Asthma is a chronic inflammatory disorder of the airways whereby bronchial hyperresponsiveness from exposure to a variety of stimuli results in an exaggerated bronchoconstrictor response, causing recurrent episodes of coughing, wheezing, breathlessness, or chest tightness. The resulting airflow obstruction is usually reversed spontaneously or with asthma treatment.
Often misused interchangeably with asthma, “reactive airway disease” is a non-specific term that does not indicate a specific diagnosis and should not be considered synonymous with asthma.
Clinical diagnosis of asthma is likely when episodic wheezing, dyspnea or cough improve with an inhaled bronchodilator, but should be confirmed with spirometry by demonstrating the reversibility of airflow limitation.
Cough (often reported to be worse at night)
These symptoms are typically episodic in nature with resolution noted on removal of exposure to the trigger or with use of anti-asthma medications.
Commonly reported triggers include: allergens (e.g. dust, mold, furred animals, pollen), cold air, exercise, viral infections, occupational irritants, tobacco smoke, and rarely aspirin.
A personal or family history of atopy (seasonal allergic rhinitis/conjunctivitis, atopic dermatitis or hives) also suggests the diagnosis of asthma in a patient with typical respiratory symptoms.
Asthma affects approximately 300 million individuals worldwide. Over the past 20 years, the prevalence of asthma has increased significantly. Although 75% of cases are diagnosed by the age of seven, asthma may develop at any age. New-onset asthma is an uncommon diagnosis in the elderly population.
Development of asthma appears to be the result of interplay between genetic susceptibility and environmental exposure during a crucial time in immune system development.
Environmental exposures that play a role in the development of asthma include airborne allergens, viral respiratory infections (e.g. respiratory syncytial virus and rhinovirus), and to a lesser degree, tobacco smoke, air pollution and diet (obesity or low intake of antioxidants and omega-3 fatty acids).
Chronic obstructive pulmonary disease (COPD): significant smoking history of more than 20 pack years.
Cardiac asthma: wheezing caused by bronchospasm in congestive heart failure. History reveals paroxysmal nocturnal dyspnea, pedal edema, or other symptoms of congestive heart failure (CHF).
Pulmonary embolism: history suggests risk factors for venous thromboemboli or presence of deep vein thrombosis.
Mechanical obstruction of airways by either foreign body aspiration or external compression of trachea/bronchi.
Vocal cord dysfunction (VCD): symptoms suggestive of asthma but spirometry may show inspiratory loop flattening and response to asthma medications will be poor.
Gastroesophageal reflux: reports of heartburn, dysphagia or regurgitation.
High-pitched, multiphasic or musical wheeze most often heard during expiration but sometimes audible during inspiration. The presence or absence of wheeze does not predict the severity of airflow obstruction.
Findings in severe airflow obstruction include inability to speak in full sentences, tachycardia, tachypnea, use of accessory muscles, prolonged expiration, and sitting in the “tripod position” (extending arms to support the chest).
Finding pale, swollen nasal mucosa suggests allergic rhinitis and the presence of nasal polyps could represent concomitant aspirin sensitivity.
The preferred method for establishing the diagnosis of asthma is spirometry, which objectively measures airflow limitation and reversibility. An increase in forced expiratory volume 1 (FEV1) of at least 12% and 200 milliliters (ml) after administration of a bronchodilator indicates reversible airflow obstruction consistent with asthma.
Occasionally, spirometry will be normal and bronchoprovocation with methacholine, histamine, cold air, or exercise challenge may be necessary to diagnose asthma.
Certain pulmonary function studies are helpful in differentiating asthma from alternative diagnoses: chronic obstructive pulmonary disease (COPD) (diffusing capacity), restrictive lung disease (measuring lung volumes, FEV1/FVC [forced vital capacity] ratio), VCD (evaluating inspiratory flow-volume loops).
Laboratory studies are usually not indicated for the diagnosis of asthma, but can be useful in tailoring treatment regimens, assessing severity of exacerbation and for monitoring response to therapy.
Complete blood count (CBC): eosinophilia greater than 4% supports the diagnosis. If greater than 8%, consider allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome or eosinophilic pneumonia.
Serum immunoglobulin (Ig) E level: may be elevated to more than 100 international units (IU), but it is non-specific.
