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Asthma: An Evidence-Based Management Update

February 2001
Volume 3, Number 2
Authors Mary K. Reilly, MD Chief Resident, Emergency Medicine, Case Western Reserve University/MetroHealth Medical Center, Cleveland, OH. Michael A. Kaufmann, MD Chief Resident, Emergency Medicine, Case Western Reserve University/MetroHealth Medical Center, Cleveland, OH. Rita K. Cydulka, MD, FACEP Associate Professor, Case Western Reserve University; Attending Physician, MetroHealth Medical Center; Consultant, Cleveland Clinic Foundation; Cleveland, OH. Peer Reviewers Alfred Sacchetti, MD, FACEP Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Jeffrey Mann, MD Attending Emergency Physician, Somerset Medical Center, Somerville, NJ. CME Objectives

HE young man looks bad. The medics struggle to keep him upright as they wheel him past, but his skin is slippery from the torrents of sweat that surge from his cyanotic torso. You yell to him, but he does not respond. His whole being is focused on getting one more nearly impossible breath. The boys neck muscles strain, his chest heaves, but you detect no breath sounds as you quickly listen to his lungs. As the team moves him to the ED stretcher, the terrified light in his eyes begins to dim, and the gasps start to quiet. This young asthmatic is slipping away. In the past two decades, our knowledge and understanding of the pathophysiology and treatment of asthma has steadily increased. We rely on an ever-growing pharmacological armamentarium and continue to expand our means of preventative care. Furthermore, as increasing numbers of patients seek emergency care for the treatment of their asthma, the role of the emergency physician also grows. Our task now includes not only acute treatment, but also initiation of preventative and maintenance care. This issue of Emergency Medicine Practice addresses acute treatment decisions involved with patients with an acute asthma exacerbation, as well as their long-term care requirements.

Epidemiology And Pathophysiology

Despite continuing advances in treatment and prevention, asthma is increasing in prevalence worldwide,1 reaching 4%-5% in the developed nations2,3 and affecting more than 15 million Americans.4 In the United States, it is the most prevalent chronic disease among children.4 The death rate from asthma among those 19 years and younger has increased by almost 80% since 1980.4 Asthma carries higher morbidity and is even more lethal in the elderly, among whom 7%-10% are affected.5,6

Upon completing this article, you should be able to: 1. assess the severity of an acute asthma exacerbation; 2. treat a range of asthma exacerbations, from mild to severe; and 3. identify the appropriate disposition for an asthmatic presenting to the ED.

Date of original release: February 9, 2001. Date of most recent review: February 7, 2001. See Physician CME Information on back page.

Stephen A. Colucciello, MD, FACEP, Assistant Chair, Director of Clinical Services, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Associate Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC.

Associate Editor
Andy Jagoda, MD, FACEP, Professor of Emergency Medicine; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY.

Editorial Board
Judith C. Brillman, MD, Residency Director, Associate Professor, Department of Emergency

Medicine, The University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM. W. Richard Bukata, MD, Assistant Clinical Professor, Emergency Medicine, Los Angeles County/ USC Medical Center, Los Angeles, CA; Medical Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Chest PainStroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga, TN. Valerio Gai, MD, Professor and Chair, Department of Emergency Medicine, University of Turin, Italy. Michael J. Gerardi, MD, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency Medicine, Childrens Medical

Center, Atlantic Health System; Chair, Pediatric Emergency Medicine Committee, ACEP. Michael A. Gibbs, MD, FACEP, Residency Program Director; Medical Director, MedCenter Air, Department of Emergency Medicine, Carolinas Medical Center; Associate Professor of Emergency Medicine, University of North Carolina at Chapel Hill, Charlotte, NC. Gregory L. Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc., Ann Arbor, MI; Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI; President, American Physicians Assurance Society, Ltd., Bridgetown, Barbados, West Indies; Past President, ACEP. Jerome R. Hoffman, MA, MD, FACEP, Professor of Medicine/ Emergency Medicine, UCLA

