The Asthma Center

Asthma - adult and adolescent

 

 

I. Introduction

Asthma affects at least 15 million Americans. Symptoms of coughing, chest tightness, wheezing, and/or shortness of breath are common among asthma sufferers. Asthma is often easily diagnosed and modern medication generally relieves symptoms. However, the correct diagnosis and optimum treatment of asthma may remain elusive for some patients.
 
Although physicians have long been aware that “all that wheezes is not asthma,” asthma continues to be misdiagnosed at times. In such cases, poor initial response to treatment may result in the administration of increased doses of asthma medications, including repeated courses of oral corticosteroids. In this latter instance, a patient’s persistent symptoms often lead to emergency room visits and hospitalizations.
 
A systematic evaluation is particularly valuable in both confirming the diagnosis of asthma and identifying other medical problems masquerading as asthma (e.g., paradoxical vocal cord dysfunction). Such an evaluation should include objective pulmonary function studies and appropriate lab, radiographic, and allergy testing, etc. These studies should help identify the presence of comorbidities (e.g., GERD, chronic sinusitis, etc.), along with the patient’s type of asthma (e.g. allergic, aspirin sensitive, etc.).
 
The response to asthma treatment can also vary greatly. In order to optimize treatment, the physician should determine:
  • The patient’s type of asthma (e.g. allergic asthma, exercise-induced asthma, etc.)
  • Specific triggers of symptoms
  • Responses to various classes of medications
  • The patient’s home/work environment and lifestyle
  • The presence of comorbidities
 
Even though patients’ symptoms may be controlled, it still may not mean they are receiving optimal treatment. For example, in allergic asthma, continued exposure to an asthma-triggering allergen (e.g., dust mites) can perpetuate airway hyperreactivity, a precursor to asthma symptoms. Medication may suppress symptoms but not deal with the triggering event. In the case of dust mites, allergen avoidance measures should be employed to reduce the allergen in the environment and perhaps the patient might also undergo immunotherapy, reducing specific-allergen hypersensitivity. It is optimal to eliminate the cause when possible, rather than simply suppress symptoms with medications.
 
Sub-optimal treatment may lead to an increase in airway hyperreactivity and, in some cases, persistent inflammation can be associated with permanent airway remodeling. Remodeling can result in irreversible airway damage leading to chronic airway obstruction.
 
II. Asthma defined
Asthma is an inflammatory disease of the bronchial airways associated with airway hyperreactivity. Symptoms include coughing, wheezing, dyspnea, chest tightness and congestion. Asthma symptoms are often worse at night or early in the morning. Mast cells located in the bronchial mucosa are triggered to release chemical mediators that result in airway inflammation. Inflammatory cells (e.g., eosinophils, neutrophils, lymphocytes) accumulate in the bronchial mucosa. The release of mediators can cause bronchospasm, bronchial muscle hypertrophy, edema, and the production of copious amounts of mucous, often filled with inflammatory cells. Eosinophils are often found in the sputum of active asthma patients. The inflammatory process is also associated with bronchial hyperresponsiveness, a key element in asthma severity. Airway inflammation leads to varying degrees of airway obstruction, which may be reversible.
 
III. Recognizing asthma triggers
Although asthma patients may have similar symptoms, the trigger(s) and/or the mechanism(s) involved may vary greatly among individuals.
 
Possible asthma triggers:
  • Inhaled allergens (pollen, dust mite, pet dander, cockroach, mold, food allergens, etc.)
  • Respiratory tract infections (e.g., influenza)
  • Inhaled irritants (cigarette smoke, pollution, chemicals)
  • Physical activity (running, sports)
  • Environmental factors (temperature and humidity)
  • Hormonal fluctuations (menstrual cycle)
  • Medications (aspirin, beta blockers)
  • Stress and psychopathology (e.g., anxiety)
 
A. Inhaled allergens: Asthmatics with seasonal allergies tend to suffer symptoms mostly in the spring and fall. Year-round asthma symptoms may be due to perennial allergens such as cat dander or dust mite. Associated symptoms of hay fever and/or atopic dermatitis may suggest allergy as a possible trigger of asthma. Other potential indoor aeroallergens include: cockroach, mold, rodents, feathers, and other airborne allergens related to hobbies and occupations.
 
