Asthma

Basics

Description

Characterized by three components:
- Reversible airway obstruction
- Airway inflammation
- Airway hyperresponsiveness to a variety of stimuli
Diagnosis (the three “R”s)
- Recurrence: Symptoms are recurrent.
- Reactivity: Symptoms are brought on by a specific occurrence or exposure (trigger).
- Responsiveness: Symptoms diminish in response to bronchodilator or anti-inflammatory agent.

Epidemiology

1 out of 10 school-aged children in the United States has asthma, making it one of the common chronic illnesses in children.
Current asthma prevalence among children in the United States is 8.6% and has been rising since the early 1980s across all age, sex, and ethnic groups.
Incidence is >5 times higher in younger children (age 0 to 4 years) than older children (age 5 to 17 years).
Incidence and prevalence vary widely based on geographic, ethnic, and socioeconomic factors.
- Prevalence and rate of exacerbations is highest in Puerto Ricans compared to all ethnic groups.
Up to 75% of adolescents who wheeze will have asthma which persists in to adulthood, especially if comorbidities are present.
Impact
- Asthma accounts for 25% of all emergency room visits annually and is the third ranking cause of hospitalization in children <15 years.
- Asthma is leading cause of school absenteeism in children ages 5 to 17 years, accounting for nearly 14 million missed school days per year.
Disparities
- Morbidity and mortality are disproportionately higher among low-income, minority, and inner-city children likely due to limited access to culturally sensitive care.
- African American children are >3 times more likely to be hospitalized or die from asthma compared to Caucasian children.
- Minority children are less likely to use controller medications, which may be due in part to underprescribing, limited access to care, and poor adherence.
Mortality
- Overall, death from asthma in children has decreased by 26% since 1999, perhaps owing to better recognition and increased use of anti-inflammatory medications.
- Death from asthma may occur in any asthma of any severity but is more likely when asthma is poorly recognized and under controlled.

Risk Factors

Family history of asthma
- Parental history of asthma increases a child’s risk of asthma 3 to 6 fold, with slightly higher risk thought to be conferred in maternal asthma.
Prematurity
Allergic rhinitis and atopic dermatitis
Obesity/overweight
History of viral infections in early childhood
Tobacco smoke exposure
Exposure to inhaled allergens (such as dust mite, mold) or chemical irritants

Genetics

Asthma is a heterogenous condition; identification of phenotype can help stratify asthma subgroups and better predict individual clinical response to therapy.
In addition to previously identified allergic and nonallergic phenotypes, other features such as age at onset, degree of airway obstruction, and endotype have been included in the refinement of asthma phenotypes.
Several studies have suggested that epigenetics may have a role in the pathogenesis of asthma via mechanisms such as DNA methylation (reversible DNA modification in response to environmental influence).
Emerging methods such as genome-wide association studies (GWASs) have identified genetic polymorphisms that help explain certain ethnic disparities as well as variations in atopic pathogenesis, severity, and response to medications.

General Prevention

Currently, no known methods for primary prevention of asthma
Once asthma is diagnosed, strategies focus on preventing of severe exacerbations and lost work/school days as well as comorbidities such as obesity, depression.
All children with asthma should receive the inactivated influenza vaccine annually, starting at age 6 months.
Effective measures (see “Patient Education”) include:
- Good adherence with environmental, behavioral, and medical treatment plan
- Written asthma action plan: shown to reduce emergency department visits and lost school/work days
- Education about and avoidance of triggers

Pathophysiology

Immune and inflammatory responses in the airways are triggered by an array of environmental antigens, irritants, or infectious organisms.
Airway is stimulated and primary inflammatory mediators released
Airway is invaded by inflammatory cells (mast cells, basophils, eosinophils, macrophages, neutrophils, B and T lymphocytes).
Inflammatory cells respond to and produce various mediators (cytokines, leukotrienes, lymphokines), augmenting the inflammatory response.
Airway epithelium is inflamed and becomes disrupted, and basal membrane is thickened.
Airway smooth muscle is hyperresponsive, and bronchoconstriction ensues.
Eosinophilia and the ability to make excess IgE in response to antigen are associated with increased airway reactivity.
Viral infections, particularly respiratory syncytial virus (RSV) during infancy, may play a role in the development of asthma or may modify the severity of asthma.
Airway smooth muscle hypertrophy and airway epithelial hyperplasia are characteristic chronic changes resulting from poorly controlled asthma.

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