School of Medicine; Attending Physician, UCLA Emergency Medicine Center; Co-Director, The Doctoring Program, UCLA School of Medicine, Los Angeles, CA. John A. Marx, MD, Chair and Chief, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Michael S. Radeos, MD, MPH, FACEP, Attending Physician in Emergency Medicine, Lincoln Hospital, Bronx, NY; Research Fellow in Emergency Medicine, Massachusetts General Hospital, Boston, MA; Research Fellow in Respiratory Epidemiology, Channing Lab, Boston, MA. Steven G. Rothrock, MD, FACEP, FAAP, Associate Professor of Emergency Medicine,

University of Florida; Orlando Regional Medical Center; Medical Director of Orange County Emergency Medical Service, Orlando, FL. Alfred Sacchetti, MD, FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Department of Emergency Medicine, Vanderbilt University Hospital, Nashville, TN. Mark Smith, MD, Chairman, Department of Emergency Medicine, Washington Hospital Center, Washington, DC. Thomas E. Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL.

Asthma is the third-leading cause of preventable hospitalization in the United States7 and each year accounts for approximately 2 million visits to the nations EDs.8 The direct costs for the treatment of asthma are projected to have been higher than $14.5 billion in the year 2000, more than double the cost one decade ago.4 Although asthma is characterized by reversible airflow obstruction, it is a chronic disease with long-term implications. It can cause a permanent decline in lung function, resulting in increased mortality.9,10 Appropriate treatment and long-term care, therefore, are critical to preserve normal lung function and minimize long-term mortality. The pathophysiology of asthma is multifactorial. Asthma is a chronic inflammatory condition, which is caused by an array of factors, including genetic, allergenic, infectious, socioeconomic, psychosocial, and environmental triggers.11-14 Because all of these can influence the pattern of episodic and variable airflow obstruction, treatment involves understanding and addressing the underlying etiologies. (See Table 1.) Despite this seemingly complex array of inciting factors, emergency treatment of the asthmatic patient traditionally has included pharmacological therapy that works in one of two ways: by relaxing bronchial smooth muscle (bronchodilation) or reducing airway inflammation (anti-inflammatory action).15 While pharmacologic therapy is the mainstay of emergency treatment of asthma, we can improve long-term outcomes by recognizing the genesis of the disease.

exposure to various chemicals, dusts, or fumes. The astute emergency physician should be able to differentiate these common presentations with a careful history and physical, combined with the judicious use of diagnostic studies. Past medical history can be an important determinant. Has the patient ever had a history of asthma or wheezing before? Has he or she ever used an inhaler? A history of CHF or cardiac disease may increase the likelihood of pulmonary edema masquerading as reactive airway disease. Healing, Papa would tell me, is not a science, but the intuitive art of wooing nature. W.H. Auden

Clinical Practice Guidelines And Systematic Reviews

The National Heart, Lung, and Blood Institute of the National Institutes of Health (NIH) first published guidelines for the diagnosis and management of asthma in 1991 and updated these recommendations in 1997. However, there is no consistent or widespread acceptance of these guidelines.16 In fact, the management of asthma in many EDs deviates significantly from published guidelines.17 Furthermore, there is little evidence that these (or other) guidelines actually improve outcomes.18 As we will show in the ensuing pages, many of the NIH guidelines are not evidence-based. A number of recommendations are based on the opinion of the panel, and unlike most evidence-based guidelines, they did not use a ranking system to establish a hierarchy of best evidence. (In such a hierarchical system, a large, prospective, randomized, controlled trial free from significant bias is specifically designated as more valid than a case report.) Nonetheless, as many as 40% of hospitals have developed some critical pathways for asthma. Hospitals that use asthma clinical guidelines are more likely to engage in asthma-specific quality improvement efforts than hospitals that do not use such guidelines.19 There is some evidence that an acute asthma quality improvement initiative can advance patient care. In one urban teaching hospital, such an initiative decreased delays to -agonist and steroid therapy by approximately 16 minutes and 34 minutes, respectively. The program decreased median ED length of stay by 58 minutes and resulted in fewer inpatient admissions.20 In some hospitals, the triage or treatment area nurses will initiate asthma protocols in order to speed interventions and decrease resource utilization. One study prospectively examined 149 patients with asthma treated by a pathway protocol and compared them with a historical cohort of 97 patients with asthma who were treated by conventional means. Protocol patients had less oxygen use, fewer handheld nebulizer treatments, fewer saline locks, and received fewer intravenous steroids. There was a significant increase in the use of metereddose inhalers with spacer and oral steroids in patients treated by protocol.21 Even scientific reviews and meta-analysis regarding

