Evaluating and Treating Asthma

Emerg Med 37(4):20-29, 2005

How do you gauge the severity of an asthma attack? What does wheezing signify? What are the red flags in an arterial blood gas analysis? The authors address these and other clinical issues and discuss the therapeutic merits of beta agonists, systemic steroids, leukotriene antagonists, heliox therapy, anticholinergics, magnesium, and immune modulators.

By Seema S. Aceves, MD, PhD, and Stephen I. Wasserman, MD

Acute asthma management confers a significant burden on the health care system in the United States. Acute asthma annually accounts for two million emergency department visits, with a hospitalization rate of 20% to 30% and a relapse rate within two weeks of 10% to 20%.

Millions of people suffer from chronic asthma, with prevalence rates in many countries estimated to be between 4% and 6%. Longitudinal cohort studies from New Zealand, Australia, and the United States have demonstrated that persistent asthma has its roots in early childhood. Such studies have demonstrated that wheezing that begins before age 5 and persists into adulthood results in an increased risk for impaired lung function. On the other hand, children who begin to wheeze after age 5 have a reduced risk of lung function abnormalities even if their wheezing persists into adulthood. Thus, it is becoming apparent that prevention of adult asthma often needs to begin during childhood.

Risk factors for the development of asthma in childhood include a maternal history of asthma, exposure to tobacco smoke, and the development of allergic diatheses such as food allergy, eczema, and allergic rhinitis. In difficult cases, once asthma has developed, the patient also tends to display allergies to foods and to the outdoor mold Alternaria.
 

UNCLEAR ETIOLOGY

The etiology for the increasing incidence of asthma is unclear but likely involves multiple genetic, immunologic, and environmental influences. Exposure to endotoxins and natural infections in early childhood appear to protect against the development of atopic asthma, and avoidance of these infections through interventions such as mass immunization and antibiotic use is correlated with an increased incidence of atopy. This association has led to the theory popularly referred to as the "hygiene hypothesis," in which the failure to strengthen the developing immune system by exposing it to stimuli that interact with it leads to dysfunctional immune responses, such as allergy and asthma, in children.

In addition, increasing exposure to environmental pollutants and tobacco smoke also is likely to influence the development of persistent airflow obstruction. Lastly, differences in genetic backgrounds, such as polymorphisms in the beta-adrenergic receptor and various cytokine genes, are likely to play an important role in the predisposition to asthma and its severity.

Management of the patient with asthma requires an approach that has been well thought out and is accepted by those responsible for the delivery of care. For example, using a standardized protocol has been shown to improve asthma management in the emergency department. Such standardized protocols demand an understanding of the nature of the disorder, education of patients and care providers, and a commitment to their implementation.
 

CLINICAL POINTS

Certain clinical points are of paramount importance when taking a history from a patient experiencing an acute asthma exacerbation. Patients with a history of brittle asthma with quick declines in lung function, exemplified by multiple emergency department visits despite compliance with controller medications, a poor ability to sense dyspnea, a history of intubation, and the need for frequent systemic courses of steroids, will require more aggressive and prompt intervention. Studies done in both adult and pediatric patients have demonstrated that patients with lower socioeconomic status, a history of frequent emergency department visits, and more prescriptions, as well as more prescribers of asthma medications, are more likely to require hospitalization during an asthma exacerbation. Pediatric prospective cohort studies based in the emergency department found that risk factors for requiring beta-agonist therapy for 12 hours or longer following systemic corticosteroid administration included a history of ICU admission for asthma, an oxygen saturation of 92% or lower, and the need for hourly administration of albuterol.

Historical clues regarding the etiology of an asthma exacerbation should be elicited. Most clinicians have heard the phrase "all that wheezes is not asthma," and it serves us well to keep this pearl in mind when evaluating a wheezing patient. In adults, the differential diagnosis for acute wheezing includes cardiac disease (such as heart failure), chronic obstructive pulmonary disease, emphysema, pneumonia (especially with Mycoplasma or Chlamydia), and localized obstruction due to a foreign body or tumor. Sometimes wheezing is caused by acute viral or bacterial bronchitis, but again, consider the history; recurrent episodes of wheezing "bronchitis" may in fact be asthma. Pulmonary embolus, aspirin-exacerbated respiratory disease, and anaphylaxis must also be considered.