B. Infection: Respiratory infections can trigger acute asthma. Influenza in particular can lead to severe and possibly life-threatening asthma exacerbations. However, influenza immunization and/or pneumococcal immunization can diminish risk for these specific infections.
 
C. Irritants: Passive exposure to tobacco smoke can trigger asthma symptoms--especially in children. Other potential triggers include air pollution, fireplace smoke, irritants at work, perfumes, cooking odors, aerosol sprays, cleaning products, out-gassing from newly installed carpeting or home furnishings, formaldehyde out-gassing, fresh paint, and chlorine-based materials such as bleach.
 
D. Physical activity: Aerobic activity such as running and other sports can trigger asthma symptoms. Pre-treatment with a bronchodilator or other anti-asthma medication may prevent symptoms.
 
E. Hormonal influences: Among women with asthma, up to one-third observe a correlation between worsening asthma symptoms and their menstrual cycle. Asthma may also worsen during pregnancy in approximately one-third of women.
 
F. Medications: Some medications may exacerbate asthma symptoms. Patients sensitive to aspirin and NSAIDs are often diagnosed with triad asthma (sinusitis, nasal polyps and severe asthma). This occurs in less than 5% of asthmatics. Βeta blockers also have a clear potential to worsen asthma symptoms in both their oral and topical forms.
 
G. Stress and psychopathology: Asthma patients may experience a worsening of symptoms with stress. Panic disorder, Munchausen syndrome and paradoxical vocal cord dysfunction can also cause symptoms that mimic asthma. Objective studies for asthma, such as spirometry, will help identify symptoms due to bronchospasm versus those due to psychopathology.
 
IV. Asthma: physical findings
Examining the patient’s chest during the physical examination is a valuable way to identify signs of asthma and perhaps determine its severity.
 
The sounds of air entry in mild and well-controlled asthma are easily heard on deep inspiration/expiration, and the sounds are usually equal in both sides of the chest. However, during an acute severe episode of asthma, air entry may diminish and/or become asymmetrical.
 
Diffuse, high-pitched wheezing is typical of asthma but not specific for asthma. Wheezing in asthma is usually best heard on expiration, however, as asthma worsens, wheezing may also be heard during inspiration. Asthmatic wheezing can be heard at various pitches, starting and stopping at different points in the respiratory cycle. In contrast, wheezing due to a local bronchial narrowing (for example, when a foreign body or tumor obstructs the bronchi) is associated with mono-phasic wheezing.
 
Patients with asthma often have wheezing throughout the chest. In contrast, upper airway obstruction produces wheezing sounds that appear to be transmitted prominently from the upper airway and are loudest over the trachea. These transmitted sounds (e.g., stridor) are most prominent during inspiration and often noted in paradoxical vocal cord dysfunction, croup, or laryngeal edema.
 
During an acute exacerbation of asthma, the expiratory portion of the inspiratory/expiratory cycle is prolonged. The patient begins to use accessory breathing muscles, and in severe cases, a patient may develop pulsus paradoxus and/or cyanosis indicating a potential life-threatening situation.
 
V. Pulmonary function testing
Pulmonary function testing (an objective measurement of lung function) is necessary to diagnose asthma, determine the severity of asthma, and establish a benchmark value used in future assessment of the disease process.
 
