INTRODUCTION — The best strategy for management of acute exacerbations of asthma is early recognition and intervention, before attacks become severe and potentially life threatening. Detailed investigations into the circumstances surrounding fatal asthma have frequently revealed failures on the part of both patients and clinicians to recognize the severity of the disease and to intensify treatment appropriately [1,2].
The National Asthma Expert Panel has published useful algorithms on the management of acute exacerbations of asthma, both in the home and acute care settings (figure 1 and figure 2) . These algorithms may be used for asthma exacerbations of any severity. A table outlining the emergency management of severe asthma exacerbations in adults is provided (table 1).
The basic principles of care are the following:
The management of acute asthma exacerbations will be presented here. Mechanical ventilation in severe exacerbations of asthma is discussed separately. (See "Mechanical ventilation in adults with acute exacerbations of asthma".)
INITIAL RESPONSE — Instructions to a patient regarding self-administration of medications and self-monitoring differ depending upon the patient's history (eg, medications currently used to treat asthma, prior history of severe exacerbations, and prior experience with oral glucocorticoids) and ability to understand and follow directions. An individualized written "asthma action plan" that is based upon symptoms and peak flow measurements can be provided to patients to provide clear instructions on how to detect and respond to changes in symptoms and peak flow readings (figure 3) . Peak flow meters are available at low cost (eg, $30 or less).
Detecting the onset of an exacerbation — Some patients are very sensitive to increased asthma symptoms, while others perceive reduced airflow only when it becomes marked. For the latter group, a decrease in peak expiratory flow may be the first sign that asthma control is deteriorating. A decrement in peak flow of greater than 20 percent from normal, or from the patient's personal best value, signals the presence of a deterioration and helps one gauge the severity of the change. A fall to less than 50 percent of baseline should be considered a severe attack. (See "Peak expiratory flow rate monitoring in asthma".)
When patients recognize the onset of an exacerbation, they should self-administer an inhaled short-acting beta agonist as follows:
The patient should then repeat a peak flow measurement. Based upon the initial response to the inhaled beta agonist, the patient should either continue self-care or seek medical attention, as described below (figure 1).
Good response to initial home treatment — If the repeat peak flow measurement increases to above 80 percent of the patient's personal best, then the patient may safely continue self-treatment (figure 1). Other important early interventions include removal of or from the offending stimulus (if known), continued administration of inhaled short-acting beta agonists, and consideration of a short course of oral glucocorticoids if beta agonists do not fully correct the decrement in peak flow.
Quadrupling the dose of inhaled glucocorticoids in the setting of mildly increased asthma symptoms, rather than initiating oral glucocorticoids, may be of some benefit, although this approach has not been studied sufficiently . Doubling the dose of inhaled glucocorticoids appears to be ineffective and is not recommended . In a well-executed double blind placebo controlled trial of 390 patients with asthma, subjects were randomly assigned to treatment with twice their usual dose of inhaled glucocorticoid or placebo (delivered using an identical inhaler) when asthmatic symptoms worsened . Over the course of the one-year study, over half of all patients experienced an episode of worsening of their asthma, and 12 percent eventually required systemic glucocorticoid therapy with prednisolone to control their symptoms. There was no significant difference in the need for systemic glucocorticoid therapy between groups, suggesting that, in general, doubling the inhaled glucocorticoid dosage in the acute setting has little clinical impact on the progression of an acute exacerbation.
The patient should initiate contact with the clinician for instructions about how to continue care. The asthma action plan should include clear instructions about how to reach the clinician during exacerbations.
Incomplete response to initial home treatment — In patients with an incomplete response to inhaled short-acting bronchodilator, if the repeat peak flow measurement increases to the range of 50 to 79 percent of the patient's personal best, then the patient should initiate oral glucocorticoids and contact the clinician urgently for advice (figure 1). Other early interventions include removal of or from the offending stimulus (if known), continued administration of inhaled short-acting beta agonists, and intermittent measurements of peak flow to assess response.
Timely administration of oral glucocorticoids for serious asthmatic exacerbations is probably the single most effective strategy for reducing emergency department visits and hospitalizations for acute asthmatic attacks. Patients with serious exacerbations frequently require evaluation in the office, and may need to proceed to the emergency department if improvement is not apparent.