In children, the etiology for acute wheezing can be similar to that in adults but also includes cardiac disease such as congenital heart disease, as well as foreign body aspiration, gastroesophageal reflux disease, bronchiolitis (usually caused by respiratory syncytial virus or metapneumovirus), chronic lung disease in a child who was a premature infant, and vocal cord dysfunction.
 

PHYSICAL EXAM FINDINGS

Clues to the severity of an asthma exacerbation can be quickly gleaned on physical examination. An inability to speak in complete sentences, breathlessness, or labored and fast respirations, particularly with retractions and accessory muscle use, should alert the clinician to severe airflow obstruction. Auscultation may reveal diffuse wheezes or poor breath sounds, especially in the lung bases. Crackles may be heard over atelectatic areas.

A quiet chest with little wheezing in a dyspneic patient is indicative of a severe airflow obstruction. Paradoxically, in this situation, beta-agonist therapy will often induce wheezing, reflecting improved air exchange. Cardiac causes for wheezing are suggested when the examination reveals cardiac gallops, heaves, and elevated jugulovenous distension as in heart failure. In children, tachycardia, tachypnea, and hepatosplenomegaly are cardinal signs of heart failure. Examination of the extremities may reveal edema in cardiac-related wheezing, cyanosis in extreme hypoxia or poor circulation, and clubbing in the patient with persistent hypoxia.

If the patient routinely monitors his or her peak flow, a quick objective measurement of airway obstruction can be obtained and compared to the normal predicted value. In general, peak flows that are 60% to 80% of the predicted value demonstrate a mild to moderate airflow obstruction, while peak flows that are 60% to 50% or lower of the predicted value indicate a severe exacerbation of expiratory flow (see table below). Indeed, patients with peak flows below 50% of the predicted value following beta-agonist and steroid therapy are at increased risk of requiring subsequent hospitalization.
 

Although useful in guiding chronic asthma management, evaluation of forced expiratory flows and volumes is generally not necessary in the assessment of acute asthma.
 

LABORATORY EVALUATION

Simple maneuvers such as monitoring the patient's blood oxygen saturation level and treating hypoxia with supplemental oxygen should be performed promptly in cases of acute asthma exacerbations. Many studies have demonstrated that the degree of hypoxia correlates with the clinical course. Patients with oxygen saturations of 92% or lower are more likely to require subsequent hospitalization. Earlier and more aggressive intervention may reduce hospitalization rates in the hypoxic patient.

If the history and physical examination leave diagnostic questions as to the etiology of an acute wheezing episode, certain laboratory studies may be useful. Although not necessary in a routine asthma exacerbation, a chest x-ray in both the anteroposterior and lateral views can be a helpful aid. Patients with asthma may have x-ray findings of hyperinflation, subsegmental atelectasis, and bronchial cuffing, reflecting increased airway wall thickness. In addition, a patient with severe dyspnea, focal loss of breath sounds, complaints of chest pain, or subcutaneous emphysema may have x-ray findings consistent with pneumothorax or pneumomediastinum.

Chest x-rays are also helpful in evaluating for pulmonary edema and cardiac size in heart failure and for focal infiltrates consistent with pneumonia in a patient with crackles of unclear etiology. Occasionally, a radiopaque foreign body may be identified.

Invasive laboratory studies such as arterial blood gas (ABG) analysis should be considered in the hypoxic patient with increased work of breathing indicative of severe airflow obstruction. Early findings on ABG analysis include a normal PaO₂ with respiratory alkalosis and hypocarbia as the tachypneic patient expires carbon dioxide. With worsening airflow obstruction, hypoxia ensues and the blood pH becomes increasingly acidic due to retention of carbon dioxide.

The physiology of the ABG changes is explained by the patient's response to airflow obstruction. Initially, tachypnea can compensate for the hypoxia and hypercarbia that result from the obstruction. However, a combination of worsening pulmonary obstruction and respiratory fatigue from prolonged accessory muscle use will eventually compromise oxygenation and ventilation. This results in hypoxia and an increase in PaCO₂ with respiratory acidosis. Therefore, a normal and, even more so, a rising PaCO₂ and decreasing pH in the face of hypoxemia should quickly alert the clinician to impending respiratory failure. Such ABG findings necessitate more aggressive interventions and transfer of the patient from the primary care physician's office to the emergency department.