Differential Diagnosis
Although wheezing, cough, and dyspnea are the clinical hallmarks of asthma, all that wheezes is not asthma. Other common conditions present in a similar fashion. Differential diagnoses include pneumonia, bronchitis, croup, bronchiolitis, chronic obstructive lung disease, congestive heart failure, pulmonary embolism, allergic reactions, and upper airway obstruction. Less common entities include cystic fibrosis, hypersensitivity pneumonitis, and carcinoid syndrome. Even those with no predisposition to asthma may develop wheezing after

Table 1. Pathophysiology Of Asthma.

Etiology Cellular Relevance to treatment Interaction of mast cells with IgE molecules leading to the flood of pro-inflammatory molecules in the pulmonary system10,13 Connection between viral respiratory infections and the development of asthma14 Psychological and emotional factors that act via modification of vagal efferent activity Influence of other precipitants like environmental pollutants and pharmacologic agents

Infectious disease


Public health

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asthma are plagued with problems (except perhaps this one). In a systematic review of systematic reviews, the asthma literature was found wanting. Half of the reviews and meta-analyses never included a comprehensive search or reported their methods. Few included measures to avoid selection bias, evaluated study validity, or used appropriate criteria for validity assessment.22

Prehospital Care
The prehospital care of the asthmatic closely parallels the ED management. Medics should either give oxygen to patients with asthma, measure their oxygen saturation using pulse oximetry, or both. Patients with minimal symptoms, however, may require neither. Clinical trials demonstrate that the prehospital administration of either aerosolized albuterol or subcutaneous terbutaline significantly reduces respiratory distress.23 In this study, albuterol provided greater subjective improvement. Some limited data suggest that 125 mg of intravenous methylprednisolone given by paramedics may reduce the need for admission in asthmatics.24 Once again, patients with mild exacerbations would not require this intervention.

ED Evaluation
The acute asthmatic can present with an array of signs and symptoms. Some patients complain of wheezing and shortness of breath, while others report a relentless cough. The degree of dyspnea will dictate the ability to perform a thorough history and physical. Immediate attention must be directed to the patients appearance, vital signs, and chest examination. If needed, aggressive therapy directed at relieving airway obstruction must begin as soon as the diagnosis is suspected.

The patients history will not only help determine the course of immediate treatment in the ED, but it will also place the exacerbation in the context of the disease.

respond as rapidly to therapy. In one study, patients with sudden-onset asthma were less likely to report an upperrespiratory-tract infection (17% vs 40%) and more likely to have an unidentifiable trigger (40% vs 19%) than those with a less subacute attack. Contrary to the ED mythology that sudden-onset asthma presages respiratory failure, a recent study concluded that sudden onset of symptoms predicted rapid response to therapy and was less likely to lead to admission.25 Confirm whether the current attack feels like their typical exacerbation; if it does not, find out why. Identify any factors that may lead to concomitant or even contrary diagnosis, such as fever or a productive cough. Acuteonset chest pain may denote potential pneumothorax, pneumomediastinum, pneumonia, or pulmonary embolism (in addition to possible cardiac disease). Newonset wheezing in a person with no prior attacks may not represent asthma. (Of course, wheezing in a known asthmatic may also be due to causes other than reactive airway disease. The prior history just makes asthmarelated bronchospasm more likely.) There appear to be significant differences in the way different ethnic groups describe the symptoms of asthma. In one study, African-Americans used upper-airway terms such as tight or itchy throat, scared-agitated, voice tight, and tough breath. Whites were more likely to use lower-airway or chest-wall descriptors such as deep breath, light-headed, out of air, aware of breathing, and hurts to breathe.26 Next, determine the type of medication and amount used prior to arrival in the ED. This information will help guide therapy, both in the ED and beyond. Ask when the patient was last on steroids. Patients with a chronic disease such as asthma are often the best judges of their own condition. Ask the patient how the current attack compares to prior episodes. Some physicians have the asthmatic rate the present episode on a visual analog scale. These scales correlate well with pulmonary function tests (PFTs) in individual patients.27

