What every physician needs to know:
Asthma is common disease in both adults and children. It ranks as the second leading cause of hospital admission for children. Accurate determination of the prevalence of asthma is difficult, however, because clinicians and researchers use many definitions of the disorder. Presentations of asthma are variable, and an understanding of asthma pathophysiology is incomplete. Furthermore, significant individual variability exists with regard to genetic predisposition, co-morbid conditions, and triggering exposures.
Despite significant recent advances, a unified understanding of the physiology, histology, and immunology of asthma remains elusive, in part because of the lack of a clear correlation among symptoms, triggers, and treatment efficacy. However, several characteristics of asthma are common to many phenotypes, including airway inflammation, airway hyper-responsiveness, and reversible airflow obstruction.
Definition of Asthma
Asthma is a heterogeneous disease, whose pathologic features most often include reversible airway obstruction, chronic airway inflammation, bronchial hyperreactivity (BHR), and airways remodelling. With BHR, bronchospasm is easily initiated in response to various triggers and is likely the result of underlying chronic airway inflammation. Unfortunately, in children, BHR is difficult to assess; in adults, factors other than asthma, such as chronic bronchitis, may cause BHR.
According to the National Heart, Lung and Blood Institute (NHLBI) Expert Report 3 (EPR3) – Guidelines for the Diagnosis and Management of Asthma, asthma is defined as “a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role: in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. Reversibility of airflow limitation may be incomplete in some patients with asthma.”
This definition is relatively nonspecific and likely includes other diseases. However, the definition is useful in identifying patients for whom a particular management strategy is likely to be effective. Given this definition, asthma may present in a variety of ways that vary by age, severity, co-morbidities, triggering stimuli, and ability to detect BHR.
Asthma in Children
Asthma in young children may be difficult to diagnose with certainty because of difficulty in determining quantitative measures of BHR. In addition, symptoms may be transient, occurring only during upper respiratory tract infections. In children over the age of five, spirometry may performed effectively and obstruction detected; in younger children, pulmonary function testing is usually not possible or is inaccurate. Many young children who have symptoms characteristic of asthma, including wheezing and coughing (especially at night), may not have chronic airway inflammation.
The diagnosis of asthma becomes more likely when respiratory symptoms are recurrent or associated with an extrinsic trigger, such as cold air, exercise or activity, or allergens or irritants. Many children have wheezing associated with viral illnesses. Some will develop asthma as older children or adults, but many do not. In fact, two-thirds of children labeled as “transient wheezers” early in life no longer have symptoms by the time they are ten.
Asthma in Adults
Symptoms of adult asthma include dyspnea, chest tightness, cough, and wheezing. However, just as in children, not all symptoms may be present in an individual patient. Assessment of BHR in adults is much easier than it is in children, and BHR is often the basis on which the diagnosis of asthma is made. However accurate testing requires properly performed spirometry, including a good effort by the patient. Pulmonary function testing reveals a decreased ratio of Forced Expiratory Volume in one second (FEV1) to Forced Vital Capacity (FVC). An FEV1/FVC ratio less than 70 percent is considered an “obstructive” pattern. FEV1 is the used to grade the degree of obstruction. An improvement in FEV1 or FVC of at least 12 percent and 200 mL following bronchodilator administration is also highly suggestive of asthma.
There is a newly identified entity know as asthma-COPD overlap syndrome (ACOS), which includes patients with features of both COPD and asthma. These diagnoses have classically differed in their pathophysiology and clinical presentations. For details please refer to other chapters (Asthma: Clinical Manifestations and Management and COPD: Clinical Manifestations and Management).
Briefly, as noted below asthma is classically thought to be due to an IgE and Th2 mediated pathway. COPD on the other hand is marked by neutrophilic and CD8+ infiltration. Clinical presentations tend to vary by age (asthma tends on occur earlier in life) and clinical risk factors (e.g., allergens trigger asthma vs. tobacco use predisposing to COPD). Symptoms are more often episodic in asthma and chronic in COPD. However, recent investigation has shown that these two diseases are not always completely distinct.