Spirometry is easy to perform and provides an objective measurement of the forced expiratory volume in one second (FEV₁). Examination of the flow volume loop (FVL) may allow one to differentiate between obstructive and restrictive pulmonary disease. Further, the shape of the FVL can also detect the presence of an upper airway obstruction such as paradoxical vocal cord dysfunction. Finally, spirometry can also identify the reversibility of the obstruction following the use of a bronchodilator consistent with the presence of asthma.
 
Lung volumes can differentiate between restrictive and obstructive lung disorders, as well as identify the presence of air trapping as seen in poorly controlled asthma.
 
Finally, the diffusing capacity (DLCO) in asthma should either be normal or elevated. A decreased DLCO often suggests an alternative diagnosis involving the parenchyma of the lung (e.g., sarcoidosis, emphysema, interstitial lung disease).
 
When pulmonary function studies are normal and the diagnosis of asthma remains in doubt, a positive methacholine challenge can provide evidence of airway hyperreactivity, which is diagnostic of asthma.
 
In contrast to spirometry which is performed in the office, the peak expiratory flow rates (PEFR) can be performed anywhere. PEFR is measured during a brief forceful exhalation. This test can be self-administered with a small peak flow meter at home or at work. This measurement is particularly valuable for patients who have difficulty perceiving the severity of their airway obstruction. A sharp fall in PEFR can predict an asthma exacerbation, and increasing variability between morning and evening values can also predict worsening asthma.
 
Exhaled nitric oxide is a more recent method used to diagnose and monitor asthma. The presence of nitric oxide in the patient’s exhaled breath increases with bronchial inflammation. However, this approach has not yet received widespread acceptance as a standard part of asthma evaluation.
     
VI. Other studies for asthma evaluation
A. Chest x-ray: While asthma patients usually have normal chest x-rays, an x-ray may uncover evidence of air trapping, aspiration of a foreign body, cystic fibrosis, eosinophilic pneumonia, tuberculosis, bronchopulmonary aspergillosis, congestive heart failure, cancer or other pathology.
 
B. Laboratory studies: Testing blood or sputum for an elevated eosinophil count can support the diagnosis of asthma, while an elevated total IgE or a RAST assay can identify the presence of allergy. Tests for cystic fibrosis, immunodeficiency (quantitative immunoglobulins), alpha-1 antitrypsin and others may aid in the differential diagnosis of asthma.
 
C. Allergy skin testing: Allergy skin testing is still the most sensitive way to screen for allergy as a possible trigger of asthma.
 
VII. Differential diagnosis
In the adult asthma patient, alternative diagnoses and comorbidities may include: GERD, congestive heart failure, post viral cough syndrome, sarcoidosis, hypersensitivity pneumonitis, alpha-1 antitrypsin disease, COPD, immunodeficiency, eosinophilic lung disease, bronchiolitis, lung cancer, pulmonary embolus, psychological disorders, and chronic sinusitis.
 
Particular considerations:
Heart failure versus asthma: When heart failure is mild, it may be difficult to distinguish from asthma, especially if the patient is suffering from both heart failure and asthma concomitantly. An arrhythmia such as atrial fibrillation can also mimic some of the symptoms of asthma, such as cough and dyspnea.
 
VIII. Types of asthma
 
  • Allergic asthma
  • Non-allergic asthma
  • Aspirin-sensitive asthma
  • Occupational asthma
  • Exercise-induced asthma
  • Cough-variant asthma
  • Factitious asthma
  • Potentially fatal asthma
  • Coexistent asthma and chronic obstructive pulmonary disease
 
A. Allergic asthma: Asthma symptoms may flare following exposure to allergens such as cat or dog dander or to outdoor pollen during the spring and fall seasons. Common indoor allergens include mold, dust mite, cockroach, and animal dander (domestic and rodents). Symptoms may worsen in a dusty home or after mowing the lawn. Physical signs of allergy may include: allergic shiners, swollen nasal turbinates and a nasal crease. Allergy skin testing or the laboratory RAST assay may help identify the presence of specific allergies. However, it is the correlation of the patient’s allergy tests and clinical symptoms linked to the allergen exposure that helps support the diagnosis of allergic asthma.
 