In the pediatric patient, ABG analysis should not be performed routinely. Such an invasive intervention can result in worsening respiratory distress and fatigue, defeating the purpose of the laboratory evaluation. In cases where monitoring pH and carbon dioxide levels seems imperative, it is wiser to do a venous blood gas analysis and monitor oxygen tension indirectly with an oxygen saturation probe. It is important to keep in mind that the oxygen saturation reading may drop initially after beta-agonist treatment as a result of a ventilation-perfusion mismatch. However, with increased airflow, oxygen saturation will improve.

Although not useful in guiding acute asthma management, a complete blood cell count with differential may demonstrate eosinophilia in the asthmatic patient. In addition, the degree of eosinophilia and peripheral level of eosinophil products can serve as a surrogate marker of disease severity.

Lastly, if the possible etiology of the wheezing is an anaphylactic response to venom (from a bee sting, for example), medication, or food, the level of serum tryptase can be evaluated. The beta form of tryptase is a mast cell product released on degranulation. It has a serum half-life of approximately two hours, and its presence can be used as a surrogate marker for anaphylaxis. Although its measurement can provide diagnostically important information, it is not quickly available and thus cannot guide immediate clinical interventions. It is also important to keep in mind that serum tryptase levels may not be elevated in anaphylaxis, especially if it is secondary to food ingestion, or if the onset of the anaphylaxis was more than four hours earlier.
 

EVALUATION OF CHRONIC ASTHMA

Pulmonary flow-volume studies are the current mainstay of asthma diagnosis and, if available, also contribute to asthma management. In combination with clinical symptoms, pulmonary function testing (PFT) results are the backbone of consensus guidelines (see table below). However, new evidence suggests that PFTs may not be the best gauge of pulmonary inflammation. Although not used routinely except in study protocols, exhaled nitric oxide has been shown to correlate with other markers of inflammation (blood and sputum eosinophils, serum eosinophil cationic protein levels, and IgE) and with disease severity, but not with measures of pulmonary flow.
 

In addition, recent studies using sputum eosinophils to guide asthma therapy demonstrated threefold fewer asthma exacerbations, sixfold fewer hospitalizations, and improved bronchial hyperreactivity when compared to asthma management based on British Thoracic Society guidelines. In these studies, sputum is induced with ultrasonically nebulized hypertonic saline. The sputum is separated into cell pellet and supernatant following treatment with dithiothreitol. The total cell count is done using a hemocytometer, and differential cell counts are subsequently performed following Wright's stain. Sputum eosinophil counts can correlate with other markers of inflammation, such as exhaled nitric oxide, but they tend not to correlate with markers of pulmonary flow, such as forced expiratory volume in one second (FEV₁) and post-bronchodilator FEV₁. Green and colleagues reported that neither beta-agonist use nor asthma quality of life scores correlated with decreasing sputum eosinophils.

The results of these studies utilizing sputum eosinophils are intriguing. However, the feasibility of inducing sputum and the paucity of current evidence supporting the use of sputum eosinophils as a surrogate marker for asthma control in the mild to moderate asthmatic make this approach less attractive to the primary care practitioner.

Assessment of bronchial hyperreactivity following a methacholine challenge can be useful in the diagnosis of asthma. For example, a patient with a history of cough and a normal physical examination may have a decreased FEV₁ following treatment with methacholine, which would be consistent with a diagnosis of asthma as the cause of the cough. In addition, an exercise challenge can be done in a patient with exercise-induced asthma.
 

USE OF BETA AGONISTS

The standard of care for management of acute exacerbations of asthma is undisputedly systemic corticosteroids to hasten resolution of inflammation and beta-agonist therapy to resolve bronchial constriction. However, the best route for therapy has been debated. Recent clinical trials have demonstrated that the use of a metered-dose inhaler is equivalent to wet nebulizer therapy as long as sufficient doses of a beta agonist are administered. Moreover, inhaled therapy is superior to intravenous (IV) therapy.

Recent clinical trials have evaluated the use of intermittent versus continuous nebulizer therapy. Meta-analysis of eight randomized, controlled, mostly unblinded trials of adults (six trials) and children (two trials) demonstrated that the relative risk of hospital admission was reduced by almost 50%, and small but statistically significant increases in peak expiratory flow and FEV₁ were seen after two to three hours of continuous beta-agonist nebulization versus intermittent nebulization. The dose of beta agonist used in adults varied from 5 to 30 mg over 120 minutes, and in a single pediatric trial a 15-mg dose was used. All patients were concomitantly treated with systemic steroids; an anticholinergic and oxygen were given at the physician's discretion.