Airway reversibility was thought to be a hallmark of asthma. However, over time airways remodelling in asthma can lead to irreversible airways obstruction, and there is a subset of COPD patients with a bronchodilator response. Patients with COPD may also have an allergic phenotype. As such, ACOS is becoming an accepted clinical entity and is thought to make up 15-45% of obstructive airways disease. Both diseases can show airways hyperreactivity, and patients with COPD can also have eosinophilic airways inflammation and atopy. It is suggested that ACOS responds better to inhaled corticosteroids than COPD alone, but current guidelines do not yet address management of ACOS.
Occupational or work-related asthma is the most common chronic occupation lung disease in the United States occurring in 250-300 cases per 1 million people per year. It occurs most often in the manufacturing industry and is also commonly seen in health care and education. Occupational asthma is defined as asthma triggered by allergens isolated to the work place environment. Once a patient is sensitized to the trigger, very low dose exposures can trigger symptoms, which are often accompanied by allergic rhinitis and conjunctivitis. There are, however, other exposures that produce irritant-induced asthma symptoms and are not associated with the allergic phenotype.
Occupational asthma is an under diagnosed and undertreated clinical entity. About 16% of all adult-onset asthma is attributed to occupational asthma, and it should be considered in all cases of adult-onset asthma.
Are you sure your patient has asthma? What should you expect to find?
See chapter, Asthma: Clinical Manifestations and Management.
Beware: there are other diseases that can mimic asthma:
In adults, other diseases, such as COPD, are characterized by obstructive lung disease. However, in COPD the improvement in airflow obstruction following bronchodilator is smaller and less complete than in asthma. Other diseases may mimic or co-exist with asthma: Allergic Bronchopulmonary Aspergillosis (ABPA), aspirin-exacerbated respiratory disease (AERD), and vocal cord dysfunction (VCD), among others, must be considered.
How and/or why did the patient develop asthma?
The pathophysiology of asthma is characterized by: bronchoconstriction, airway edema, airway hyperresponsiveness, and lastly airway remodeling. Pathological examination of the lungs may identify cellular and other components of airway inflammation. Nearly 50% of all asthma is allergic asthma.
What is Airway Inflammation?
Airway inflammation is thought to be a major underlying cause of asthma. However, details of the inflammatory process are a source of considerable controversy. Furthermore, mechanisms other than inflammation may be important since not all asthma responds to glucocorticoids or anti-IgE therapy. A variety of cells from various portions of the immune system are present in airway biopsies obtained from asthmatics.
Whether asthma is primarily a disease of innate immunity involving cells like eosinophils and neutrophils or primarily an abnormal adaptive immune response driven by lymphocytes remains unclear. Regardless of its cause, chronic inflammation leads to the classic sequelae of tissue damage and fibrosis, as evident in thickening of the lamina reticularis and smooth muscle hypertrophy. Chronic inflammation also promotes bronchial hyper-responsiveness, which is the hallmark of asthma.
Role of Eosinophils
Eosinophils are characteristically associated with both allergic disease and asthma. Biopsies from most patients with asthma demonstrate eosinophils, and the degree of eosinophilic infiltration correlates with disease severity. Furthermore, eosinophils produce large quantities of biologically active compounds (Table 1) that modulate immune function and impact other tissues, including nerves and endothelial cells. Although eosinophils are often present in asthmatic airways, eosinophil-driven inflammation does not mediate pathogenesis of the disorder in all asthma phenotypes.
Role of Neutrophils
Neutrophils appear to play an important role in asthma pathogenesis for some subtypes of the disease. Neutrophils are present in higher numbers in patients who have more severe disease, such as steroid-dependent asthma or fatal asthma. Like eosinophils, neutrophils generate a host of biologically active compounds that promote further inflammation and tissue damage (Table 1). However, it remains unclear whether neutrophils are directly responsible for asthma symptoms or are simply recruited to areas of pre-existing inflammation.