B. Non-allergic asthma: In non-allergic asthma, there is no evidence of IgE-mediated hypersensitivity affecting the patient’s symptoms. More common in adults, symptoms may be triggered by respiratory tract infections, air pollution, or temperature changes. Many of these patients also have comorbidities such as chronic sinus disease or GERD driving their symptoms.
 
C. Aspirin hypersensitivity related asthma (triad asthma): Non-steroidal anti-inflammatory drugs (NSAIDs) can result in a severe, life-threatening flare of asthma symptoms in an aspirin-sensitive asthmatic. To diagnose aspirin-sensitive asthma, the patient must undergo an aspirin challenge conducted in a controlled environment capable of managing a severe acute asthma flare. Many triad asthma patients present with a syndrome of aspirin hypersensitivity, nasal polyps and chronic sinusitis.
 
D. Occupational Asthma:
There are hundreds of known inhaled workplace agents that can cause asthma flares in perhaps 10 percent of asthma patients. Occupational asthma results from either IgE-mediated sensitization to a workplace allergen or non-specific chemical irritation of the airway. It is for this reason the physician must take a work/hobby history as part of the asthma investigation to gauge the possible exposure to irritants, allergens, toxic gases, reactive metals, insecticides or organic chemicals.
 
Asthma symptoms may also follow an acute exposure to highly toxic materials over short periods of time (e.g., a chemical spill). This may induce reactive airway dysfunction syndrome (RADS), which is non-immunologic in nature, but triggers long-lasting airway hyperreactivity.
 
A diagnosis of occupational asthma is suspected when the
patient demonstrates:
  • Specific IgE antibodies to the suspected workplace allergen
  • Worsening of symptoms following work exposure
  • Diminution of symptoms following removal from the environment
  • Correlation of symptoms and pulmonary function measurements with allergen/irritant exposure at work
 
E. Exercise-induced asthma: Exercise-induced asthma (EIA) is characterized as wheezing, coughing or shortness of breath following exercise. EIA may occur as a discrete problem, only following exercise, or EIA may coexist with ongoing asthma. Exercise-induced asthma is usually more severe with running than with biking and is least common with swimming. In part, exercise-induced bronchospasm is thought to result from cooling of the airways by inhaling cool, dry air. Symptoms usually begin some 5-15 minutes after exercise ends. The FEV₁ usually decreases by 15% or more.
 
F. Cough-variant asthma: Cough-variant asthma is characterized by a persistent or recurrent dry hacking cough. It is not usually associated with wheezing or shortness of breath; however, patients may complain of chest tightness. Coughing may be provoked by exercise or exposure to strong odors, allergens, or upper respiratory tract infections. Anti-tussives are not very effective in controlling this cough, while treatment with inhaled albuterol (bronchodilator) will often be successful. Response to asthma medication along with evidence of airway hyperreactivity support the diagnosis.
 
G. Factitious asthma: Factitious asthma is a condition in which the patient has asthma-like symptoms (coughing wheezing or shortness of breath) that are self-induced or due to psychopathology. These patients often do not respond adequately to asthma medications. In fact, they may get worse with treatment. Patients may present with paroxysmal coughing, which may sound like a seal barking. One of the key differential factors is that in factitious asthma, symptoms often resolve during sleep. In contrast, severe asthma symptoms typically awaken patients at night.
 
H. Potentially fatal asthma: These patients are at risk of dying from an acute asthma attack. They often have a prior history of status asthmaticus and/or admission to the ICU. Such patients may have had an episode of respiratory failure requiring endo-tracheal intubation. Steroid-dependence is also a risk factor. Increased risk is noted for those who have had episodes of pneumomediastinum or pneumothorax complicating their asthma. Finally, asthma patients with severe obstruction on pulmonary function studies with modest reversibility and frequent need for oral corticosteroids are also considered high-risk.
 