Subgroup analysis demonstrated that the patients with severe exacerbations benefited most from continuous beta-agonist therapy. It also found that 10 patients would need to be treated in order to save one patient from hospital admission. Surely, in terms of management, the simplicity of continuous nebulization is clear.
 

SYSTEMIC STEROID THERAPY

Steroids reduce inflammation by affecting the transcription of genes that produce pro-inflammatory cytokines and mediators. Thus, their effects are not immediate. Although multiple expert committees, including the Canadian Association of Emergency Physicians, the United States National Asthma Education and Prevention Plan, and the British Thoracic Society, have agreed that systemic glucocorticoids should be used to decrease the inflammation in acute asthma, the route and timing of steroid therapy have been controversial. Multiple clinical trials in children have demonstrated that the oral or IV routes for steroid dosing are equally effective. Such data does not exist in adults; most trials of severe asthma exacerbation in adults have used IV steroid dosing. However, it is clear that oral steroids are more efficacious than inhaled glucocorticoids in the treatment of acute asthma.

A meta-analysis of 12 trials of steroids in adults and children with asthma concluded that steroid usage within the first hour of presentation to the emergency department reduces the odds of hospital admission by 50%. Patients with severe exacerbations benefited the most from this intervention. It is prudent to wait two to four hours, if possible, before making a decision to admit the patient. This time frame allows glucocorticoids to exert their transcriptional effects. Further analysis has shown that low-dose steroid therapy, defined as less than 80 mg in adults, is just as effective as higher doses in reducing the inflammation associated with acute asthma.

Treatment with steroids on discharge from the emergency department should continue to complete a three- to five-day course. In children, it has been shown that doses of 1 and 2 mg/kg/day are equivalent and that a three-day course is equivalent to a five-day course in terms of asthma control. On the other hand, the side effect of behavioral changes increases in incidence with higher doses and longer courses of systemic steroids in children.

Multiple trials have also compared the use of systemic corticosteroids to inhaled corticosteroids following discharge from the emergency department. Although there was no difference in relapse rates between patients on either systemic or inhaled therapy, these studies involved patients with mild asthma. Given the significant expense of inhaled corticosteroids and the known safety of short bursts of oral corticosteroids, plus the lack of data on the utility of inhaled corticosteroids for acute severe asthma exacerbations, it is prudent and economical to treat patients being discharged from the emergency department with short courses of oral corticosteroids. It should be noted that steroids can be given intramuscularly if IV access is not available and an oral trial is not tolerated.
 

USE OF ANTICHOLINERGICS AND MAGNESIUM

An anticholinergic agent such as ipratropium bromide exerts its effect by competing with acetylcholine for binding to the muscarinic receptor. This results in smooth muscle relaxation and bronchodilation. When used in pulmonary diseases such as chronic obstructive pulmonary disease (COPD) and asthma, anticholinergic agents do not reduce the viscosity, clearance, or volume of mucus production. Studies done in both children and adults with severe asthma exacerbations have demonstrated that expiratory flows increase by 10% or more and the odds of hospital admission decrease when inhaled ipratropium is added to beta-agonist therapy during the first 90 minutes of treatment.

Therefore, in addition to standard therapy with a systemic steroid and a beta agonist, the addition of an inhaled anticholinergic is a rational therapeutic intervention for adult and pediatric patients with a severe asthma exacerbation. The recent approval of a long-acting anticholinergic agent (tiotropium) for use in COPD will certainly prompt studies of this drug for asthma as well.

Multiple trials in children and adults have been done to evaluate whether IV magnesium sulfate, when added to bronchodilator therapy, can improve pulmonary function and reduce hospital admissions in patients with an acute asthma exacerbation. Two independent meta-analyses of these trials have been performed and have demonstrated that a 1.2- to 2-gm IV bolus dose of magnesium can improve peak flow, FEV₁, and reduce hospital admissions in the subset of patients with asthma who have a severe exacerbation. Such an exacerbation was defined differently in every trial, but in general it was defined as an FEV₁ below 30% or peak flow of less than 60% of the predicted value. The overall increase in FEV₁ in the patients with a severe exacerbation was 10%, and the decrease in the odds ratio for hospitalization rate ranged from 0.04 to 0.27.