Allergen skin testing or measurement of allergen specific IgE can help to identify risk factors.
Arterial blood gas: helpful in assessing the severity of an acute exacerbation of asthma by evaluating for hypoxemia or hypercarbia.
Chest X-ray (CXR) and computed tomography (CT) chest scan are almost always normal in patients with uncomplicated asthma and usually unnecessary in the diagnosis of asthma. However, they may be useful if there is high suspicion for alternative diagnoses (e.g. CXR revealing heart failure or external compression of trachea by a mass or CT pulmonary angiogram finding pulmonary embolus).
CXR and CT scans are unnecessary for establishing the diagnosis of asthma and should only be performed when the presentation is atypical (i.e. excessive mucus production or rapid decline in lung function).
Depends on severity of the acute exacerbation, which can be assessed by physical exam (auscultation, use of accessory muscles, heart rate, respiratory rate) and objectively by measuring peak expiratory flow rate (PEFR). PEFR less than 40% of predicted or patient’s personal best implies a severe exacerbation.
Supplemental oxygen (O2) to keep saturation of peripheral oxygen (SpO2) greater than 90%. Intubation with mechanical ventilation in cases of impending or actual respiratory arrest.
Inhaled short-acting beta2 agonists (SABAs) by nebulizer given every 20 minutes in the first hour. In severe exacerbations, add ipratropium by nebulizer every 20 minutes.
Systemic corticosteroids: should be given to all patients with severe exacerbation and to those with mild to moderate exacerbations who fail to respond to nebulized SABAs. There is no proven difference in the efficacy of oral versus parenteral steroids. Use parenteral steroids in those unable to tolerate it orally (e.g. intubated patients).
Magnesium sulfate intravenous (IV) has some bronchodilator activity, but has not been proven to be more effective than placebo in the treatment of severe asthma exacerbations.
Monitor heart rate: most patients are tachycardic during an acute exacerbation. Supraventricular tachycardia can be seen in theophylline toxicity.
Monitor lung sounds: assessing for adequate air entry, expiratory wheezes.
Continuous pulse oximetry: monitor for severe hypoxemia (SpO2 < 95% in spite of supplemental O2 via non-rebreather mask).
The following clinical danger signs are indicative of imminent respiratory arrest: inability to maintain respiratory effort, cyanosis and depressed mental status.
PEFR less than 200 liters/minute in adults is indicative of severe obstruction. It takes less than 1 minute to perform and can be repeated at various intervals to monitor response to therapy. Additionally, PEFR measurements are valuable predictors for the possibility of hypercapnia. Hypercapnia usually only occurs when PEFR is less than 25% of normal.
Arterial blood gas (ABG) monitoring is also useful in assessing respiratory status. An ABG showing new respiratory acidosis indicates respiratory musculature fatigue and is an indication for intubation.
Regimens for the long-term management of asthma are dependent on the severity of the patient’s asthma.
Two or less daytime asthma symptoms per week, two or less nocturnal awakenings per month, use of SABAs for symptom relief less than two times per week, normal FEV1 measurements and FEV1/ FVC ratio between exacerbations, oral corticosteroid use only once or less per year, and no limitations with normal activities in between exacerbations.
Symptoms more than twice a week (but not daily), three to four nocturnal awakenings per month, use of SABAs more than twice a week (but not daily), FEV1 measurements and FEV1/FVC ratio within normal range, oral corticosteroid use two or more times per year, and minor limitation in normal activities.
Any of the following: daily asthma symptoms, nocturnal awakenings more than once a week, daily use of SABAs, FEV1 is 60-80% of predicted, reduced FEV1/FVC ratio, oral corticosteroid use two or more times per year, and some limitation in normal activity.
One or more of the following: symptoms throughout the day, nightly awakenings, use of SABAs for relief multiple times a day, FEV1 less than 60% of predicted, FEV1/FVC ratio reduced, oral corticosteroid use two or more times per year, and extreme limitation in normal activity.
Once the severity is categorized, a stepwise approach developed by the 2007 National Asthma Education and Prevention Program (NAEPP) expert panel report is used to guide treatment. A stepwise escalation and de-escalation of therapy based on control of symptoms is recommended using the following approach.
Step 1 (intermittent): intermittent asthma is best treated with SABAs as needed.