IX. Comorbid conditions
Comorbid medical conditions can exacerbate a patient’s asthma symptoms or mimic asthma symptoms. Until the comorbid condition is identified and controlled, it may not be possible to control the patient’s asthma. Comorbid conditions include: gastroesophageal reflux (GERD), sinusitis, congestive heart failure, bronchopulmonary aspergillosis, sleep apnea, vocal cord dysfunction, and psychopathology.
 
X. Management of asthma
Establishing clearly defined goals early on in treatment sets both the doctor and patient on the path that can yield optimal results.
 
Goals for optimum asthma management:
  • Control of daily symptoms
  • Prevention of exacerbations of asthma
  • Attainment of personal best pulmonary function
  • Prevention of permanent changes in the airway (remodeling)
 
Too often, treatment is directed primarily at relief of symptoms (e.g., wheezing or dyspnea) and managed with a limited course of medications. Short-term treatment of acute symptoms without defining and adequately managing asthma triggers, comorbidities, airway hyperreactivity and degree of airway obstruction may lead to sub-optimal control of asthma. Persistence of airway hyperreactivity—indicating an unstable airway—usually leads to worsening asthma symptoms, which are at times associated with ER visits, airway damage, and poor quality of life.
 
In contrast, a comprehensive approach takes into consideration all the issues mentioned above, along with patient education, which usually results in increased compliance with recommendations, and ultimately best outcomes.
 
Asthma treatment has made great strides in the past 40 years. National guidelines for the evaluation and treatment of asthma by the NIH have been established along with a language used to describe types of asthma and classification of asthma medications. Asthma is categorized as either intermittent or persistent. Persistent asthma is divided into mild, moderate, or severe, depending on symptoms and pulmonary functions. Understanding the type and severity of a patient’s asthma directs a rational approach to initiating treatment. Intermittent asthma is episodic with symptom-free periods between episodes often lasting weeks or months in duration while off of medications. Persistent asthma is a chronic form of asthma which is characterized by symptoms at least two times per week and requires daily medication for best control.
 
Asthma medications are conceptualized as either reliever or controller medications. Reliever medications are used intermittently to provide rapid relief of bronchospasm. For example, albuterol is a rescue medication which is inhaled and can quickly relieve bronchospasm or prevent bronchospasm when administered pre-exercise.
 
In contrast, controller medications are aimed at reducing the underlying bronchial inflammation, which is the underlying cause of asthma. Controller medications are usually administered daily to control symptoms and lower airway hyperreactivity. Controller medications such as inhaled corticosteroids or leukotriene antagonists suppress the inflammatory response caused by mediator release from mast cells and other inflammatory cells in the bronchial tree.
 
Intermittent asthma is usually associated with transient bronchospasm that will often respond to a reliever medication such as a β-2 agonist (e.g., albuterol). Treatment can be modest in intermittent asthma. For example, treatment might only consist of the use of a reliever (rescue) medication such as a β-2 agonist (e.g. albuterol) administered on an as-needed basis. However, even a mildly affected patient with intermittent asthma may at times have a severe flare of symptoms requiring aggressive treatment, including nebulized β-2 agonists and oral corticosteroids. For example, a child with a respiratory tract infection may have a severe bout of asthma once a year and remain symptom-free for the rest of the year off of medications.
 
In contrast, individuals with persistent asthma respond best to daily administered anti-inflammatory controller medications such as inhaled corticosteroids or oral leukotriene antagonists.
 
Patients with moderate or severe persistent asthma who are using daily inhaled corticosteroids may find that the addition of inhaled long-acting β-agonists (LABAs, e.g., salmeterol) combined with inhaled corticosteroids offers them better control of symptoms than corticosteroids alone.
 
It has been observed that well controlled asthma patients have an infrequent need for reliever medications. Overuse of albuterol (e.g., more than four times per day) or similar reliever medications is a danger sign of poorly controlled asthma.
 