Past Exacerbations
The patients history offers the backdrop for his current exacerbation. Does the patient have a history of asthma? Many patients will report no history of asthma but admit

History Of Present Illness

Establish any precipitants of the attack and its duration. Be aware of attacks that are prolonged, as they may not

Key Points In Treating The Asthmatic Patient

1. Most asthmatics can be appropriately assessed with a history and physical, vital signs, PEFR, or spirometry and ongoing clinical evaluation. Specific signs and the severity of the asthmatics exacerbation should guide the addition of extra tests, such as ABG and chest radiography. 2. Always place the context of the asthmatics current attack into his past historysignificant differences in this presentation should spur consideration of alternative or concomitant diagnoses. 3. Every asthmatic requiring more than one -agonist treatment should receive corticosteroids in the ED and should be discharged to home on a pulse regimen. 4. Suggest short-term follow-up (within 3-4 days of the ED visit) to patients with asthma. Tell them to return to the ED if they get worse. v

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they wheeze all the time or have lots of bronchitis attacks. Ask whether he or she has ever been given an inhaler or breathing treatments in the past. Document the frequency of ED visits, prior hospitalizations (including admission to intensive-care settings), a previous need for steroids, and most recent steroid use. Recent discontinuation of steroids may be a factor in the current attack. Determine any history of intubation or noninvasive ventilation. Prior history of intubation or chest-tube placement is an important predictor of severe disease. In one study of near-fatal asthma, univariate analysis identified a history of previous mechanical ventilation (OR: 27.5); admission to the intensive care unit (OR: 9.9); history of worse asthma during January and February (OR: 3.5); and use of air-conditioning (OR: 15.0) as important risk factors for respiratory failure.28 A nearfatal episode of asthma is a risk factor for future lifethreatening attacks; approximately 10% of such patients die in the year after the event.29

a variety of the clinical clues outlined below. No one fakes diaphoresis. Ancient ED saying

General Appearance
The patients general appearance will often determine the pace of subsequent interventions. Upon entering the room, assess for the general level of distress. A patient who is sweating and unable to speak in full sentences is in trouble. The number of seconds a patient can spend counting correlates well with pulmonary function.30 In the first several moments, quickly appraise the patients mental status. Both lethargy and agitation presage respiratory failure. Cyanosis is a very late finding in asthma. By the time it appears, it is likely that the patient is moribund.31 While these suggestions are considered common knowledge, studies that focus on clinical examination show that inter-observer agreement regarding respiratory signs in adults is low.32 However, one study indicates that inter-observer agreement may be better in the assessment of acute asthma in children.33

Past Medical History, Social History, Medications

Obtaining a history of other medical problems, allergies, current medications, and social history is vital to the course of medical management. The patient with a history of asthma may also have a history of cardiovascular disease, pulmonary embolism, or DVT. Ignoring this history could lead to misfortune if shortness of breath is automatically attributed to asthma. This is especially important if the patient states that the current problem is not similar to previous attacks. Ask patients whether they are using an inhaler, and in particular whether they are using it with a spacer chamber. How many puffs a day are they using? Many patients may list albuterol as one of their medications without informing the physician that their inhaler is empty. Because proper technique is critical to the efficacy of an MDI, have them demonstrate how they use their inhaler. This simple intervention may have a dramatic impact on their disease if they are able to learn the proper technique. Questioning the patient about tobacco use or exposure may lead to an explanation for the asthmatic who seems to be on the right pharmacologic regimen but continues to have frequent exacerbations. Finally, the ubiquitous list of meds can offer insight into both this exacerbation and the severity of the patients asthma. For example, recently prescribed timolol ophthalmic drops may have worsened the disease due to their -blocking effect.

Vital Signs
Tachycardia and tachypnea do not always correlate with the degree of airway obstruction.34,35 Tachycardia will often resolve with appropriate -agonist therapy, not worsen. A decreasing respiratory rate can simply mean the patient is tiring, rather than improving. There is little research that examines the relationship of blood pressure to respiratory distress. However, if the blood pressure is extremely high (or extremely low), consider cardiac etiologies such as CHF or cardiogenic shock in the differential diagnosis of wheezing. If the determination of fever is important, consider obtaining a rectal temperature. Oral temperatures are notoriously inaccurate in patients with tachypnea.

