Asthma is among the most common chronic diseases, affecting millions of Americans across all ages, genders, ethnicities, and socioeconomic strata.1,2 In 2020, the Global Initiative for Asthma (GINA) and an expert panel working group from the National Heart, Lung, and Blood Institute (NHLBI) coordinated with the National Asthma Education and Prevention Program (NAEP) Committee to develop focused updates to the diagnosis and management of asthma.3,4 These changes were related to the use of inhaled corticosteroids, immunotherapy, indoor allergen mitigation, fractional exhaled nitric oxide (FeNo) testing, and bronchial thermoplasty. This article discusses recent updates on the clinical management of asthma and outlines ways for nurses to engage patients in the management of their disease.
Asthma is a chronic airway disorder characterized by a complex cascade of pathophysiologic changes that result in airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation.5 Approximately 25 million Americans, or 1 in 13, have asthma.6,7 In adults, it is more common in females (9.8%) than men (6.1%). However, in children, the occurrence is higher in boys (8.3%) than in girls (6.7%), with the highest incidence in teenagers.7-9 Due to the insidious and chronicity of symptoms, children and young adults continue to be underdiagnosed and undertreated, contributing to 9.8 million medical office visits and 1.6 million ED evaluations.10,11 The updated guidelines recommend individualized asthma action plans to promote self-management and involvement of individuals living with asthma so they can actively participate in the management of their disease.3,4
A case in point
DD is a 19-year-old male who presents to a health clinic because in the past 72 hours, he has experienced a nonproductive cough, chest tightness, and increased breathlessness that began shortly after the onset of a low-grade temperature (99.1[degrees] F) and rhinorrhea 5 days prior.
While his initial health history is being obtained in the exam room, he becomes agitated and starts coughing and speaking in short phrases. Physical assessment findings include tachypnea of 26/minute and peripheral capillary oxygen saturation via pulse oximetry (SpO2) of 93% on room air. His breath sounds are slightly diminished with expiratory wheezes throughout. The NP performs a COVID-19 rapid test followed by a peak expiratory flow (PEF) measurement. The COVID-19 test result was negative, and the PEF is 260 L/min (normal for DD based on age, height, and gender: 460 L/min). A chest X-ray and blood work are done in the clinic. (See Case study: Initial test results.)
DD's respiratory effort improves, and he appears more comfortable after an albuterol nebulizer is administered. Prior to leaving his appointment, the NP reviews with DD how to use a peak flow meter and an asthma action plan. (See Visit 1asthma action plan for DD.) DD gives a return demonstration of the proper use of a metered-dose inhaler (MDI). He is encouraged to drink six to eight glasses of water per day to replace fluids lost because of low-grade fever and rapid breathing, and aid in reducing the viscosity of mucus. He leaves the appointment with prescriptions for an intranasal H1-antihistamine twice daily for 5 days, albuterol MDI as needed for 5 days, a methylprednisolone dose pack, and azithromycin for 5 days, and instructions for a follow-up visit in 7 days.
Pathophysiology
The airway epithelium is continuously in contact with the environment, which exposes the lungs to irritants, sensitizers, and chemicals that lead to hypersensitivity of the airway if inhaled.12 Awareness and avoidance of potential triggers are the bases for secondary prevention.3,13 The air, both outdoor and indoor, can contain environmental allergens (aeroallergens), potentially harmful chemical, physical, and biological agents. (See Common sensitizers for asthma.) Indoor irritants include dust mites, tobacco smoke, mold, pet dander, irritants (perfume, aerosolized household scents), and pollen. Nonallergenic triggers are also a major factor in asthma exacerbation. Infections, such as chronic sinusitis, localized upper respiratory tract infections, and viral respiratory infections (influenza, colds, respiratory syncytial virus) can all trigger an uncontrolled eosinophilic state triggering an asthma exacerbation.14,15 Other factors that interplay with asthma exacerbation include increased body mass index, gastroesophageal reflux disease (GERD), and cough induced by angiotensin-converting enzyme (ACE) inhibitors.15-17
Airway irritants can trigger an immune response that lead to airway edema, bronchoconstriction, and airway hyperresponsiveness.3,18 This proinflammatory state includes an interplay of many cells and inflammatory mediators, including mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells, chemokines (chemoattractants of white blood cells), cytokines (chemicals that trigger an inflammation cascade), cysteinyl leukotrienes (bronchoconstrictors), and nitric oxide (a vasodilator).18,19 In some individuals, genetics play a role in airway responsiveness that predisposes an individual to an imbalanced regulation of proinflammatory cytokines.17,20
Airway flow adaptations