Role of Macrophages
Macrophages are important regulatory cells of the innate immune response. In response to stimulation, macrophages may enhance inflammation both directly and by recruiting other immune cells. Macrophages also produce anti-inflammatory cytokines, such as IL-10, and can re-orient the immune response by secreting IL-12, thereby promoting TH1, rather than allergic TH2, responses. In addition, macrophages and dendritic cells are potent antigen-presenting cells that activate adaptive immune responses and direct the nature of that response by secreting TH1- or TH2-promoting cytokines. Macrophages may also constitute a link between asthma and infections like respiratory syncitial virus (RSV).
Role of Mast Cells
Mast cells are important mediators of allergic disease, and they also play a role in host defense. Mast cells produce compounds, such as histamine, that cause allergic disease, and they drive allergic inflammation through production of cytokines and proteases. The classic trigger for mast cell activation is cross-linking of IgE on the cell surface; however, other non-specific triggers also induce mast cell activation.
Mast cells are key mediators of allergic disease and of allergy-associated asthma phenotypes. Consistent with this notion is the observation that administration of anti-IgE monoclonal antibody (omalizumab) effectively reduces symptoms for some patients with asthma. However, the response is variable, which underscores the fact that no single inflammatory pathway is responsible for all forms of asthma or all manifestations of the disorder.
Role of Lymphocytes
Lymphocytes, particularly CD4+ helper T cells, direct immune system activation. Asthma is considered an atopic disease in about half of all cases, which results in so-called Th2 skewing, a CD4+ profile that favors Th2 over Th1 expression. Patients with this asthma phenotype have a Th2 imbalance that results in T-cell-production of IL-4, IL-5, and IL-13, leading to local IgE class-switching by B-cells and eosinophil infiltration. Additionally, type 2 innate lymphoid cells (ILC2s), another newly discovered cell type that is distinct from Th2 cells but acts similarly, are stimulated by IL-33, IL-24, and IL-2 and potentiate the Th2 response (Table 1). As such, ILC2s are implicated in allergic asthma as well. Together, in addition to the inflammatory pathway, Th2 and ILCs also play a role in maintaining/restoring epithelial integrity after injury. However, Th2 skewing is neither necessary nor sufficient for development of asthma, and recent evidence suggests that Th1 may also have a role in asthma pathogenesis.
IFNγ-induced promotion of Th1 responses does not decrease asthma severity. IFNγ itself has been found to be elevated in some patients during asthma flares, and those with severe asthma have a fourfold increase in IFNγ-positive T-cells compared to mild or moderate asthma. Together, these data suggest that Th1 activity is also implicated in some subtypes of asthma, particularly asthma that is more difficult to control.
Other T-cells, namely Th9, Th17, Th22, and regulatory T-cells, have also been more recently implicated in asthma. Th9 cells, which secrete IL-9, are also upregulated in asthma and seem to be involved in allergic inflammation, While IL-9 and Th9 cells can propagate Th2-induced inflammation, IL-9 inhibition does not decrease airways inflammation. Therefore, the Th9 cell is not sufficient for asthmatic inflammation, and instead may be a marker of disease severity. Th17 cells secrete IL-17 and may lead to formation of dual positive Th2/Th17 cells. The presence of these cells in BAL fluid is related to increased peripheral eosinophilia is some asthma patients. IL-22, which is secreted by Th22 as well as other T-cells, is implicated in asthma. However, IL-22 can be both protective and pro-inflamatory, so further study needs to investigate the role of IL-22 and Th22 in asthma. Lastly, absence or dysfunction of regulatory T-cells may also play a role in asthma pathogenesis through failure to promote tolerance to inhaled agents, including allergens.