Poor response to initial home treatment — Patients should seek immediate medical attention if they have a peak expiratory flow rate that remains less than 50 percent of baseline, symptoms or signs of severe exacerbation (eg, marked breathlessness), or are at high risk for a fatal attack. Inhaled beta agonists should continue to be administered while help is arriving. Risk factors for a fatal asthma attack include:
SEVERITY ASSESSMENT — Once the patient presents for evaluation, a number of clinical findings and objective tests may assist the clinician in assessing the severity of an asthma attack (figure 2).
Clinical findings — The presence of certain clinical findings may help to identify patients having severe asthma attacks. Pulsus paradoxus (ie, a fall in systolic blood pressure by at least 12 mmHg during inspiration), use of accessory muscles of inspiration (eg, sternocleidomastoid muscles), diaphoresis, and inability to lie supine due to breathlessness all are indicative of severe airflow obstruction . Unfortunately, these findings are not sensitive indicators of severe attacks; up to 50 percent of patients with severe airflow obstruction will not manifest any of these abnormalities .
Peak flow — Measurement of expiratory airflow with a peak flow meter (or spirometer) is the best method for objective assessment of the severity of an asthma attack. Peak flow measurements take less than one minute to perform, are safe and inexpensive, and, when repeated over time, can be used to monitor a patient's response to treatment. They are also useful as a predictive marker for the possibility of hypercapnia, as discussed below. Normal values differ with gender, height, and age (table 2A-C), but a peak flow rate below 200 L/min indicates severe obstruction for all but unusually small adults . (See "Peak expiratory flow rate monitoring in asthma".)
Gas exchange — Marked hypoxemia (arterial partial pressure of oxygen [PaO2] <60 mmHg [8 kPa], oxygen saturation [SaO2] <90 percent) is infrequent during asthma attacks; however, it remains a potential cause of severe complications and death. The ready availability of transcutaneous oximetry (ie, pulse oximetry) allows noninvasive screening for hypoxemia among patients with severe asthma attacks. Current guidelines recommend the use of transcutaneous pulse oximetry monitoring particularly among patients who are in severe distress, have a forced expiratory volume in one second (FEV1) or peak expiratory flow that is less than 40 percent of baseline, or are unable to perform lung function measures . There is no contraindication to the use of continuous transcutaneous oximetry during all asthmatic attacks.
Assessing hypercapnia — An assessment of arterial partial pressure of carbon dioxide (PaCO2) is important in patients with a severe asthma attack. Respiratory drive is almost invariably increased in acute asthma, resulting in hyperventilation and a correspondingly decreased PaCO2. Thus, an elevated or even normal PaCO2 indicates that airway narrowing is so severe that the respiratory system cannot respond adequately to the output of the respiratory center. Hypercapnia and respiratory failure can then develop rapidly with any further airway obstruction or with respiratory muscle fatigue.
Simple peak flow measurements provide a useful screening tool for the possibility of hypercapnia (in contrast to hypoxemia) and obviate the need for routine arterial blood gases in acutely ill patients. In the absence of respiratory depressant medications such as narcotics or sedatives, hypercapnia occurs only when the peak expiratory flow falls below 25 percent of normal [8,9]. Thus, arterial blood gas measurements in acute asthma are generally indicated only among patients with persistent dyspnea (despite initial bronchodilator therapy) whose peak expiratory flow remains below 25 percent of normal. They may also be necessary in the patient who is too ill to perform a peak flow measurement.
Chest radiograph — Chest radiographs are generally unrevealing in acute asthma attacks . The most common abnormality is pulmonary hyperinflation. Other abnormal findings (eg, pneumothorax, pneumomediastinum, pneumonia, or atelectasis) are infrequent, occurring in only about 2 percent of chest radiographs obtained among patients presenting to emergency departments for the treatment of acute asthma [11,12].
Similarly, chest radiographs in patients hospitalized for their asthma can be limited to those patients with suspected complications (eg, temperature >38.3ºC, unexplained chest pain, leukocytosis, or hypoxemia). They are also useful for patients at high risk for comorbidities (eg, based upon a history of intravenous drug abuse, immunosuppression, granulomatous disease, recent seizures, cancer, chest surgery, or heart failure) [10,13].
TREATMENT — A table outlining the emergency management of severe asthma exacerbations in adults is provided (table 1).
The primary goals of therapy for acute severe asthma are the rapid reversal of airflow obstruction and the correction, if necessary, of severe hypercapnia or hypoxemia. Airflow obstruction is most rapidly alleviated by the combination of repeated administration of inhaled bronchodilators and early institution of systemic glucocorticoids (figure 1 and figure 2). Until their respiratory distress has abated, patients should receive close monitoring, including serial measurements of lung function (eg, peak expiratory flow), to assess the response to treatment.