Pulse Oximetry
Pulse oximetrythe fifth vital signis often useful in the assessment of asthma. It will rapidly alert the ED staff to hypoxia and the need for supplemental oxygen. Hypoxemia generally reflects the extent of ventilation/ perfusion mismatch.36 Remember, however, that pulse oximetry does not reflect ventilation status. Patients with near-normal saturations while on oxygen may be hypercarbic and in danger of incipient respiratory failure. Pulse oximetry may also predict the need for admission in children. Children with initial low oxygen saturation (below 90% or 91% depending on the study) often require admission regardless of their response to therapy.37-39 In one study, children who presented with an oxygen saturation level of 92% or less had a greater-thansixfold relative risk for requiring prolonged treatment.40 Another study showed that in children, a posttreatment SpO2 level of 91% or less increased the odds of admission 16-fold.41 As opposed to some previous studies, this study found pretreatment SpO2 levels to be a relatively poor predictor of admission. The initial room air pulse oximetry can accelerate

Physical Examination
Be wary when performing the physical exam. A patients ventilatory status can change rapidly. Remember that patients with no wheezing may actually be in extremis; they cannot move enough air to produce the turbulent whistle of asthma. Such patients, however, will appear dyspneic and will not be able to speak normally. Others who are just holding their own may tire and rapidly become acidotic and hypercarbic. Many experienced physicians use their gestalt to rapidly assess the severity of distress. They may overtly or subliminally incorporate

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treatment intervention in adults (if low) or provide reassurance (if high). However, the initial oxygen saturation has little prognostic utility in the adult asthmatic.42

patient. The short-term prognosis in the acute asthmatic is challenging and often not obvious. In addition to the history and physical exam, diagnostic studies may prove useful in determining the disposition for some patients.46

Head And Neck

A careful cardiopulmonary evaluation is central to the ED evaluation. Findings such as increased jugular venous pressure, lymphadenopathy, and carotid bruits may signal alternative diagnoses. Pay special attention to the patients neck veins. If they distend during inspiration (Kussmauls sign), then the patient has a significant increase in right-sided venous pressure that might possibly be due to right ventricular infarction, tension pneumothorax, pulmonary embolism, or pericardial tamponade.43 In the unlikely event of a deviated trachea, consider the possibility of a tension pneumothorax on the side opposite the deviation. The strap muscles of the anterior neck will bulge when the patient is in significant distress in an attempt to pull air into the lungs. Those in respiratory distress may breathe with pursed lips.

Asthma Index Scores And Pulmonary Function Tests

Scoring systems are usually employed to help with management and triage decisions. Asthma index scores, once commonly used for predicting emergency disposition and treatment, have proven to be no better than clinical judgment in predicting outcome.47-49 The peak expiratory flow rate (PEFR) measures the obstruction in larger airways.50 Beware of the patient making a poor effort with his peak flow; peak flow data alone should not dictate disposition but should be used in the context of the patients overall clinical picture. Despite its shortcomings, PEFRs are easy to obtain, inexpensive, and less time-consuming than FEV1 measurements. In the appropriate setting, with good patient cooperation, many emergency physicians consider them useful. In addition, PEFRs may be used to avoid other invasive tests (see the Arterial Blood Gas section later in this article). The forced expiratory volume in the first second (FEV1) tends to be a more sensitive reflection of the patients overall airway obstruction, as well as the patients ability to ventilate.51 In addition, FEV1 is much less dependent on patient effort, making it more reliable than PEFR. However, FEV1 requires a more involved maneuver and significant patient cooperation.52-55 A pretreatment PEFR or FEV1 of less than 50% predicted indicates severe obstruction.56 The National Guidelines recommend PEFR or FEV1 measurements to assist in ED management decisions. While pulmonary function tests such as PEFR may be valuable in the home management of asthma, there is considerable controversy regarding their utility in the ED. Only one study shows that the use of PEFR initially and at 30 minutes (combined with assessment of accessory muscle use) might help predict which patients may require hospitalization.57 However, a better-designed large prospective trial demonstrated that peak flow rates could not predict which patients would return to the ED with a relapse.58 Another study looked at the personal best PEFR scoresa value that the asthma guidelines champion as an important benchmark for ED managementamong inner-city ED patients with acute asthma. The authors found that the personal best PEFR was inaccurate and argue that in contradistinction to NAEPP guidelines, these values should not be used routinely (or preferentially) as part of the ED discharge decision.59 Other studies confirm that PEFRs do not correlate well with need for admission or with return visits to the ED.60,61