In children, the usual magnesium dose is 25 mg/kg, which can be given intramuscularly if IV access has not been obtained. Whether that standard dose is adequate to maximally improve pulmonary function remains uncertain. No trials have been conducted to evaluate doses of magnesium used in other clinical settings, such as uterine tocolysis, in which a 6-gm bolus dose of magnesium, followed by a continuous infusion at 2 gm/hour, is used.
 

LEUKOTRIENE ANTAGONIST AND HELIOX THERAPY

Sulfido-peptide leukotrienes, produced from arachidonic acid during the breakdown of membrane lipids, are inflammatory mediators and potent bronchoconstrictors. Asthmatic patients have increased levels of urinary leukotriene E₄ during an exacerbation. In addition, leukotriene pathways appear to play an important role in other asthmatic disorders, such as aspirin-exacerbated respiratory disease, and these patients too may benefit from daily antileukotriene therapy. Although IV leukotriene receptor antagonists can increase expiratory flow, no improvements in hospitalization or relapse rates have been documented. Registration studies of oral leukotriene receptor antagonists demonstrated about an 8% improvement in FEV₁ with initial dosing, suggesting the potential for a modest benefit in acute asthma.

Although multiple studies have been done using heliox, a helium-oxygen mixture thought to increase laminar flow through the airways, meta-analyses have not demonstrated an improvement in FEV₁, peak expiratory flow, or hospitalization rates in patients receiving this agent.
 

ADMITTING THE ASTHMATIC PATIENT

The decision as to whether or not to admit a patient with an acute asthma exacerbation depends on the patient's history, physical examination, and response to interventions performed. Patients who clearly meet criteria for admission would be those whose oxygen saturation remains below 92%, those whose peak flow remains at 60% or lower of the predicted value, and those who continue to have significant work of breathing with tachypnea, dyspnea, or accessory muscle use despite one hour of beta-agonist therapy (preferably with concurrent anticholinergic therapy) and steroid treatment. Other, nonclinical issues must also be considered. For example, a patient with a long-standing history of noncompliance with medical regimens is a likely candidate for hospitalization. The same is true of patients living in remote areas and those who do not have access to transportation or a telephone.

Finally, a consideration of the patient's medical history, such as a need for intubation, a poor ability to sense dyspnea, or hesitancy to seek medical care should factor into the decision-making process. If available, a short-term observation and treatment unit can provide a good option for continued patient evaluation and treatment without hospital admission.
 

GUIDELINES FOR DIAGNOSING ASTHMA

In 1997, an expert panel consensus was obtained for the purpose of allowing clinicians to more consistently diagnose and manage asthma. In 2002, an update to these guidelines was made by a expert panel known as the Global Initiative for Asthma (GINA), which established that the diagnosis of asthma depends on the constellation of daytime and nighttime symptoms in conjunction with changes in PFTs (see table above). Although PFTs have been an integral part of asthma diagnosis and management, especially in the specialist's office, they are imperfect measurements of asthma severity. For example, FEV₁ is often the primary outcome measured in clinical trials for asthma, even though FEV₁ is an indicator of large-airway obstruction and asthma is a disease of small-airway obstruction. Indeed, it is becoming clear that assessing markers of airway inflammation, such as sputum eosinophils and exhaled nitric oxide, and altering asthma management in response to changes in these markers may provide better control than management in response to PFTs or symptoms.

Mild intermittent asthma is defined as the presence of symptoms only one or two times per week, with relatively mild exacerbations, and requires no daily therapy. Mild persistent asthma is defined as daytime symptoms that occur more than twice a week but not every day, and nighttime symptoms that occur more than twice a month but less than once a week. Pulmonary function testing demonstrates an FEV₁ that is more than 80% of the predicted value, which is considered normal. The mild, persistent asthmatic patient should be treated with a daily, low-dose, inhaled corticosteroid, although a leukotriene antagonist can be used as an alternative therapy, especially in children. Although placed on a lower tier in the management of chronic asthma, the mast-cell stabilizer cromolyn can also be a useful modality for some patients.

The definition of a moderate persistent asthmatic is a patient who has daytime symptoms daily and nighttime symptoms more than once a week, while the severe persistent asthmatic has continuous daytime symptoms that limit his or her physical activity and frequent nighttime symptoms. The moderate persistent asthmatic has an FEV₁ of 60% to 80% of the predicted value, whereas the severe persistent asthmatic has an FEV₁ below 60% of the predicted value.

