This chapter will review the recommendations from the 2007 National Asthma Education and Prevention Program Guidelines and Global Initiative for Chronic Obstructive Lung Disease 2019.
An acute or subacute episode of worsening shortness of breath, cough, wheezing, and chest tightness, or a combination of these symptoms.
Mortality risk factors
Previous severe exacerbation (e.g., intubation or intensive care unit admission for asthma).
Two or more hospitalizations or three or more emergency department (ED) visits in the previous year.
Hospitalization or ED visit for asthma in the past month.
Use of more than two canisters of short-acting β-agonists per month.
Difficulty perceiving asthma symptoms or severity of exacerbations.
Social history that includes major psychosocial problems, illicit drug use, low socioeconomic status.
Concomitant illnesses including cardiovascular diseases, psychiatric illness, or other chronic lung diseases.
|Inhaled Short-Acting β2-Agonists (SABA): cornerstone in management of acute, severe asthma. |
MOA: stimulate β2 receptors causing relaxation of respiratory smooth muscle, leading to bronchodilation and a decrease in airway obstruction.
Nebulizer solution (2.5 mg/3 mL, 5 mg/mL)
MDI or dry powder inhaler (90 mcg/puff)
|2.5–5 mg q20min ×3, then 2.5–10 mg q1–4h PRN or 10–15 mg/h continuously |
Four to eight puffs q20min up to 4h, then q1–4h PRN
May mix with ipratropium nebulizer solution
Wait 15 s between actuations
Nebulizer solution (1.25 mg/0.5 mL, 1.25 mg/3 mL)
MDI (45 mcg/puff)
1.25–2.5 mg q20min ×3, then 1.25–5 mg q1–4h PRN
See albuterol MDI dose
|Continuous nebulization not evaluated |
Levalbuterol one-half the mg dose of albuterol provides comparable efficacy and safety
|Systemic β2-Agonists (Subcutaneous): if no response to inhaled therapy after a few hours.|
|Epinephrine 1:1,000 (1 mg/mL)||0.3–0.5 mg q20min ×3||No proven advantage of systemic therapy over aerosol|
|Terbutaline (1 mg/mL)||0.25 mg q20min ×3|
|Anticholinergics: given in combination with SABA |
MOA: bind to muscarinic receptors on respiratory smooth muscle, leading to reduction in bronchoconstriction
|Ipratropium bromide |
Nebulizer solution (0.25 mg/mL)
MDI (18 mcg/puff)
0.5 mg q20min ×3, then PRN
Eight puffs q20min PRN up to 3 h
|Not a first-line therapy; should be added to SABA for severe exacerbations |
May mix with albuterol nebulizer solution
|Ipratropium with albuterol |
Nebulizer solution (0.5 mg/2.5 mg per vial)
MDI (18 mcg/90 mcg per inhalation)
|3 mL q20min ×3, then PRN |
Eight puffs q20min PRN up to 3 h
|Adding ipratropium to albuterol has shown benefit in severe exacerbations, not in mild or moderate exacerbations|
|Systemic Corticosteroids : for moderate-severe exacerbations or for patients with inadequate response to SABA treatment.|
|MOA: decrease airway obstruction by reducing inflammation and airway edema, increase the number of β2 receptors and their responsiveness to β-agonists, and suppress proinflammatory cytokines.|
|Prednisone||40–80 mg/day in one to two divided doses until PEF 70% of predicted or personal best||Duration: 3–10 days (no tapering necessary)|
Chronic obstructive pulmonary disease (COPD) exacerbation
A change in the patient’s baseline dyspnea, cough, or sputum production necessitating additional treatment.
Common causes of acute COPD exacerbation
Respiratory tract infection (most common).
Bacterial: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis .
Viral: influenza, rhinovirus, parainfluenza, respiratory syncytial virus.
Mechanical ventilation: noninvasive or invasive.
Acute therapy ( Table 16.2 ).