Pulmonary And Cardiac Exam

The chest exam is, of course, central to the evaluation of an asthmatic. Look for intercostal retractions and accessory muscle use. Next, careful auscultation of the lungs may reveal wheezing, rhonchi, rales, or a silent chest. The latter can be ominous, as wheezing can be absent when airflow is minimal.34 The presence of unilateral wheezing or rales should lead one to consider the possibility of pneumonia or other causes of obstruction. Unequal breath sounds suggest a variety of diagnoses. While this finding may be present in asthma, it also occurs with pneumothorax, pulmonary embolism, pneumonia, pleural effusion, or foreign body. Stridor should be distinguished from wheezing. When listening with a stethoscope, stridor is most prominent over the glottis, while wheezing is louder in the chest fields. Stridor is associated with tracheal or laryngeal obstruction and is usually more distinct upon inspiration. A complete cardiac exam includes evaluation of the heart sounds. A gallop rhythm, in particular an S3, is evidence of cardiac failure. Pulsus paradoxus (> 20 mmHg) is associated with severe obstruction in some individuals, although it is absent in up to one-third of severe asthmatics.34 It is not clear that this finding is useful in clinical practice. No study proves that it adds any further information to that provided by routine clinical assessment. In one British trial, pulsus paradoxus did not correlate with either the severity of acute asthma in individuals or with peak flow. The authors suggested that it be abandoned as an indicator of asthma severity.44 Furthermore, physicians differ widely in their ability to measure pulsus paradoxus.45

Diagnostic Studies
The therapeutic quandary with asthma is not usually in the diagnosis, but in the treatment and disposition of the

Chest Radiography
Chest radiography should not be routine in the ED evaluation of acute asthma. Unless the patients history or physical exam suggests the possibility of additional or

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competing diagnoses, such as congestive heart failure, foreign body, pneumonia, or pneumothorax, chest radiography is probably not warranted. White et al carried out a prospective study of asthmatics that identified a major abnormality in 34% of chest radiographs in patients requiring admission for acute asthma.62 Major abnormality included infiltrate, pneumothorax, and cardiomegaly.62 The prevalence of abnormal chest radiographs in all-comers to the ED (not just those ill enough to require admission) is significantly lower.63,64 Indications for chest films may include:63,64 Asthma severe enough to require hospitalization Severe respiratory distress Clinical suspicion of pneumothorax, CHF, pneumonia, or foreign body Failure to improve in the ED Compromised host Unexplained fever Patients with COPD are more likely to have abnormalities on chest film, and their need for chest radiography depends on a variety of factors.65

corticosteroid treatment can cause modest leukocytosis,66 which can mislead the physician into diagnosing an infectious etiology. Finally, a theophylline level should be obtained in those patients maintained on chronic therapy.

The most urgent goal in the ED is to rapidly reverse airflow obstruction and ensure adequate oxygenation. The initial therapeutic interventions in any asthmatic should include the basic ABCs, with intravenous access, oxygen, and cardiac monitoring instituted for those in severe distress. It is useful to quickly identify the asthmatic as either unstable or stable (recognizing that the initial designation is subject to rapid change). The clinical pathway Management Of Patients With An Acute Asthma Exacerbation on page 14 begins with this classification. The unstable patient mandates emergency airway equipment at the bedside (including the availability of rapid-sequence intubation agents). Systemic -agonists (e.g., subcutaneous terbutaline or epinephrine) may replace or be combined with aerosolized treatments. Assess the improvement of that patient with several measures: mental status, air exchange, oxygenation, and ventilation. Progressive deterioration or failure to improve with maximal therapy may require intubation. Thankfully, the majority of asthmatics who present to the ED will not require such extreme measures. The most standard therapies can be grouped into three primary categories: -adrenergic agonists, glucocorticoids, and anticholinergics. A fourth category of drugs, the methylxanthines, has no significant role in emergency management, while a fifth and sixth category of drugs, the cromones and leukotriene modifiers, are generally reserved for maintenance therapy. Magnesium is emerging as a treatment for very severe asthma exacerbations. The role of other agents, including agonist isomers (e.g., levalbuterol), heliox, anesthetics, and anti-hypertensive agents are currently the topics of intensive clinical research in the management of acute asthma exacerbations.