Role of Epithelial Cells
Epithelial cells contribute to the structure of the airways and provide a barrier to inhaled particles and other agents. In addition, airway epithelial cells are highly responsive to their environment and may influence local inflammation. In response to endogenous signals, as well as through interactions with immune cells, endothelial cells alter the expression of adhesion molecules on their surfaces and production of biologically active molecules, including cytokines and proinflammatory mediators (Table 1). These molecules act to recruit inflammatory cells to sites of epithelial cell damage, thus directly promoting inflammation. Some also have local effects, causing increased proliferation of endothelial cells and surrounding connective tissue, resulting in airway remodeling.
Epithelial damage and repair processes, as reflected in increased epidermal growth factor receptor (EGFR) levels, correlate with asthma severity. Whether impaired epithelial repair processes drive the chronic inflammation or dysregulated inflammation results in chronic tissue damage remains unclear.
What is Airway Hyper-responsiveness?
The bronchial smooth muscle in asthma is more likely to constrict in response to stimuli compared with normal airways. Such heightened responsiveness can be demonstrated by performing provocative lung testing, such as methacholine challenge testing (MCT). Inhalation of methacholine, a cholinergic agonist, produces more bronchoconstriction in response to a given dose in asthmatics than in individuals without asthma. Just as exogenously administered chemical agents may cause bronchoconstriction, other stimuli, such as cold air, particulates, allergens, and physical stimuli like exercise, may also induce contraction of bronchial smooth muscle.
Airway Hyper-responsiveness in Asthma
The individual response to bronchospasm-inducing stimuli varies widely. Most asthmatics demonstrate some degree of increased tendency for bronchospasm, but the range of responses among individuals without asthma is broad, and there is overlap between hyper-responsive non-asthmatics and minimally responsive asthmatics. Consequently, a clear cut-off that defines asthma on provocation challenge does not exist. A “positive” challenge is not required and is not used regularly for establishing the diagnosis. However, the extent of airway hyper-responsiveness does appear to correlate with severity of symptoms.
Cause of Airway Hyper-responsiveness
Airway inflammation is believed to underlie bronchial hyper-responsiveness. The number of inflammatory cells (including eosinophils, neutrophils, and T-cells) recovered from bronchoalveolar lavage fluid from asthmatics who undergo bronchoscopy correlates with airway hyper-responsiveness. Adequate treatment with an inhaled corticosteroid decreases hyper-responsiveness, presumably by reducing cellular infiltration and resulting inflammation. However, the effect that inflammation has on airway smooth muscle cells and underlying connective tissues responsible for the hyper-responsiveness, and whether hyper-responsiveness is a direct effect of the inflammation or a consequence of long-term, chronic injury remains unknown.
The Role of Airway Hyper-responsiveness in Asthma Symptoms
Airway hyper-responsiveness leads to airway obstruction, largely a reversible process, with essentially normal airway lumen size in between asthma exacerbations. Notably, however, some degree of irreversible airway narrowing can occur over time as a result of airway remodelling, as described previously. Other factors, such as mucus plug formation, may also affect lumen patency.
Treatment of airway inflammation with oral or inhaled corticosteroids is aimed at reducing airway inflammation and mitigating airway remodelling, airway hyper-responsiveness, and mucus production. In contrast, use of inhaled beta-agonists and other such agents targets a reduction in smooth muscle contraction. Although important in treating acute symptoms, the latter group of medications is short-acting and does not address the underlying cause of asthma symptoms.
Finally, other agents target specific pathways involved in inflammation; examples include leukotriene antagonists (e.g., montelukast, zafirlukast, and zileuton), antihistamines, and anti-IgE monoclonal antibody (e.g., omalizumab). Since each of the affected pathogenic pathways plays a variable role in each asthma patient, the clinical benefit of each class of medication varies from person to person.
One consequence of chronic airway inflammation in asthma is so-called “airway remodeling,” the histologic and cellular characteristics of which can be seen in specimens obtained through biopsy, although not routinely used for clinical purposes in diagnosing or managing asthma. The following cell types are involved in airways damage and remodelling.