Step 2 (mild persistent): start daily long-term controller, preferably low-dose inhaled corticosteroid (ICS).
Step 3 (moderate persistent): either low dose ICS plus long-acting beta2 agonist (LABA) or medium doses of ICSs.
Step 4 (severe persistent): medium dose ICS plus LABA.
Step 5 (severe persistent): high dose ICS plus LABA. Consider omalizumab for patients with allergies.
Step 6 (severe persistent): high dose ICS plus LABA plus oral corticosteroid. Consider omalizumab for patients with allergies.
Despite which step they are on, all patients should use SABAs as needed for quick symptom relief.
ICSs are the most consistently effective long-term control medication. Regular use of ICSs decrease the need for SABAs for symptom relief and decrease the risk of severe exacerbations. Nearly all patients with exacerbations severe enough to warrant an emergency department visit should be started on ICSs regularly.
Alternative long-term controllers include leukotriene receptor antagonists, cromolyn or theophylline.
Identify and avoid precipitating factors.
Omalizumab (an antibody to IgE) may be recommended by an asthma specialist for patients over 12 years of age who are sensitive to relevant allergens. Indications for treatment include diagnosis of moderate-to-severe persistent asthma, asthma symptoms not well controlled with inhaled glucococorticoids, total IgE level ranging from 30 to 700 international units/liter, and positive allergy testing to an allergen present year-round.
No change in standard management.
No change in standard management.
No change in standard management.
Use of beta-blockers for coronary artery disease can worsen bronchial obstruction and airway reactivity in patients with chronic asthma and should generally be avoided. Although not contraindicated in patients with asthma, angiotensin-converting enzyme (ACE) inhibitor use has an uncommon effect of worsening bronchial obstruction in asthma.
Oral glucocorticoid use causes hyperglycemia and adjustments to diabetes regimens should be considered to manage this side effect. Chronic steroid use also causes suppression of the hypothalamic-pituitary-adrenal axis.
No change in standard management.
Recurrent asthma exacerbations requiring chronic steroid use can cause immunosuppression. Use of inhaled corticosteroids is frequently associated with oral thrush. Patients should be advised to rinse mouth after use of ICS.
Asthma and COPD are increasingly recognized as heterogeneous and sometimes overlapping syndromes. The prevalence of Asthma-COPD overlap syndrome (ACOS) increases with age. ACOS is characterized by increased neutrophilic mucosal inflammation and airway obstruction, with limited reversibility with bronchodilators. Due to the lack of randomized studies evaluating ACOS, there is no change in the acute management of an exacerbation.
Ulcers, gastritis and gastrointestinal bleeding can occur as the result of systemic steroid use. In patients with pre-existing peptic ulcer disease, consider adding gastrointestinal prophylaxis if a prolonged course of steroids is anticipated.
No change in standard management.
No change in standard management.
Taper steroids as respiratory symptoms improve. Patient should be started on inhaled corticosteroid therapy prior to hospital discharge.
Anticipated length of stay for an uncomplicated asthma exacerbation is 2 to 3 days.
When the patient has no signs of respiratory distress, does not require any supplemental O2 to maintain adequate O2 saturation (>93%), is able to tolerate oral glucocorticoids, and is using bronchodilators less frequently (every 6 hours or less).
Recommend outpatient follow-up with primary care doctor within 3 to 5 days. If patient experiences frequent symptoms or has difficult to control asthma, a referral to a pulmonologist or allergist is warranted. When possible, scheduling the appointments prior to discharge and a reminder phone call within 48 hours of discharge can help in compliance with outpatient follow-up.
Identify asthma triggers and emphasize avoiding them.
Demonstrate the proper technique of using inhalers.
Strongly advice smoking cessation.
Demonstrate to the patient the proper technique of measuring PEFR. Patients should also be advised to measure a baseline peak flow to compare to during periods of acute exacerbations.
There are currently no Joint Commission core indicators for asthma in the adult population.
Standard recommendations should be applied for initiation of deep vein thrombosis prophylaxis. Consider adding peptic ulcer disease prophylaxis if patient will be receiving systemic glucocorticoids and aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) concurrently.
Almost all patients with asthma exacerbations significant enough to warrant an emergency department evaluation should be discharged home on a short course of oral glucocorticoids and with recommendations to start inhaled corticosteroids regularly if not started prior to discharge.
