Asthma is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles


  • Asthma is a heterogeneous airway disease characterized by chronic inflammation, hyperresponsiveness with exposure to a wide variety of stimuli, and variable airflow obstruction. As a consequence, patients have paroxysms of cough, dyspnea, chest tightness, and wheezing.
  • Asthma is a chronic disease with episodic acute exacerbations that are interspersed with periods of symptomatic variability. Exacerbations are characterized by a progressive increase in asthma symptoms that can last minutes to hours. They are associated with viral infections, allergens, and occupational exposures, and occur when airway reactivity is increased and lung function becomes unstable.


  • Asthma severity should be classified based on both level of impairment (symptoms, lung function, daily activities, and rescue medication use) and risk (exacerbations, lung function decline, and medication side effects).
  • At the initial evaluation, this assessment will determine the level of severity in patients not on controller medications (Table 9-10). The level of severity is based on the most severe category in which any feature appears. On subsequent visits, or if the patient is on a controller medication, this assessment is based on the lowest step of therapy to maintain clinical control (Table 9-11). Control of asthma is based on the most severe impairment or risk category.
    Table 9-10: Classification of Asthma Severity on Initial Assessment

    IntermittentMild PersistentModerate Persistent
    Severe Persistent
    Daytime symptoms≤2 d/wk≥2 d/wk but not dailyDaily
    Throughout the day
    Nighttime symptoms≤2×/mo3–4×/mo≥1×/wk but not nightly
    Activity limitationsNoneMinorSome
    Reliever medicine use≤2 d/wk≥2 d/wk but not dailyDaily
    Several times per day
    ManagementStep 1Step 2Step 3Step 4Step 5
    Low-dose ICSLow-dose ICSMedium- or high-dose ICS + LABAAdd-on therapy: i.e., anti-IL-5/α, anti-IL4α, omalizumab, bronchial thermoplasty
    AlternativeLow-dose ICS
    LTRA, cromolyn, theophyllineHigh-dose ICS + LTRA or theophyllineConsider low-dose OCS
    In 2–6 wk, evaluate level of asthma control and adjust therapy accordingly.

    Data from the 2018 GINA Report: Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma – GINA. Updated 2018. Accessed September 13, 2018 and Asthma NAE and PP Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 32018 GINA Report: Guidelines for the Diagnosis and Management of Asthma. National Heart, Lung, and Blood Institute (US); 2007.

    FEV1, forced expiratory volume in 1 second; ICS, inhaled corticosteroid; IL, interleukin; LABA, long-acting β-adrenergic agonist; LTRA, leukotriene receptor antagonist; OCS, oral corticosteroid.

    Table 9-11: Assessment of Asthma Control

    Well ControlledNot Well ControlledVery Poorly Controlled
    Daytime symptoms≤2 d/wk>2 d/wkThroughout the day
    Nighttime symptomsNone1–3×/wk≥4×/wk
    Activity limitationsNoneSomeExtreme
    Reliever medicine use≤2×/wk>2×/wkFrequent
    FEV1 or PEF≥80%60%–80%<60%
    Validated questionnaireACT ≥20
    ACQ <0.75
    ACT 16–19
    ACQ >1.5
    ACT ≤15
    ManagementMaintain at lowest step possible
    Consider step down if well controlled for ≥3 mo
    Step up one stepStep up one to two steps and consider short-course OCS
    Follow-up1–6 mo2–6 wk2 wk

    Data from the 2018 GINA Report: Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma – GINA. Updated 2018. Accessed September 13, 2018 and Asthma NAE and PP Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. National Heart, Lung, and Blood Institute (US); 2007.

    ACT, Asthma Control Test; ACQ, Asthma Control Questionnaire; FEV1, forced expiratory volume in 1 second; OCS, oral corticosteroids PEF, peak expiratory flow.

  • During an exacerbation, the acute severity of the attack should be classified based on symptoms, signs, and objective measures of lung function (Table 9-12).
    Table 9-12: Classification of Asthma Exacerbation Severity

    ModerateSevereImpending Respiratory Arrest
    FEV1 or PEF predicted or personal best40%–69%<40%<25% or unable to measure
    SymptomsDOE or SOB with talkingSOB at restSevere SOB
    ExamExpiratory wheeze
    Some accessory muscle use
    Inspiratory and expiratory wheeze
    Increased accessory muscle use
    Chest retraction
    Agitation or confusion
    Wheeze may become absent
    Accessory muscle use with paradoxical thoracoabdominal movement
    Depressed mental status
    VitalsRR <28/min
    HR <110 bpm
    O2sat >91% RA
    No pulsus paradoxus
    RR >28/min
    HR >110 bpm
    O2sat <91% RA
    Pulsus paradoxus >25 mm Hg
    Same as severe but could develop respiratory depression and/or bradycardia
    PaCO2Normal to hypocapnia>42 mm HgHypercapnia is a late sign

    Data from the 2018 GINA Report: Global Strategy for Asthma Management and Prevention. Global Initiative for Asthma – GINA. Updated 2018. Accessed September 13, 2018 and Asthma NAE and PP Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. National Heart, Lung, and Blood Institute (US); 2007.