Inhaled beta agonists — The mainstay of bronchodilator treatment is inhalation of short-acting beta-2-selective adrenergic agonists, such as albuterol, levalbuterol, metaproterenol, or pirbuterol [3,14]. The standard regimen for initial care in the emergency department has become albuterol (or an equivalent) 2.5 to 5 mg by continuous flow (also called "hand-held" or "updraft") nebulization every 20 minutes for three doses, then 2.5 to 10 mg every one to four hours as needed . Another protocol calls for administration of albuterol by MDI with a spacer, four puffs every 10 minutes, or eight puffs every 20 minutes, for up to four hours, then every one to four hours as needed. For critically ill patients, some clinicians prefer continuous nebulization, administering 10 to 15 mg over one hour. (See "Beta agonists in asthma: Acute administration and prophylactic use".)
Nebulizer versus MDI — The relatively large particle size generated by continuous flow nebulizers and the loss of medication from the expiratory port of the nebulizer system make this method of delivery relatively inefficient compared to a metered dose inhaler (MDI). Comparisons of MDI plus spacer systems (eg, Aerochamber®, Optichamber®, Vortex®, and others) to nebulizer delivery, using the same beta agonist but in much reduced doses, have demonstrated comparable improvements in lung function [15-18]. (See "Delivery of inhaled medication in adults".)
As an example, one prospective but unblinded trial analyzed data from 2342 emergency department visits by 1420 patients and noted that admission rates were the same in patients treated with albuterol by nebulizer or by MDI with a spacer . Furthermore, MDI treatment was associated with significantly shorter emergency department stays (164 versus 175 minutes), greater improvements in peak flow (127 versus 112 L/min), and a lower cumulative dose of albuterol (1125 mcg versus 6700 mcg).
Four to six carefully administered inhalations from an MDI with spacer have generally been found to equal one nebulizer treatment, although the equivalent dose has not been precisely defined. In comparative trials, administration of beta agonist by MDI with spacer was directly supervised to ensure the patient's proper coordination and inhalational technique.
Many emergency departments (including our own) continue to rely on nebulized administration of beta agonists for acutely ill asthmatic patients, taking advantage of the simplicity of delivery during the patient's tidal breathing. Nevertheless, one implication of equivalency of the two delivery methods is that maximal bronchodilator therapy can be delivered using routinely available supplies in the home or clinician's office, even without availability of a compressor and nebulizer. In addition, as patients recover in the hospital from acute, severe attacks, the transition can be made from nebulized beta agonists to beta agonists by MDI with spacer without loss of efficacy and with the opportunity for patient education in proper inhaler technique. (See "The use of inhaler devices in adults".)
Inhaled anticholinergics — The most recent guidelines for asthma management prepared by the Expert Panel of the National Asthma Education and Prevention Program (Expert Panel Report III) recommend the addition of ipratropium for patients with severe exacerbations who are in the emergency department, but not during hospitalization .
The adult dosing of ipratropium for nebulization is 500 mcg every 20 minutes for three doses, then as needed . Alternatively, ipratropium can be administered by MDI at a dose of eight inhalations every 20 minutes, then as needed for up to three hours.
Some investigators have reported that the combination provides greater bronchodilation than beta agonists alone, particularly among patients with the most severe airflow obstruction [19-21]. Meta-analyses also have supported the use of ipratropium in the setting of very severe airflow obstruction [22-24]. (See "Anticholinergic agents in the management of acute exacerbations of asthma".)
However, positive findings have not been universal. As examples, a 1996 multicenter trial involving more than 300 adults treated in emergency departments for asthma exacerbations could find no advantage to combined albuterol and ipratropium over albuterol alone, either for the entire population of patients or for any identifiable subgroups . A second trial of 254 patients also failed to demonstrate any benefit from the addition of ipratropium during acute attacks of asthma . This controversy continues with the conflicting results of a large trial conducted in New Zealand, in which for the group as a whole, greater bronchodilation was achieved with the combined use of albuterol and ipratropium, but no advantage could be found among those with the most severe obstruction (FEV1 <1 L) on presentation .
At present, the use of inhaled ipratropium is usually reserved for patients with severe airflow obstruction failing to improve despite repeated administration of inhaled beta agonists. Other special circumstances in which such parasympatholytic therapy may be of particular benefit include treatment of patients on monoamine oxidase inhibitor therapy (who may have increased toxicity from sympathomimetic therapy due to impaired drug metabolism), patients with chronic obstructive pulmonary disease with an asthmatic component, and patients whose asthma has been triggered by beta-blocker therapy.