Questioning patients regarding their ability to function at home or work, or tolerate physical exertion, quickly leads to an understanding of how the patient’s asthma affects his/her quality of life. The patient’s ACT score completes the picture of the degree of asthma control.
 
Pulmonary function studies objectively identify the degree of airway obstruction and help define the severity of the patient’s asthma as well as the degree of reversibility. Frequent use of oral corticosteroids to treat asthma symptoms also indicates poor asthma control. Other indications of the severity of asthma include: the number of nocturnal awakenings due to asthma, emergency room visits and hospitalizations. Patients who have required ICU admission(s) in status asthmaticus and/or intubation and ventilator support are at particularly high risk for life-threatening asthma.
 
Once persistent asthma symptoms are controlled, it is a good idea to attempt to reduce (step-down) the level of asthma medications while carefully monitoring the patient’s response. This is carried out in conjunction with minimizing the effects of triggers and comorbidities. The goal is to determine the minimum amount of medication for optimal asthma control.
 
Moderate to severe asthma may require treatment with two controller medications, for example, an inhaled corticosteroid combined with a long-acting β agonist (LABA). Patients with severe asthma may require an initial course of oral corticosteroids in addition to inhaled medications.           
 
A comprehensive evaluation is needed to optimize care. Such an evaluation includes objective findings from pulmonary function studies to both confirm the diagnosis as well as define the response to therapy. The use of peak flow meters at home for pulmonary function self-measurement may help assess daily asthma control. Completing physical examinations, x-rays, laboratory tests, allergy studies, and checking for comorbidities lay the foundation for optimizing treatment.
 
Patient education is another key factor leading to better understanding of the disease process and compliance with treatment recommendations. In addition, all asthma patients should be armed with an “asthma action plan” which clearly outlines what to do should symptoms suddenly worsen. For example, patients with moderate to severe asthma should have a back up emergency plan with immediate access to nebulized albuterol and perhaps a course of prednisone for severe exacerbations. This is the same treatment given in emergency rooms and works best when administered early in the course of an acute flare of severe asthma symptoms unresponsive to rescue medications.
 
Environmental controls for asthma management
When a known allergen triggers asthma symptoms, patients would be wise to either modify their exposure or decrease their sensitivity to these allergens. Encasement of pillows and bedding in dust-mite-proof membranes or placing HEPA filter air cleaners in the home are common methods for decreasing allergen exposure. Pets triggering asthma may be removed from the home, while mold allergy sufferers may need to dry up basements, use dehumidifiers, or improve ventilation.Another approach to dealing with allergen triggers is to induce tolerance to the allergens.
 
There are times when one cannot completely eliminate an allergen trigger. For example, little can be done to control outdoor exposure to high concentrations of aeroallergens, such as pollens and mold. Further, even good environmental controls cannot completely eliminate the presence of animal dander, dust mite allergen, or mold within the home.
 
In such cases, if it becomes apparent that allergen exposure is significantly contributing to the patient’s asthma symptoms, then the physician should consider lowering the patient’s sensitivity to the offending allergen through immunotherapy. Specific immunotherapy (allergy shots) can induce tolerance to various allergens (e.g., pollen, dust mite, animal dander and mold) through a series of injections of the offending allergens. This form of therapy is commonly used in treating allergic asthma and respiratory allergy. Most patients experience significant clinical improvement, since the offending allergen is better tolerated and therefore its role as a trigger of asthma symptoms is diminished. Sublingual immunotherapy, a potential alternative to injections, is not yet FDA-approved for use.
 