Arterial Blood Gas

Measurement of arterial blood gases is expensive, painful, and is occasionally associated with significant morbidity (arterial thrombosis). It is also unnecessary in the vast majority of patients who are suffering an acute exacerbation. ABG may be useful in patients experiencing severe or prolonged attacks, those with a PEFR or FEV1 less than 25% of predicted who appear in significant distress,56 or in those with altered mental status. Pulmonary function tests can usually exclude the possibility of respiratory failure. Martin et al demonstrated that PEFR accurately predicted hypercarbia or acidosis. In his study, no patient with a PEFR greater than 25% predicted had a PaCO2 greater than 45 or a pH less than 7.35.36 When an ABG is obtained, some pitfalls await the unwary physician. In the patient with significant tachypnea, a normal PaCO2 is actually a worrisome finding, since the tachypneic patient is expected to be hypocarbic. A near-normal value reflects the fact that the patient is tiring and should warn of impending ventilatory failure.


Electrocardiography And Cardiac Monitoring

Cardiac monitoring and ECG testing are not indicated in the evaluation of the acute asthmatic unless co-existing cardiac conditions are suspected. When present, typical ECG patterns include findings consistent with pulmonary disease, including right ventricular strain, right atrial enlargement or nonspecific ST-T wave abnormalities that resolve with treatment.

-adrenergic agonists are the mainstays in the treatment of acute bronchospastic disease. They exert their effects by increasing cyclic adenosine monophosphate (cAMP). A series of interactions cause intracellular calcium to bind to cell membranes with greater affinity, thus dropping the myoplasmic calcium concentration. This results in bronchial smooth-muscle relaxation, inhibition of mediator release, and increased mucociliary clearance.

Routine Laboratory Evaluation

Blood tests, including a complete blood count, are rarely indicated in the evaluation of acute asthma exacerbations. Again, the exceptions may include those patients in whom other diagnoses are being considered. If a CBC is obtained, note that -agonist therapy and

Types Of Agents
The older catecholamine bronchodilators include isoproterenol, isoetharine, and epinephrine. Isoproterenol is a more selective -adrenergic agent than epinephrine, but a number of deaths were associated with isoproterenol inhalation in England in the 1960s. Use of this agent

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is not generally warranted. Isoetharine is also a more 2-selective agent than epinephrine and is as effective a bronchodilator as albuterol.67 It is available as a metered-dose inhaler or as an aerosol solution. Doses may be repeated every 20-30 minutes during an acute attack. Epinephrine is a nonselective - and -adrenergic agonist. While it can be nebulized, it is usually administered subcutaneously, and occasionally intravenously for the patient in extremis. It is found in over-the-counter inhalers and the nebulized form increasingly used in the treatment of bronchiolitis. Complications of its use include myocardial irritability, dysrhythmias, and nervousness. However, in one interesting study, when patients with a history of recent myocardial infarction or of angina were excluded, the administration of subcutaneous epinephrine did not cause an increase in dysrhythmias, despite the fact that it was given to asthmatics as old as 96.68 The subcutaneous dose in adults is 0.3-0.5 cc of a 1:1000 solution, which may be repeated every 20 minutes to a total of three doses. The agents listed above have nearly been replaced by newer, longer-acting derivatives and, with the exception of epinephrine, do not have a place in the routine care of asthmatics. Albuterol is currently one of the most widely used of the -agonists. Despite its popularity, researchers have not consistently validated its clinical superiority.69 Other -agonists include metaproterenol, terbutaline, fenoterol, and carbuterol. They are similar to albuterol in that they all share greater 2-specificity and longer duration of action than the catecholamines.