Systemic glucocorticoids — Patients with continued wheezing and shortness of breath despite intensive bronchodilator therapy most likely have persistent airflow obstruction on the basis of airway inflammation and intraluminal mucus plugging. Their rate of improvement typically slows after the first hour of treatment, since airway edema, cellular infiltration, and mucus hypersecretion resolve with a tempo far slower than smooth muscle constriction . Among patients with significant airflow obstruction despite intensive treatment with bronchodilators, systemic glucocorticoids speed the rate of improvement .
Current guidelines encourage early systemic glucocorticoids for all patients who have a moderate (peak expiratory flow <70 percent of baseline) or severe exacerbation (peak expiratory flow <40 percent of baseline; in the urgent care setting, the criterion for a severe asthmatic attack changes from the <50 percent used for decision-making at home to <40 percent), or in whom inhaled short-acting beta agonists do not fully correct the decrement in peak flow . In the past, systemic glucocorticoids were commonly withheld for many hours and even days, while treating with bronchodilators and awaiting gradual spontaneous improvement in airway inflammation. Supplemental systemic glucocorticoids should be administered promptly to any patient who develops an asthma exacerbation despite daily or alternate day oral glucocorticoid therapy.
In general, the onset of action of systemic glucocorticoids is not clinically apparent until as long as six hours after administration. Thus, the beneficial effect is not likely to be observed during the few hours that the patient spends in the medical office or emergency department . Early administration helps to minimize the delay in improvement anticipated with systemic glucocorticoids .
Administration — The optimal dose for systemic glucocorticoids in asthmatic exacerbations remains unknown, although the equivalent of a prednisone dose of 40 to 60 mg per day in a single or divided dose is typical (table 3) .
In the absence of vomiting, oral administration can be used instead of intravenous administration. Oral prednisone and methylprednisolone are rapidly absorbed (peak serum levels achieved at one hour after ingestion) with virtually complete bioavailability, and their efficacy is comparable to intravenous methylprednisolone. Thus, 40 to 60 mg of prednisone administered in a medical office may provide the maximal benefit to be derived from systemic glucocorticoids in acute asthma.
Intravenous glucocorticoids should be given to patients who present with impending or actual respiratory arrest, or patients who are intolerant of oral glucocorticoids . The exact dose of glucocorticoids to use for patients with life-threatening asthma is largely based on expert opinion . A higher initial dose of methylprednisolone 60 to 80 mg every 6 to 12 hours is often chosen for patients who are admitted to the intensive care unit. A lower initial dose of 40 to 60 mg every 12 to 24 hours is likely adequate for patients who are admitted to the hospital, but do not require intensive care. A massive initial dose (eg, methylprednisolone 500 mg intravenous bolus) is no more effective than a large initial dose (125 mg) .
Transition to oral administration of glucocorticoids can occur when the patient can tolerate and absorb oral medication. When comparable doses are administered, the effect of glucocorticoids by oral and intravenous routes of administration is identical.
Intramuscular injection of long-acting glucocorticoid formulations administered at the time of discharge from the emergency department appears to be as effective as oral therapy [34-38]. In a randomized trial of 190 adult patients with acute asthma, intramuscular injection of long-acting methylprednisolone (160 mg) resulted in a similarly low rate of relapse as oral methylprednisolone given in a tapering schedule over eight days (total dose = 160 mg) . This approach may be beneficial for patients without access to oral medication or at high risk of medical noncompliance.
Duration — The duration of a systemic therapy necessary to effect complete resolution of symptoms and return of lung function to baseline varies from patient to patient and attack to attack. As a rough guide, most severe attacks that require hospitalization will resolve (with return of lung function to baseline) in 10 to 14 days. Alternatively, patients can stop their oral glucocorticoids based on resolution of their symptoms and self-monitored peak flow values (eg, when peak expiratory flow is greater than 70 percent of baseline).
Tapering oral glucocorticoids is not necessary if the duration of glucocorticoid treatment is less than three weeks (a duration too brief to cause adrenal atrophy) and if inhaled glucocorticoids are concomitantly prescribed for ongoing therapy (to prevent relapse).
