• 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.


  • 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


  • 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


  • 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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