If the airway is conceptualized as a simple elastic cylinder tube, then the airway caliber will mechanically stretch to accommodate the volume of air. The airway epithelium provides a mechanical barrier protecting the body from environmental elements. During inspiration, the epithelium can be exposed to allergens, toxins, pollutants, and temperature change, leading to acute structural and inflammatory changes in individuals with asthma. The epithelium and bronchial smooth muscles become thickened, leading to narrowing. This narrowing causes an increased airway resistance leading to air trapping in the lower respiratory tract. Mechanically, the airway outside the smooth muscle wall becomes thickened resulting in a decreased elastic pull exerted by the thorax on the lungs and capacity to generate inspiratory and expiratory exchange. If reversibility of airflow is limited in those individuals with moderate to severe asthma, then persistent changes in the airway structure can occur. In moderate to severe asthma, the airway wall is thickened, leading to sub-basement fibrosis, angiogenesis, and smooth muscle hypertrophy resulting in decreased airway diameter.17,18
The activation of inflammatory cells, eosinophils, mast cells, lymphocytes, monocytes, and neutrophils releases chemical mediators leading to epithelial injury and airway edema. As the epithelial lining sheds, it will lose the physical protective barrier and cilia. Interleukin 4 (IL-4) and Interleukin 13 (IL-13) are major drivers of airway inflammation, triggering epithelium thickening and goblet cell hyperplasia leading to hypersecretion and formation of inspissate mucus plugs, limiting airflow.21,22 These physiologic changes cause individuals to experience coughing, wheezing, chest tightness, shortness of breath, and decreased endurance with activities of daily living. Symptoms can last a few minutes to hours; in emergent cases, days. There is no cure for asthma. Although asthma is a chronic respiratory disease, it can be episodic where individuals can manage their disease and reduce the number of flareups with three key interventions: asthma trigger avoidance, medication adherence, and asthma flare treatment.4,16
Diagnosis and monitoring
To diagnose asthma, healthcare providers need to integrate patient reports of symptoms, clinical findings on physical assessment, and clinical response to treatment.4,16 Spirometry is the single definitive test to diagnose asthma. The availability of spirometry testing in primary and family medical offices is dependent on access to good quality equipment and technical training of the clinical staff.23-25 In primary and family medical offices, peak flow meters are portable handheld cylindrical plastic devices with a mouthpiece that are used to measure PEF. Device prices, which range from $10 to less than $100, continue to decline; these are commonly available in medical supply companies, retail drug stores, or online merchants.
Peak flow meters can be used by an individual at home to indirectly determine if they have airflow limitation or if their asthma is worsening. National, regional, and advocacy groups have printed and internet-based patient education tools demonstrating proper technique and self-monitoring guidance (See Asthma management resources for healthcare workers.) To be an effective, reliable tool, the individual must establish their personal best by using the peak flow meter twice a day for 2 consecutive weeks.16,26 Accurate assessment of asthma control can be difficult due to the pathophysiology complexity and limitation of traditional diagnostic testing. Individual self-assessment with questionaries can shed light on asthma control, since individuals may underestimate or overestimate the level of their asthma control. (See Asthma control assessment tools.)
Spirometry is a routine test for pulmonary function that measures the volume and speed of air that an individual can inhale and exhale, predicting the lung size. When a healthcare provider suspects a restriction or obstruction in the airflow volume or airway caliber, a pre- and post-spirometry will be performed to determine the magnitude of smooth muscle relaxation and degree of responsiveness to a bronchodilator (for diagnosis and effectiveness of maintenance therapy).3,4 For this test, individuals will continue their inhaled corticosteroids and leukotriene modifiers but hold their bronchodilators to determine the degree of change in lung function.27 The individual is asked to inhale fully then forcefully exhale and continue exhaling hard and fast until all the air is exhaled. During this maneuver, the volume of air exhaled in the first second (FEV1), the total amount of air that has been forcefully exhaled (forced vital capacity or FVC), and the ratio of these two measurements (FEV1/FVC) is determined. A postspirometry measurement is obtained after the administration of an inhaled bronchodilator. The desired result is an increase in FEV1 of greater than 12% and greater than 200 mL from baseline.3,4 The administration of albuterol or an equivalent short-acting beta2 agonist by MDI with a spacer or chamber device in an individual with asthma will lead to quick and effective airway opening, in contrast to a lack of change in individuals with chronic obstructive pulmonary disease (COPD). (See Spirometry measurements and Contraindications to performing pulmonary function testing.) When the pulmonary function test results are within normal limits and the healthcare provider suspects exercise-induced or allergen-induced asthma, a referral to a pulmonary or allergy specialist for bronchial provocation testing to assess airway hyperresponsiveness is appropriate. Challenging agents include inhaled methacholine and inhaled mannitol.