A newer, unique immunological treatment for moderately severe to severe asthma involves the injection of an anti-IgE monoclonal antibody. This treatment is available today using Xolair (Omalizumab) and requires an injection of monoclonal anti-IgE every 2-4 weeks. Xolair works by non-specifically reducing the amount of circulating IgE antibodies in the allergic asthma patient, rather than inducing tolerance to a specific allergen(s). The benefits of Xolair injections thus last only as long as the treatment is administered, unlike specific immunotherapy, which has the potential for long-lasting benefits far beyond the treatment period. And finally, this form of therapy can be quite expensive, ranging anywhere between $6,000 and $30,000 a year.
 
Medications commonly used to treat asthma:
  • Corticosteroids (inhaled and oral)
  • Leukotriene antagonists (Singulair, Accolate, and Zyflo)
  • Theophylline
  • Cromolyn sodium
  • Bronchodilators, short- and long-acting
  • Specific Immunotherapy
  • Xolair (Omalizumab)
 
• Fixed combinations of inhaled corticosteroids and long-acting β agonists (e.g., Advair Diskus, Symbicort HFA, Dulera HFA) are controller medications that come in various strengths, allowing for individualized dosing of medication. The dose of inhaled corticosteroids with or without LABAs needs to be adjusted with regard to the level of asthma control which can vary over time in any individual patient.
 
• Oral corticosteroids (e.g., Prednisone) are used sparingly because of their potential for severe side effects (e.g. osteoporosis, diabetes, hypertension, aseptic bone necrosis, etc.). They are best reserved for brief use during an acute flare of asthma when symptoms cannot be controlled with inhaled corticosteroids, LABAs, leukotriene modifiers, and short-acting beta agonists. As soon as the asthma exacerbation has resolved, the dose of oral corticosteroids should be decreased as rapidly as deemed safe while monitoring the patient closely. However, it should be noted that patients who have been on long-term or frequent courses of corticosteroids may be steroid-dependent, and under these circumstances, a sudden, rapid decrease of oral corticosteroids could be dangerous, since these patients are likely adrenal insufficient and sudden withdrawal of this medication could lead to a medical crisis.
   
• Leukotriene antagonist: Some patients with persistent asthma find that controller medications such as leukotriene antagonists may also bring asthma symptoms under better long-term control because of their anti-inflammatory effect. Leukotriene antagonists can also be combined with inhaled corticosteroids with a potential for synergy in long-term control. Leukotriene antagonists montelukast (Singulair™) and zileuton (Zyflo™) may be particularly helpful in patients with aspirin-induced asthma or exercise-induced asthma. Patients receiving leukotriene antagonists should have liver function studies performed to determine whether or not they are tolerating these medications, since hepatitis—although uncommon—is a known side effect.
 
• Theophylline: Long-acting theophylline preparations can be useful in some patients who do not have complete control of their asthma. Theophylline preparations are used less frequently today because of their high potential for toxicity and side effects and the need to monitor blood levels. As a result, theophylline treatment is usually reserved for patients not adequately responding to inhaled steroids, LABAs, and leukotriene antagonists. It should be noted that theophylline is very inexpensive and since it is an oral preparation, its delivery is more easily carried out than inhaled preparations.
 
• Thermoplasty: A newly FDA-approved treatment for patients with moderately severe to severe asthma has met with initial success. This treatment targets reducing airway obstruction in asthma patients due to bronchial muscle hypertrophy. A cardinal feature of asthma is hypertrophy or thickening of the bronchial smooth muscle. At times, the bronchial smooth muscle wall is so thick that it results in persistent and severe narrowing of the bronchial passageway, thus limiting airflow. Patients not responding to conventional therapy who have persistent, severe airway obstruction might be candidates for this new form of treatment. Patients undergo bronchoscopy, in which heat is applied to the local bronchial smooth muscle, resulting in a shrinking or diminution in the bronchial smooth muscle mass, and thus, increasing the airway lumen diameter, resulting in decreased airway obstruction. This is a new technique which is invasive and associated with a potential for adverse events.
 