    DOE, dyspnea on exertion; FEV1, forced expiratory volume in 1 second; HR, heart rate; O2sat, oxygen saturation; PEF, peak expiratory flow; RA, room air; RR, respiratory rate; SOB, shortness of breath.

  • Patients who have had two or more exacerbations requiring systemic corticosteroids in the past year may be considered in the same category as those who have persistent asthma, regardless of level of impairment.


In the United States:

  • Asthma is a highly prevalent problem, affecting 8.3% of American adults and children.1
  • The prevalence of asthma is highest among black children, with 15.7% of that population carrying the diagnosis.


Possible factors for asthma development can be broadly divided into host, genetic, and environmental factors.

  • There have been multiple genes, chromosomal regions, and epigenetic changes associated with the development of asthma. Racial and ethnic differences have also been reported in asthma and are likely the result of a complex interaction between genetic, socioeconomic, and environmental factors.
  • There are multiple environmental factors that contribute to the development and persistence of asthma. Severe viral infections early in life, particularly respiratory syncytial virus and rhinovirus, are associated with the development of asthma in childhood and play a role in its pathogenesis.
  • Childhood exposure and sensitization to a variety of allergens and irritants (e.g., cigarette smoke, mold, pet dander, dust mites, cockroaches) may play a role in the development of asthma, but the exact nature of this relationship is not yet fully elucidated. By contrast, early-life exposure to indoor allergens together with certain bacteria (microbiome) may be protective for urban children. The prevalence of asthma in children raised in a rural setting is reduced, although the reason for this is not fully known.


Asthma is characterized by airway obstruction, hyperinflation, and airflow limitation resulting from multiple processes:

  • Acute and chronic airway inflammation characterized by infiltration of the airway wall, mucosa, and lumen by activated eosinophils, mast cells, macrophages, and T lymphocytes. Components of innate immunity including natural killer T cells, neutrophils, and innate lymphoid lymphocytes are also implicated.
  • Bronchial smooth muscle contraction resulting from mediators released by a variety of cell types including inflammatory, local neural, and epithelial cells.
  • Epithelial damage manifested by denudation and desquamation of the epithelium leading to mucous plugs that obstruct the airway.
  • Airway remodeling characterized by the following findings:
    • Subepithelial fibrosis, specifically thickening of the lamina reticularis from collagen deposition
    • Smooth muscle hypertrophy and hyperplasia
    • Goblet cell and submucosal gland hypertrophy and hyperplasia resulting in mucous hypersecretion
    • Airway angiogenesis
    • Airway wall thickening due to edema and cellular infiltration

Risk Factors

A number of factors increase airway hyperresponsiveness and can cause an acute and chronic increase in the severity of the disease:

  • Allergens such as dust mites, cockroaches, pollens, molds, and pet dander in susceptible patients.
  • Viral upper respiratory tract infections.
  • Many occupational allergens and irritants such as perfumes, cleaners, or detergents, even in small doses.
  • Changes in weather (i.e., from warm to cold), strong emotional stimuli, and exercise.
  • Indoor and outdoor pollutants, such as nitrogen dioxide (NO2) and tobacco and wood smoke, can trigger acute bronchospasm and should be avoided by all patients.
  • Obesity is associated with increased asthma severity.
  • Medications such as β-blockers (including ophthalmic preparations), aspirin, and NSAIDs can cause the sudden onset of severe airway obstruction.


  • Strict compliance and appropriate follow-up can help prevent worsening of asthma control.
  • Identification and avoidance of risk factors (allergens, irritants) that exacerbate symptoms play a key role in prevention.
  • Recognition and management of comorbidities such as obesity, sinonasal diseases, gastroesophageal reflux disease (GERD), and psychiatric disorders are important.
  • All patients with asthma should receive a yearly influenza vaccination.

Associated Conditions

  • Rhinosinusitis, with or without nasal polyps, is frequently present and should be treated with intranasal or oral corticosteroids, saline rinses, and/or antihistamines. Antibiotics should be reserved for superimposed bacterial infections.
  • Vocal cord dysfunction (VCD) can coexist with or masquerade severe, uncontrolled asthma. Diagnosis often requires provocation testing with laryngoscopy, otherwise the findings are often normal. Treatment consists of speech and, if needed, behavioral therapy.
  • Symptomatic GERD can cause cough and wheezing in some patients and may benefit from treatment with H2 blockers or proton pump inhibitors. Empiric treatment of GERD in asymptomatic patients with uncontrolled asthma is not an effective strategy.
  • Obesity is increasingly being recognized as a comorbid condition as well as possibly playing a role in worsening asthma control. This may be related to altered lung mechanics, altered respiratory patterns, or an increase in systemic inflammation. Obese patients should be strongly encouraged to focus on weight loss through diet and exercise.
  • Smoking prevalence in patients with asthma is the same as the general population. Although no convincing evidence links tobacco use with developing asthma, it may make patients less responsive to ICSs and more difficult to control. Tobacco cessation should be encouraged in all patients.
  • Obstructive sleep apnea (OSA) may make asthma more difficult to control and should be addressed with an overnight polysomnogram if suspected.

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