The fractional concentration of exhaled FeNO testing is recommended by GINA and NAEEP to confirm uncertain asthma based on history, physical exam, and inability to accurately complete spirometry (conditional recommendation, moderate certainty of evidence).3,4 FeNo testing is not supported as a tool for predicting exacerbations or primary assessment for asthma control (strong recommendation, low evidence). The individual is asked to breathe slowly and steadily into a mouthpiece as a machine measures the level of nitric oxide (NO) in their expired breath. FeNO is a biomarker used to determine if an individual's asthma is correlated with eosinophilic airway inflammation. In allergic asthma (eosinophilic asthma), the inflamed epithelial cells of the bronchial wall release higher-than-normal levels of NO. The findings of this test (conditional recommendations, low evidence) aid the practitioner to determine if the individual is adherent with their treatment regimen, and can be used to determine responsiveness to inhaled corticosteroids, or consideration before initiating biologic therapy.28-30 When used as a surveillance tool, a 20% decrease in FeNO value from the baseline supports a positive response to the anti-inflammatory therapy.31 The cost, maintenance, and healthcare worker training associated with the equipment might be cost-prohibitive for a primary care office or clinic. Referral to a pulmonary specialist may be warranted.32
Past guidelines advised all individuals to improve their indoor air quality, allergy, and asthma control by limiting their indoor allergen sources, including wall-to-wall carpet, stuffed toys, soft furniture, mattress, pillows, and bedding. Careful inspection of the home-dwelling for mold sources was also recommended.32 However, the guidelines published by GINA and NAEPP now advise this action only to individuals who have symptoms related to exposure to indoor or outdoor allergens to take steps to mitigate exposure (conditional recommendation, low evidence).3,4 Guidelines offer guidance on pest management strategies (mice, rat, or cockroaches), washable pillow and mattress covers, and use of high-efficiency particulate filters for vacuums. Changing clothing, taking a shower, using shampoo after working, or spending time outdoors can mitigate pollen triggers. Allergen testing may be warranted based on clinical presentation and history of exposure.3,4
Management
The updated asthma guidelines published by GINA and NAEEP noted a conditional recommendation on shared decision-making between healthcare providers and individuals living with asthma.3,4 The updated guidelines moved from daily inhaled short-acting beta2-agonist (SABA) to daily inhaled corticosteroids for acute asthma exacerbation and mild-persistent and mild-to-moderate persistent asthma (conditional recommendation, high, moderate level of evidence). Patients with any features of asthma should not be treated with a long-acting beta2-agonist (LABA) or long-acting muscarinic antagonist (LAMA) alone, without an inhaled corticosteroid (ICS).3 (See Asthma medications.)