Both the moderate and severe persistent adult asthmatic patient should be treated with a daily inhaled corticosteroid in combination with a long-acting beta agonist. In the moderate persistent asthmatic child, a leukotriene antagonist can be substituted for a long-acting beta agonist as add-on therapy with an inhaled corticosteroid. However, it is recommended that the severe persistent asthmatic child should receive an inhaled corticosteroid in combination with a long-acting beta-agonist. Both adults and children with severe disease may require daily oral steroids in addition to inhaled therapy (see table above).
 

IMMUNE MODULATORS AND ASTHMA THERAPY

Because persistent exposure to allergens perpetuates the cycle of airway inflammation, allergen avoidance can reduce the symptoms of asthma in atopic patients. The first immunomodulatory therapy to be used was specific allergen immunotherapy, commonly known as "allergy shots." By changing the immune response from one of allergic inflammation to one of tolerance in response to the offending allergen, such treatment can improve both allergic rhinitis and asthma.

Trials of new immunologic agents have been done in the moderate to severe adult asthmatic population. The most recently approved agent is omalizumab, a molecule that blocks the binding of IgE to its receptor on mast cells and basophils, thereby inhibiting the release of inflammatory mediators in response to an allergen. Therapy with this agent has proven beneficial by permitting a decrease in oral or inhaled corticosteroid usage and in the prevention of exacerbations of asthma and hospitalizations when added to standard treatment for atopic asthma. Use of omalizumab is indicated for patients who are allergy skin test positive and with moderate to severe persistent asthma whose symptoms are inadequately controlled on standard anti-inflammatory regimens.

Drawbacks to omalizumab include the cost, the time to demonstrated efficacy, and an unproven and not statistically significant association with cutaneous malignancy. This finding, which usually occurs within months of initiation of treatment, does not make biological sense and was not considered to be of sufficient concern to delay drug approval.

Other immune-modifying anti-inflammatory agents may be useful in the treatment of asthma. To date, trials with anti-IL-5, a cytokine that plays a key role in eosinophil migration and survival, have not demonstrated a decrease in bronchial hyperreactivity or asthma symptoms. Although this therapy did result in a marked decrease in blood and sputum eosinophils, pulmonary tissue eosinophils were only decreased by 50%. Thus, these trials likely did not provide adequate reduction in tissue eosinophils, perhaps due to insufficient duration of treatment.

Multiple immunologic agents currently being marketed for various other diseases may also prove to be useful in the management of asthma. Included among these is natalizumab, an antibody that blocks the binding of inflammatory cells to activated vascular endothelium by interfering with the interaction of the surface molecules VLA-4 and VCAM, which is being developed for inflammatory bowel disease and possibly multiple sclerosis. Other agents, such as those directed against interleukin 4 and tumor necrosis factor-alpha, have been suggested as potentially useful in asthma.
 

CARING FOR THE ASTHMATIC PATIENT

The asthma guidelines developed by the expert committees of the National Heart, Lung, and Blood Insitute and the GINA panel are meant to facilitate the care of the asthma patient. However, significant barriers to care exist. Many studies have demonstrated poor continuity of asthma care in the neediest patients—specifically patients, especially children, with persistent asthma living in urban settings. In addition, patients frequently do not follow up with primary care physicians following emergency department visits for asthma exacerbations. Although patients who have had appointments scheduled with their primary care physician through the emergency department are more likely to follow up, the majority of patients who visit the emergency department do not have such appointments made there.

Unfortunately, even patients who do follow up with their primary care physician are no less likely to return to the emergency department for an asthma exacerbation, nor are they likely to miss fewer days of school or work. One intervention that has been shown to decrease the likelihood of emergency department visits and nocturnal asthma symptoms is seeing an allergy specialist. Our feeling is that most patients benefit from specialist care, especially early in the diagnosis. It provides the opportunity for identifying potential allergic triggers, evaluation of pulmonary function, in-depth asthma teaching, and asthma home visits, if available. In addition, periodic re-evaluation of asthmatic patients for new anti-inflammatory treatments such as omalizumab can be done through an asthma specialist's office.

Interactions between an allergist or pulmonologist and the primary care physician will serve to facilitate appropriate asthma management. Recently, the assignment of patients to an asthma nurse specialist was shown to decrease hospitalizations by 60%, but not to decrease emergency department visits. It is clear that the patient with asthma will benefit from the insights of health care personnel who are expert in the management of this disorder.

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