• Assessing control:  Patients with persistent asthma should have regular and timely medical evaluations in order to assess their response to therapy. During visits, the physician analyzes the patient’s asthma control by a validated asthma questionnaire (ACT scoring), medical history, physical examination and pulmonary function studies. If the patient’s asthma appears well-controlled, it would be worthwhile to attempt to decrease the patient’s level of medication in order to determine minimum dose(s) needed to achieve optimum control. One should also evaluate the patient’s compliance with recommendations and inhaler technique. One should also search for the presence comorbidities such as sinus disease, GERD, exposure to cigarette smoke or allergen triggers. It is also helpful to identify the patient's other medical problems (e.g., congestive heart failure) and treatments (e.g., use of beta blockers) in order to identify potential conflicts in treatment.
 
XI. Patient education
Successful asthma management depends on patients’ fundamental understanding of:
  • The disease process of asthma
  • The names of their medications and how they work
  • How their medications are best administered
  • The importance of patient compliance with the physician’s recommendations
  • An emergency action plan
 
Open and clear physician-patient communication creates a partnership, empowering the patient to take an active role in effective asthma management. Patients should be aware of the dangers of overuse of beta agonists and corticosteroids, as well as when best to communicate concerns to the physician.
 
Patients should be evaluated for their competence in the use of inhaled medication devices, and when appropriate, the use of a nebulizer. Patients should know when to initiate a course of oral corticosteroids and/or nebulized albuterol. A review of the use of specialized devices such as a peak flow meter can enable objective measurement of pulmonary functions at home or at work. The use of a spacer device (holding chamber for an MDI) may benefit those who have difficulty using inhalers, whereas dry powder inhalers (DPI) that are breath-activated may better suit patients with coordination issues.
 
Finally, the structure of an optimal asthma management program is based on timely physician assessments, clear and comprehensive medical directions, good access for communication and when necessary, accommodation for urgent office visits. In summary, all of these elements allow patients to feel confident and knowledgeable in their ability to competently manage their asthma outside of a physician’s office. Patients should initiate an emergency action plan for increased asthma symptoms, yet recognize when to contact a physician for additional guidance.
 
To learn more about asthma management, visit http://www.theasthmacenter.org for a free download of our publication, Understanding Asthma, published by The Asthma Center Education and Research Fund.
 
Severe unresponsive asthma
Although most asthma patients respond well to comprehensive treatment, a few with symptoms and signs of severe asthma supported by objective evidence of obstructive airway disease will have a decidedly inadequate response to treatment. Less than 5% of asthma patients are diagnosed with severe asthma. Among these, some fail to respond to even aggressive asthma management. Such patients are often treated with daily oral corticosteroids, and many become steroid dependent. However, some severe asthma patients have a poor response to even high doses of glucocorticosteroids. Many become steroid-dependent. The term steroid-resistant asthma has been applied to asthma patients who have little or no objective response (improvement in FEV₁) to even prolonged treatment of high-dose glucocorticosteroids.
 
Unfortunately, severe unresponsive asthma patients are often given ever-increasing doses of daily corticosteroids. As a consequence, many severe asthmatics become steroid dependent and suffer a poor quality of life resulting from their persistent symptoms and treatment side effects. Steroid-resistant asthma patients have been subject to a number of "off-label" trials using anti-inflammatory or immunological modulating treatments (e.g., Cyclosporin, IVIG, Methotrexate, etc.). The evaluation and management of severe asthma will be the subject of a future monograph.
 
It is now clear that the category of severe unresponsive asthma is heterogenous and includes not only steroid-resistant asthma, but also other severe asthmatics that are affected by various comorbidities (e.g., GERD, chronic sinusitis, paradoxical vocal cord dysfunction, bronchopulmonary aspergillosus, psychopathology, uncontrolled triggers {allergens and pollution} immunodeficiency, etc.). These patients may benefit from a consultation at a major academic center (e.g., National Jewish Health) for a second opinion, always searching for a solution.