The bronchial epithelium consists of pseudostratified, ciliated, columnar cells that sit atop a lining of basal cells that are tightly adherent to the underlying basement membrane. Desquamation of the superficial columnar cells occurs in asthma in response to exposure to allergens or other irritants. Over time, these cells are replaced by simple, stratified, non-ciliated epithelial cells.
The damage is largely caused by products of inflammation (described above). However, evidence exists that airway epithelial cells in asthmatics are more susceptible to damage from inflammatory mediators, inhaled agents, and viral infection than are those in other people. Damage to the epithelium is also caused or enhanced by underlying tissue changes, including thickening and edema of the underlying submucosal tissue, a process that may not depend on the presence of chronic inflammation.
Submucosal airway remodelling in asthma includes thickening of the lamina reticularis that underlies the basement membrane, deposition of collagen, and smooth muscle hypertrophy. The result is an increase in bronchial wall thickness that can be more than twice normal. The degree of thickening may or may not correlate with disease severity. The damage is also mediated by inflammatory cells, including those that reside normally in the tissue, such as macrophages, dendritic cells, and mast cells, as well as those recruited from the circulation, such as neutrophils, eosinophils, and lymphocytes.
Local mediators of this process include myofibroblasts, which, when activated by inflammatory signals, proliferate and increase collagen synthesis. The inflammatory signals include transforming growth factor beta (TGFβ), endothelial growth factor (EGF), tumor necrosis factor (TNF), insulin-like growth factor (IGF), platelet-derived growth factor (PDGF) and possibly vascular endothelial growth factor (VEGF).
Smooth Muscle Hypertrophy
Smooth muscle hypertrophy occurs throughout the airways of asthmatics. Much like the increase in subepithelial connective tissue cells, smooth muscle cell hypertrophy responds to chronic inflammation and repair signals, such as EGF. Repeated, aberrant smooth muscle contraction may also lead to an increase in muscle mass over time. There is increasing recent evidence that the mechanical stress from bronchoconstriction or ventilator-induced lung strategy also result in smooth muscle hyperplasia over time.
Consequences of Airway Remodelling
Airways regmodelling is a complex process and the driving force behind airway remodelling in asthma remains unclear. Regardless of the cause, thickening of the airways combined with increased smooth muscle contraction leads to airway narrowing and obstruction of airflow. Overtime, this process results in more severe disease that is less responsive to therapy and causes increased morbidity and mortality.
Which individuals are at greatest risk of developing asthma?
Important socioeconomic risks for development of asthma include:
Black race, Latino ethnicity
Important medical and environmental risks for development of asthma include:
Family history of asthma or allergies
Maternal smoking during pregnancy
Important environmental factors that decrease risk of asthma include:
Maternal vitamin D supplementation in the third trimester
Infant and childhood exposure to dogs and farm animals
Overall Prevalence of Asthma
In 2009, the National Center for Health Statistics of the Centers for Disease Control estimated the prevalence of asthma in the United States at 17.5 million (7.1%) adults and 7.1 million (9.6%) children. More than half had severe or uncontrolled asthma resulting in an asthma attack within the previous year. These patients made 17 million visits to doctors’ offices and emergency rooms and accounted for over 456,000 hospitalizations. Despite advances in diagnosis and treatment, asthma remains a serious disease that is responsible for more than three thousand deaths annually (1.1 per 100,000 total population).
From 1980 to 1997, asthma prevalence in the United States increased significantly, from 4 to 6 percent. Changes in the National Health Interview Survey in 1997 make direct comparison of more recent and historical data impossible, but asthma prevalence since 2001 also has increased (See Figure 1). However, the rate of asthma attacks, which may be a more important measure, has remained constant, suggesting either recent improvements in asthma management or inclusion of less severe phenotypes.
Asthma Prevalence by Age and Gender
Asthma prevalence is unevenly distributed across gender, age, geography, and income level. In children, asthma is significantly more common among boys (See Figure 2). In early adolescence, the prevalence is equal between the sexes, and asthma becomes more common in women throughout most of adulthood. The overall prevalence of asthma decreases with age in males, but it may increase in females, peaking in the late teenage years. It reaches a plateau by age 25 years for both genders.