An ICS can reduce the inflammatory symptoms of asthma, decreasing airway edema and mucus. The new guidelines have changed the recommendation for the daily administration of inhaled long-term corticosteroids as first-line treatment, with research supporting these individuals had fewer incidences of hospitalizations, exacerbations, and death.3 The use of combination single maintenance and reliever therapy (SMART), inhaler containing budesonide (ICS), and low-dose formoterol (a LABA) is preferred for both maintenance and quick relief in adolescent and adult patients with moderate-persistent asthma.3,4
The SABA albuterol works in an acute situation by relaxing the muscle around the airways. In 2021, GINA guidelines no longer recommend SABAs such as albuterol as daily initial treatment of asthma in adolescents and adults. SABAs are still recommended for acute episodic, as needed, and short-term management of vigorous exercise-induced asthma or first signs of asthma symptoms. A LABA, when combined with an ICS, is recommended for those with uncontrolled persistent asthma.3
LAMAs, both short- and long-acting, are no longer recommended as an add-on therapy for uncontrolled persistent asthma (conditional recommendation, moderate evidence).3,4
Leukotrienes, byproducts of arachidonic acid, are produced by a variety of tissues and cells in the body (mast cells, eosinophils, macrophages). When not blocked, they interact with specific airway receptors triggering inflammation. When stimulated, leukotriene causes airway smooth muscle contraction, increased production of mucus, chemotactic activity (attracting other inflammatory cells to the area), and airway edema. Antileukotriene agents (also known as leukotriene-modifying agents) are oral medications used for the treatment of allergic rhinitis, persistent asthma, and need to be taken at least 2 hours before activity as prophylaxis for exercise-induced bronchospasm.3,4,33
For individuals living with mild-to-moderate persistent asthma and allergic asthma, biologic medications (subcutaneous, sublingual, or I.V. route) are recommended (conditional recommendation, moderate evidence). Biologic medication (immunosuppressive therapies) target specific T-helper cells (Th2 lymphocytes) that produce IL-4, IL-5, and IL-13 cytokines that drive B cells to secrete immunoglobulin E (IgE). Mast cells bound to IgE cause degranulation and the release of chemical mediators that cause bronchoconstriction and airway edema.34-36 The most common adverse reactions to these medications include myalgia, arthralgia, headache, fatigue, localized erythema at the injection site, pharyngitis, and a rare risk for anaphylaxis.35,36 Administration of I.V. biologics can lead to additional adverse reactions including injection-site reactions, anaphylaxis, pulmonary edema, cytopenia, infections (fungal or lethal tuberculosis), drug-induced systemic lupus erythematous, and even death. These medical emergencies may require immediate administration of epinephrine with or without glucocorticoids. For this reason, the administration should be done in a healthcare setting with onsite supervision of an advanced clinical practitioner with appropriate training in biologics.37,38
With the inhibition of IL-4 and IL-13, studies suggest that the T-cell response to live vaccines may be inhibited. Prior to administering the first dose of biologic medication, healthcare practitioners should perform a Mantoux-tuberculin skin test and review individual vaccine health records for the last dose and titer for measles, mumps, rubella, varicella-zoster, rotavirus, and intranasal influenza.34,39,40 With the recent COVID-19 pandemic, attention has been drawn to the safety and administration of the COVID-19 vaccines. The COVID-19 vaccine by Pfizer/BioNTech and Moderna are messenger RNA vaccines made from a synthetic material that signal the body to produce antibodies, while the Johnson & Johnson (Jansen) vaccine is a vector vaccine.41,42 A vector vaccine works by introducing the body to a weakened (recombinant) human adenovirus containing spike protein (antigenic determinant) of COVID-19 virus, triggering our immune system to muster B and T cells.42-44 The CDC and the US FDA have stated that the COVID-19 vaccines are not live vaccines; therefore, it is safe to administer to individuals 2 weeks prior to giving them prescribed biological (immunosuppressive) medication.38,43,45
Bronchial thermoplasty is a newer invasive procedure reserved for uncontrolled moderate-to-severe asthma in adults 18 years of age or older who have failed conventional asthma therapy (conditional recommendation, low evidence).3,4 Performed under moderate sedation/analgesia, bronchial thermoplasty involves applying heat via a device that delivers localized controlled radiofrequency waves to the airways during bronchoscopy, which reduces the increased mass of airway smooth muscle associated with asthma.46,47 The procedure has a small benefit-to-risk ratio with uncertain long-term outcomes.3,4,32
Continuation of case study
DD returns in 7 days to see the NP. He reports that he continues to have episodes of coughing 5 out of 7 evenings per week. He reports using his MDI as prescribed, and shares his peak flow log that shows he has been averaging 80% of his personal best. He denies experiencing heartburn (pyrosis), chest pain, or recurrent upper respiratory complaints. DD shares that he is a nonsmoker, lives alone, and works outdoors, and he has noticed that his breathing is harder during the cold winter months and on dry hot days. His lungs are clear bilaterally and the rest of the physical exam is unremarkable. A pre- and post-spirometry demonstrate good reversibility: prebronchodilator FEV1/FVC 0.74; postbronchodilator FEV1/FVC 0.82. (See Visit 2 pulmonary function test results.) The NP has DD return demonstrate the use of an MDI. A new asthma action plan is made. (See Visit 2 asthma action plan for DD.) He is advised to continue his peak flow meter measurements and is prescribed a new corticosteroid inhaler, fluticasone propionate inhalation powder. He is referred to an immunology/allergy specialist for allergen testing. DD is scheduled to see the NP in 7 to 10 days for follow-up.
REFERENCES