“National Asthma Education and Prevention Program: Expert panel report III: Guidelines for the diagnosis and management of asthma. National Heart, Lung, and Blood Institute, US Dept of Health and Human Services”. NIH publication. 2007. pp. 08-4051.
“Global initiative for asthma (GINA): Global strategy for asthma management and prevention”. 2011.
Rodrigo, GJ, Rodrigo, C, Hall, JB. “Acute asthma in adults: a review”. Chest. vol. 125. 2004. pp. 1081-1102.
Benatar, SR. “Fatal asthma”. N Engl J Med. vol. 314. 1986. pp. 423-428.
Stein, LM, Cole, RP. “Early administration of corticosteroids in emergency room treatment of acute asthma”. Ann Intern Med. vol. 112. 1990. pp. 822-827.
McFadden, ER. “Acute severe asthma”. Am J Respir Crit Care Med. vol. 168. 2003. pp. 740-759.
Skobeloff, EM, Spivey, WH, McNamara, RM, Greenspon, L. “Intravenous magnesium sulfate for the treatment of acute asthma in the emergency department”. JAMA. vol. 262. 1989. pp. 1210-1213.
Edmonds, ML, Camargo, CA, Brenner, BE, Rowe, BH. “Replacement of oral corticosteroids with inhaled corticosteroids in the treatment of acute asthma following emergency department discharge: a meta-analysis”. Chest. vol. 121. 2002. pp. 1798-1805.
Bateman, ED, Reddel, HK, Eriksson, G. “Overall asthma control: the relationship between current control and future risk”. J Allergy Clin Immunol. vol. 125. 2010. pp. 600-608.
Castro, M, Zimmermann, NA, Crocker, S. “Asthma intervention program prevents readmissions in high healthcare users”. Am J Respir Crit Care Med. 2003. pp. 1681095-1099.
Janson, SL, McGrath, KW, Covington, JK. “Individualized asthma self-management improves medication adherence and markers of asthma control”. J Allergy Clin Immunol. vol. 123. 2009. pp. 840-846.
Cates, CJ, Wieland, LS, Oleszczuk, M, Kew, KM. “Safety of regular formoterol or salmeterol in adults with asthma: an overview of Cochrane reviews”. Cochrane Database Syst Rev. 2014.
Chung, KF, Wenzel, SE, Brozek, JL, Bush, A, Castro, M, Sterk, PJ, Adcock, IM, Bateman, ED, Bel, EH, Bleecker, ER, Boulet, LP, Brightling, C, Chanez, P, Dahlen, SE, Djukanovic, R, Frey, U, Gaga, M, Gibson, P, Hamid, Q, Jajour, NN, Mauad, T, Sorkness, RL, Teague, WG. “International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma”. Eur Respir J. vol. 43. 2014. pp. 343-73.
Goodacre, S, Cohen, J, Bradburn, M, Stevens, J, Gray, A, Benger, J, Coats, T. “The 3Mg trial: a randomised controlled trial of intravenous or nebulised magnesium sulphate versus placebo in adults with acute severe asthma”. Health Technol Assess. vol. 18. 2014. pp. 1-168.
Kew, KM, Dahri, K. “Long-acting muscarinic antagonists (LAMA) added to combination long-acting beta2-agonists and inhaled corticosteroids (LABA/ICS) versus LABA/ICS for adults with asthma”. Cochrane Database Syst Rev. 2016.
Norman, G, Faria, R, Paton, F, Llewellyn, A, Fox, D, Palmer, S, Clifton, I, Paton, J, Woolacott, N, McKenna, C. “Omalizumab for the treatment of severe persistent allergic asthma: a systematic review and economic evaluation”. Health Technol Assess. vol. 17. 2013. pp. 1-342.
Postma, Dirkje, S, Rabe, Klaus F. “"The asthma–COPD overlap syndrome."”. New England Journal of Medicine. vol. 373.13. 2015. pp. 1241-1249.
Tong, X, Guo, T, Liu, S, Peng, S, Yan, Z, Yang, X, Zhang, Y, Fan, H. “Macrolide antibiotics for treatment of asthma in adults: a meta-analysis of 18 randomized controlled clinical studies”. Pulm Pharmacol Ther. vol. 31. 2015. pp. 99-108.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.