Asthma Prevalence by Racial and Ethnic Group, Geography, and Income
Asthma prevalence varies significantly by ethnic group. Asthma is most prevalent among African Americans, who are most at risk for racial discrimination, poorer access to health care, and resultant worse long-term outcomes from asthma. In the United States, asthma affects 8.2 percent of non-Hispanic whites, 11.1 percent of non-Hispanics blacks, and 6.3 percent of Hispanics. Among Hispanics, the prevalence varies widely, with 16.6 percent of Puerto Ricans affected compared with only 4.9 percent of those of Mexican heritage. The reasons for these differences are not clear.
The prevalence of asthma in the Northeast and Midwest is slightly higher than in the South or West. Urban dwellers have a slightly lower prevalence of asthma than do those in rural areas. These differences are much smaller, however, than those observed among various ethnic groups. Finally, asthma prevalence also correlates with income level, decreasing dramatically as income increases above the poverty line.
Obesity and Asthma
Those who are obese have increased incidence of asthma. Obesity is also closely linked to lower socioeconomic status and racial disparities, but obesity alone portends a worse prognosis among those diagnosed with asthma even when race and income are controlled for. It is hypothesized that since obesity results in a proinflammatory state, there is greater risk of developing asthma due to overlap in activation of common inflammatory pathways. Obese children and adolescents also tend to be less bronchodilator responsive and have larger symptom burden compared to non-obese asthmatic controls.
Studies indicate that maternal smoking during pregnancy leads to increased risk of childhood wheezing. On the other hand, vitamin D supplementation during pregnancy has a trend towards decreased incidence of childhood wheezing, although the initial data did not reach statistical significance.
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
See chapter, Asthma: Clinical Manifestations and Management.
What imaging studies will be helpful in making or excluding the diagnosis of asthma?
See chapter, Asthma: Clinical Manifestations and Management.
What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of asthma?
Pulmonary function testing, including provocative lung testing (e.g., methacholine challenge), can be diagnostic of asthma. However, some patients with asthma may have negative pulmonary function tests. For more details, see chapter, Asthma: Clinical Manifestations and Management.
What diagnostic procedures will be helpful in making or excluding the diagnosis of asthma?
See chapter, Asthma: Clinical Manifestations and Management.
What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of asthma?
Although asthma is characterized by a familial predisposition, the disorder is polygenic and is associated with complex inheritance patterns that are strongly influenced by gene-environment interactions. There are no diagnostic genetic tests that can be performed, but it is prudent to understand gene associations, which relate to pathogenesis and clinical course of the disease.
Genetics Versus Environmental Influences in Asthma
Genetic predisposition to asthma may outweigh environmental effects. Individuals from families with a history of asthma frequently develop the disorder despite markedly different environmental exposures. Furthermore, no set of environmental exposures alone is routinely linked to development of asthma. As previously discussed, asthma is a disease with many phenotypes and is characterized by variability in severity and triggers. Application of the candidate gene approach and genome-wide association studies has resulted in identification of several genes and chromosome regions that appear to correlate with development of asthma.
Gene Associations in Asthma
Currently, more than 1800 studies that report on asthma and genetics are listed in the Genetic Association Database. However, the majority of findings in the reports have not yet been replicated or proven to have clinical significance. While many of the genes associated with asthma are involved in immune system function, others are important for maintenance of connective tissues (e.g., matrix metalloproteinases and metallopeptidases), metabolic control, or other functions.
No single gene has been convincingly identified as being causally related to asthma in a large percentage of patients. Rather, asthma is thought to be a complex disease that results from the contributions of many genes. Additionally, epigenetic changes may also play a role, as histone modifications have been associated with bronchial hyperresponsiveness and corticosteroid resistance in asthma.
If you decide the patient has asthma, how should the patient be managed?
See chapter, Asthma: Clinical Manifestations and Management.
