are excluded, but the rate increases to 12-15% of the general population if patients with underlying asthma are included. Asthma affects an estimated 300 million individuals worldwide. Annually, the World Health Organization (WHO) has estimated that 15 million disability-adjusted life-years are lost and 250,000 asthma deaths are reported worldwide.[31]

In the United States, asthma prevalence, especially morbidity and mortality, is higher in blacks than in whites. Although genetic factors are of major importance in determining a predisposition to the development of asthma, environmental factors play a greater role than racial factors in asthma onset. A national concern is that some of the increased morbidity is due to differences in asthma treatment afforded certain minority groups. Larger asthma-associated lung function deficits are reported in Hispanics, especially females.[32]

Asthma is common in industrialized nations such as Canada, England, Australia, Germany, and New Zealand, where much of the asthma data have been collected. The prevalence rate of severe asthma in industrialized countries ranges from 2-10%. Trends suggest an increase in both the prevalence and morbidity of asthma, especially in children younger than 6 years. Factors that have been implicated include urbanization, air pollution, passive smoking, and change in exposure to environmental allergens.

Asthma predominantly occurs in boys in childhood, with a male-to-female ratio of 2:1 until puberty, when the male-to-female ratio becomes 1:1. Asthma prevalence is greater in females after puberty, and the majority of adult-onset cases diagnosed in persons older than 40 years occur in females. Boys are more likely than girls to experience a decrease in symptoms by late adolescence.

Asthma prevalence is increased in very young persons and very old persons because of airway responsiveness and lower levels of lung function.[33] Two thirds of all asthma cases are diagnosed before the patient is aged 18 years. Approximately half of all children diagnosed with asthma have a decrease or disappearance of symptoms by early adulthood.[34]

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Prognosis

International asthma mortality is reported as high as 0.86 deaths per 100,000 persons in some countries. US asthma mortality rates in 2009 were reported at 1 death per 100,000 persons. Mortality is primarily related to lung function, with an 8-fold increase in patients in the lowest quartile, but mortality has also been linked with asthma management failure, especially in young persons. Other factors that impact mortality include age older than 40 years, cigarette smoking more than 20 pack-years, blood eosinophilia, forced expiratory volume in one second (FEV1) of 40-69% predicted, and greater reversibility.[35]

The estimate of lost work and school time from asthma is approximately 100 million days of restricted activity. Approximately 500,000 annual hospitalizations (40.6% in individuals aged 18 y or younger) are due to asthma. Each year, an estimated 1.7 million people (47.8% of them aged 18 years or younger) require treatment in an emergency department.[36] For 2010, the annual expenditures for health and lost productivity due to asthma was projected to be $20.7 billion.[37]

Nearly one half of children diagnosed with asthma will have a decrease in symptoms and require less treatment by late adolescence or early adulthood. In a study of 900 children with asthma, 6% required no treatment after 1 year, and 39% only required intermittent treatment.

Patients with poorly controlled asthma develop long-term changes over time (i.e., with airway remodeling). This can lead to chronic symptoms and a significant irreversible component to their disease. Many patients who develop asthma at an older age also tend to have chronic symptoms.

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Patient Education

The need for patient education about asthma and the establishment of a partnership between patient and clinician in the management of the disease was emphasized by EPR-3.[1]

The key points of education include the following:

  • Patient education should be integrated into every aspect of asthma care
  • All members of the healthcare team, including nurses, pharmacists, and respiratory therapists, should provide education.
  • Clinicians should teach patients asthma self-management based on basic asthma facts, self-monitoring techniques, the role of medications, inhaler use, and environmental control measures. [38, 39, 40]
  • Treatment goals should be developed for the patient and family.
  • A written, individualized, daily self-management plan should be developed.
  • Several well-validated asthma action plans are now available and are key in the management of asthma and should therefore be reviewed: ACT (Asthma Control Test), ATAQ (Asthma Therapy Assessment Questionnaire), and ACQ (Asthma Control Questionnaire). [41]

School-based asthma education programs improved knowledge of asthma, self-efficacy, and self-management behaviors in children aged 4-17 years, according to a systematic literature review by Coffman et al, but the programs had less effect on quality of life, days of symptoms, nights with symptoms, and school absences.[42]

The 2009 Veterans Administration/Department of Defense (VA/DoD) clinical practice guideline for management of asthma in children and adults concurs with EPR-3 in recommending self-management education for both the patient and caregiver as part of the treatment program.[43]

For excellent patient education resources, visit eMedicineHealth's Asthma Center. Also, see eMedicineHealth's patient education articles Asthma, Asthma FAQs, Asthma in Children, and Understanding Asthma Medications.