Magnesium sulfate — Intravenous magnesium sulfate (2 gm infused over 20 min) has bronchodilator activity in acute asthma, possibly due to inhibition of calcium influx into airway smooth muscle cells . Although the routine use of this agent does not seem to confer significant benefit beyond that achieved with the conventional use of beta agonists and systemic glucocorticoids, two systematic reviews concluded that it is helpful in the subgroup of patients with severe attacks [40-42].
This agent is suggested for patients who have life-threatening exacerbations or whose exacerbation remains severe (peak expiratory flow <40 percent of baseline) after one hour of intensive conventional therapy .
Intravenous magnesium has an excellent safety profile; however, it is contraindicated in the presence of renal insufficiency, and hypermagnesemia can result in muscle weakness. (See "Symptoms of hypermagnesemia".)
Nonstandard therapies — There are several therapies for acute exacerbations of asthma that may be helpful, but cannot be recommended for routine use at this time, due to insufficient evidence of efficacy. These include the use of helium-oxygen gas mixtures and leukotriene receptor antagonists, which are discussed below, and anesthetic agents (eg, ketamine), nebulized furosemide, and macrolide antibiotics, which are reviewed separately. (See "Alternative and experimental agents for the treatment of asthma", section on 'Acute asthma'.)
Helium-oxygen — Helium-oxygen (heliox) mixtures have been administered to patients with asthma in an attempt to decrease work of breathing and improve ventilation. The rationale of this intervention is based on the low density of helium, and the effects of low-density gas inhalation on airflow characteristics. In addition, nebulization of albuterol using a helium-oxygen gas mixture may increase the mass of albuterol delivered by allowing smaller particles to better penetrate to the lung periphery, compared to nebulization with air or oxygen. The physiology and clinical application of heliox are reviewed elsewhere. (See "Physiology and clinical use of heliox".)
Despite the theoretical benefits of HeO2, studies have reported conflicting results concerning its efficacy in this setting. Two critical analyses of the published literature found insufficient evidence to recommend the use of helium-oxygen gas mixtures in the treatment of asthmatic attacks [43,44]. In part, studies published to date have been small and non-randomized. In addition, it is difficult to exclude with certainty patients who improve due to treatment of their vocal cord (upper airway) dysfunction.
At this time, routine use of helium-oxygen mixture cannot be recommended due to conflicting data about its efficacy. However, for patients who have life-threatening exacerbations or whose exacerbation remains severe (peak expiratory flow <40 percent of baseline) after one hour of intensive conventional therapy, heliox-driven albuterol nebulization should be considered .
Leukotriene receptor antagonists — Leukotriene receptor antagonists are an established therapy for chronic asthma, but the role of these medications in the management of acute exacerbations is unclear [45-47].
The value of acute administration of an intravenous leukotriene receptor antagonist was assessed in a randomized controlled clinical trial of 201 adults with acute asthma . Patients who had a one-second forced expiratory volume (FEV1) <70 percent predicted following inhalation of nebulized albuterol were randomly assigned to treatment with montelukast (7 mg or 14 mg IV) or placebo. Montelukast therapy was associated with a 15 percent increase in FEV1 at both dosages, compared with a 4 percent increase in patients treated with placebo (figure 4). However, no intravenous preparation of a leukotriene receptor antagonist is currently available in the United States.
A larger randomized controlled trial assessed the effect of zafirlukast on 641 adults with acute asthma . Patients treated in the emergency department with a single oral dose of zafirlukast 160 mg (four times the usual total daily dose) were less likely than those receiving placebo to require prolonged observation or hospital admission (10 versus 15 percent, respectively). In addition, patients who received oral zafirlukast 20 mg per day for six days after leaving the emergency department were less likely than patients given placebo to require medical care for relapse during the 28-day follow up period (24 versus 29 percent, respectively).
These significant findings are of small magnitude and need to be confirmed in larger trials, but they do offer preliminary evidence that leukotriene receptor blockade could be an effective therapy for acute asthma in adults.
Ineffective therapies — The use of intravenous methylxanthines in addition to beta-agonists, and the use of inhaled glucocorticoids instead of oral or intravenous preparations in the emergency department setting have been shown to be relatively ineffective approaches that cannot be recommended .