What is the prognosis for patients managed in the recommended ways?
Consequences of Asthma
Asthma results in considerable morbidity and utilization of health care resources. In 2009, asthma-related outpatient physician visits totalled 7.8 million for adults and 7.5 million for children. In the same year, 1.1 million adults and 0.6 million children had asthma-related emergency room visits, and asthma-related hospitalizations exceeded 299,000 for adults and 157,000 for children.
A large case control study showed that adults with asthma have increased all-cause mortality compared to non-asthmatic controls over a 25-year study period, and most of the deaths in the asthmatic group were due to obstructive lung disease or status asthmaticus. Risk factors for death were older age, lower FEV1, large degree of bronchodilator response, elevated peripheral eosinophil count at time of enrolment, and prior hospital encounters for asthma.
Although black and white asthmatic patients generate the same relative numbers of ambulatory visits for asthma, black patients are more than three times as likely to visit the emergency room and nearly twice as likely to be hospitalized as white patients. Finally, of the 3447 asthma deaths reported in 2007, 185 were children. Among children with asthma, black children have over twice the likelihood of hospital readmission than white counterparts. Asthma-related mortality is higher among blacks than among other ethnic groups. Research has shown that socioeconomic disparities play a large role in the clinical outcomes of black children with asthma. Additionally black children have increased exposure to allergens, less use of long-acting bronchodilators, and increased reliance on rescue inhalers.
In addition to generating significant health care expenses, asthma accounts for substantial costs in lost productivity. Asthma is responsible for 10.5 million missed school days, as nearly 60 percent of children with asthma miss at least one day of school annually. In addition, 5.5 percent of asthmatic children have a long-term reduction in activity level compared with other children of the same age.
Employed adults with asthma miss more than 14 million workdays annually, and nearly 34 percent of adult asthmatics miss at least one day of work annually. An additional 22 million days of household work or other work are lost annually among asthmatics who are not employed outside the home. Estimates suggest that asthma-related costs were more than $56 billion in 2007, or about $3300 per asthmatic.
Natural History of Asthma
In the majority of cases, asthma begins during childhood. During the first three years of life, half of children have wheezing associated with a viral upper respiratory infection, a small proportion of which develop true asthma. Most children have resolution of their asthma as they grow. Children who are born prematurely can outgrow their asthma, but a significant number continue to have asthma-associated symptoms through adolescence and beyond or have recurrence of disease as an adult.
Unlike children, adults diagnosed with asthma rarely have complete remission of their disorder. The risk of asthma-related death increases with age and may be underreported. Asthma is a source of significant morbidity and may be life threatening, especially when it is present with other comorbidities, such as cardiac disease and severe food or medication allergies.
What other considerations exist for patients with asthma?
See chapter, Asthma: Clinical Manifestations and Management.
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- What every physician needs to know:
- Are you sure your patient has asthma? What should you expect to find?
- Beware: there are other diseases that can mimic asthma:
- How and/or why did the patient develop asthma?
- What is Airway Inflammation?
- Role of Eosinophils
- Role of Neutrophils
- Role of Macrophages
- Role of Mast Cells
- Role of Lymphocytes
- Role of Epithelial Cells
- What is Airway Hyper-responsiveness?
- Airway Hyper-responsiveness in Asthma
- Cause of Airway Hyper-responsiveness
- The Role of Airway Hyper-responsiveness in Asthma Symptoms
- Airways remodelling
- Epithelial Damage
- Submucosal Remodeling
- Smooth Muscle Hypertrophy
- Consequences of Airway Remodelling
- Which individuals are at greatest risk of developing asthma?
- What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
- What imaging studies will be helpful in making or excluding the diagnosis of asthma?
- What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of asthma?
- What diagnostic procedures will be helpful in making or excluding the diagnosis of asthma?
- What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of asthma?
- If you decide the patient has asthma, how should the patient be managed?
- What is the prognosis for patients managed in the recommended ways?
- What other considerations exist for patients with asthma?