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Contributor Information and Disclosures
Author

Michael J Morris, MD, FACP, FCCP Clinical Faculty, Pulmonary Disease/Critical Care Service, Department of Medicine, Brooke Army Medical Center; Associate Program Director, SAUSHEC Internal Medicine Residency, San Antonio Military Medical Center; Clinical Assistant Professor, University of Texas School of Medicine at San Antonio; Professor, Uniformed Services University of the Health Sciences

Michael J Morris, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Association of Military Surgeons of the US, American Association for Respiratory Care

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Boehringer-Ingelheim.

Coauthor(s)

Daniel J Pearson, MD Fellow in Pulmonary and Critical Care Medicine, San Antonio Military Medical Center

Daniel J Pearson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Helen M Hollingsworth, MD Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center

Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Pathogenesis of asthma. Antigen presentation by the dendritic cell with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.
Asthma symptoms and severity. Recommended guidelines for determination of asthma severity based on clinical symptoms, exacerbations, and measurements of airway function. Adapted from Global Strategy for Asthma Management and Prevention: 2002 Workshop Report.
Stepwise approach to pharmacological management of asthma based on asthma severity. Adapted from Global Strategy for Asthma Management and Prevention: 2002 Workshop Report.
Asthma. High-resolution CT scan of the thorax obtained during inspiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (arrow).
Asthma. High-resolution CT scan of the thorax obtained during expiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma. Note the normal increase in right lung attenuation during expiration (right arrow). The left lung remains lucent, especially the upper lobe, secondary to bronchial obstruction with airtrapping (left upper arrow). The vasculature on the left is diminutive, secondary to reflex vasoconstriction. Left pleural thickening and abnormal linear opacities are noted in the left lower lobe; these are the result of prior episodes of postobstructive pneumonia (left lower arrow).
High-resolution CT scan of the thorax obtained during inspiration demonstrates airtrapping in a patient with asthma. Inspiratory findings are normal.
High-resolution CT scan of the thorax obtained during expiration demonstrates a mosaic pattern of lung attenuation in a patient with asthma. Lucent areas (arrows) represent areas of airtrapping.
Posteroanterior chest radiograph demonstrates a pneumomediastinum in bronchial asthma. Mediastinal air is noted adjacent to the anteroposterior window and airtrapping extends to the neck, especially on the right side.
Lateral chest radiograph demonstrates a pneumomediastinum in bronchial asthma. Air is noted anterior to the trachea (same patient as in the previous image).
High-resolution CT scan of the thorax obtained during inspiration demonstrates airtrapping in a patient with asthma. Inspiratory findings are normal.
High-resolution CT scan of the thorax obtained during expiration demonstrates a mosaic pattern of lung attenuation in a patient with asthma. Lucent areas (arrows) represent areas of airtrapping (same patient as in the previous image).
Asthma. High-resolution CT scan of the thorax obtained during inspiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (arrow).
Asthma. High-resolution CT scan of the thorax obtained during expiration in a patient with recurrent left lower lobe pneumonia shows a bronchial mucoepidermoid carcinoma (same patient as in the previous image). Note the normal increase in right lung attenuation during expiration (right arrow). The left lung remains lucent, especially the upper lobe, secondary to bronchial obstruction with airtrapping (left upper arrow). The vasculature on the left is diminutive, secondary to reflex vasoconstriction. Left pleural thickening and abnormal linear opacities are noted in the left lower lobe; these are the result of prior episodes of postobstructive pneumonia (left lower arrow).
Asthma. High-resolution CT scan of the thorax demonstrates mild bronchial thickening and dilatation in a patient with bilateral lung transplants and bronchial asthma.
Asthma. High-resolution CT scan of the thorax demonstrates central bronchiectasis, a hallmark of allergic bronchopulmonary aspergillosis (right arrow), and the peripheral tree-in-bud appearance of centrilobular opacities (left arrow), which represent mucoid impaction of the small bronchioles.
 
 
 
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