Methylxanthines — The use of alternative bronchodilators such as intravenous theophylline or aminophylline, in addition to beta-agonists, is not recommended in the treatment of acute asthma exacerbations . These agents are not as potent as the beta agonists when used alone for the treatment of asthma, and provide no further bronchodilation beyond that achieved with inhaled beta agonists alone (figure 5) [49,50]. In addition, these agents appear to increase the incidence of adverse effects when combined with bronchodilators . Studies extending over several hours of emergency department care have also failed to show a benefit of theophylline therapy in terms of need for or duration of subsequent hospitalization (figure 6) . For patients who are taking oral theophylline at presentation, we typically continue maintenance oral therapy (and check a theophylline blood level); but if oral intake could no longer be continued, we would very rarely use intravenous therapy with aminophylline or theophylline.
Inhaled glucocorticoids — Some reports have suggested that high dose inhaled glucocorticoids have an effect comparable to oral or intravenous glucocorticoids following initial stabilization in the Emergency Department [52-55]. However, several larger controlled trials and meta-analyses have drawn the opposite conclusion [5,56-61]. Thus, this approach cannot be recommended.
Empiric antibiotics — Clinical practice guidelines recommend against empiric antibiotic therapy for the treatment of an asthma exacerbation, because most respiratory infections that trigger an exacerbation of asthma are viral rather than bacterial. However, the trials on which this recommendation is made did not use antibiotics that cover atypical organisms. The use of antibiotics in acute asthma is discussed in more detail elsewhere. (See "Alternative and experimental agents for the treatment of asthma", section on 'Empiric antibiotics'.)
DISPOSITION — Patients with acute, severe asthmatic exacerbations are at risk for further deterioration in lung function, respiratory failure, and asphyxic death. In many cases, airway obstruction remains labile for days following an acute exacerbation, with wide swings in expiratory flow over minutes or hours. Nocturnal deteriorations are common.
Indications for hospitalization — The purpose of hospitalization during an acute exacerbation of asthma is close observation and availability of aggressive interventions in the event of worsening asthma. It also serves to remove the patient from stimuli in the home environment that potentially aggravate asthma, ensure medication compliance, and permit inactivity during recovery from the illness.
Identifying patients who should be kept for observation or hospital admission remains largely a matter of clinical judgment. Severe symptoms of coughing, wheezing, and shortness of breath that preclude self-care are obvious indications for continued in-hospital care. Peak flow measurements are also useful for identifying patients "at risk" for poor outcomes if discharged home:
Medications upon discharge — An asthmatic attack has not fully resolved even when symptoms have abated. Residual airflow obstruction may last for several days.
Oral glucocorticoids — A short course of oral glucocorticoids significantly reduces the likelihood of a repeat severe exacerbation with emergency department bounce back ("relapse") within the succeeding two weeks, and lessens the frequency of persistent severe symptoms evaluated at a two-week telephone follow-up [62,63]. As an example, one randomized, controlled trial demonstrating efficacy used an eight day tapering schedule beginning at methylprednisolone 64 mg/day .
Nearly all patients with a significant asthma exacerbation requiring emergency department evaluation should receive a course of oral glucocorticoids for three to ten days . For steroid courses of this duration, there is no need to taper the dose if patients are also taking inhaled glucocorticoids.
Inhaled glucocorticoids — Treatment with regular inhaled glucocorticoids constitutes an important method to prevent recurrent asthma attacks after discontinuation of oral glucocorticoids and to prevent the potential decline in lung function associated with any future severe asthma exacerbation [3,31]. Virtually every patient who has suffered an asthma attack severe enough to require urgent care should receive an inhaled glucocorticoid as part of their discharge medication plan (table 4).
Among hospitalized patients, we typically begin (or resume, if previously taking) inhaled glucocorticoids as soon as patients are able to tolerate medication delivery from dry-powder inhalers or metered-dose inhalers (with spacers). Delaying initiation (or reinitiation) of inhaled glucocorticoids until the oral glucocorticoid dose has been reduced to approximately 20 mg of prednisone or the equivalent is also acceptable, but in our experience this approach more often leads to confusion and medication non-compliance.
INFORMATION FOR PATIENTS — Patients should be provided with information about asthma and, if they do not already have one, a personalized action plan (figure 3). Follow-up care with a primary provider should be facilitated whenever possible.
Educational materials on this topic are available for patients. (See "Patient information: Asthma treatment in adolescents and adults" and "Patient information: Trigger avoidance in asthma" and "Patient information: How to use a peak flow meter" and "Patient information: Asthma inhaler techniques in adults".) We encourage you to print or e-mail these topics, or to refer patients to our public web site, www.uptodate.com/patients, which includes these and other topics.
SUMMARY AND RECOMMENDATIONS — A table outlining the emergency management of severe asthma exacerbations in adults is provided (table 1).
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