exist for the latter devices: dry powder inhalers (DPIs) or an MDI utilizing a novel hydrofluorocarbon (HFC). When making this transition, physicians should be aware of potential efficacy differences between the two methods of drug delivery.78 Nebulizer therapy is still widely used in EDs, despite the fact that numerous studies show that the MDI combined with a spacer chamber is therapeutically equivalent.79-83 The combination of an MDI with spacer is less expensive, easier to administer, and provides an opportunity for the physician to evaluate whether the patient is using the device correctly (an essential component of home management). For these reasons, many hospitals have switched from the nebulizer to the MDI with spacer in the emergency treatment of asthma. Other EDs may give the first treatment via nebulizer and switch to an MDI plus spacer if the patient meets certain clinical criteria (respiratory rate, pulmonary function tests, oxygen saturation, etc.). Children randomized to an MDI plus holding chamber as compared to a nebulizer improve faster, have fewer side effects, fewer admissions, and shorter lengths of stay in the ED.79,80,84

The most effective dose of inhaled -agonist remains unknown. Standard doses of albuterol for adults range from 2.5-5.0 mg per treatment; however, continuous nebulization may involve administering 20 mg or more per hour. In one study, two 5.0 mg treatments of aerosolized albuterol at a 40-minute interval were more effective than three treatments of 2.5 mg given every 20 minutes. The high-dose regimen improved pulmonary function more rapidly and to a greater extent than standard-dose therapy and resulted in shorter ED length of stay (in addition to lower charges to third-party payors).85 -agonist doses may be administered nebulized every 15-20 minutes or as a continuous aerosol.86 Recent literature has failed to demonstrate the superiority of either method.87 Continuous nebulization has a theoretical advantage in departments with limited personnel; if the respiratory therapist or nurse is unable to return every 20 minutes to initiate additional treatments, continuous nebulization can potentially bridge these gaps in the patient who is in moderate distress. One study showed that 2.5 mg of nebulized albuterol is therapeutically equivalent to 1 mg of salbutamol by MDI/spacer (11 puffs). In this randomized trial of acute severe asthma, the MDI-spacer group received four puffs of albuterol at 10-minute intervals (24 puffs per hour). Although patients in the MDI and nebulizer group showed similar improvement, nebulizer therapy produced greater adverse side effects.88 Other studies have employed 6-12 puffs per treatment using an albuterol MDI, even in children.89

Levalbuterol And Its Isomer Counterparts

Levalbuterol is the R-isomer of racemic albuterol (a mixture of 50:50 R- and S-albuterol). The bronchodilator effects of racemic albuterol depend on the R-isomer; for many years, the S-isomer was felt to be biologically inert.70 However, a more in-depth evaluation of the S-isomer indicates that it may have pharmacological properties separate from its R counterpart.71 Theoretically, levalbuterol could provide equivalent bronchodilatation to albuterol with fewer side effects. It costs significantly more than albuterol, and its therapeutic effects have not been directly compared to albuterol in patients with acute exacerbations.72 Even when used on a non-emergent basis, the current literature does not uniformly support the use of levalbuterol over its racemic counterpart.73-75

Routes Of Administration
Aerosol therapy (either nebulization or via metered-dose inhaler [MDI]) is the preferred route for ED use. This is because aerosols achieve topical administration of drug in small doses and produce local bronchodilation with minimal systemic absorption and side effects. The addition of a spacer chamber is an important adjunct when using the MDI, dramatically increasing effective drug delivery.76,77 Worldwide, healthcare providers are transitioning from chlorofluorocarbons (CFCs) as propellants for metered-dose inhalers to non-CFC devices. Two choices

Parenteral Therapy
Parenteral -agonist therapy usually involves subcutaneous injections of epinephrine or terbutaline. These are sometimes given in the distressed patient when aerosol therapy is

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either unavailable or will be delayed. Some physicians, believing that bronchoconstriction may be so profound as to impair aerosol delivery to the lungs, use parenteral therapy in the patient in extremis. However, the presumed advantages of this approach remains unproven. The evidence regarding the utility of intravenous -agonists is limited. Although a few studies have examined intravenous terbutaline in adults resistant to maximal therapy,90,91 it is best studied in children who are in status asthmaticus. Intravenous terbutaline is well tolerated in asthmatic children at varying doses up to a maximum of 10 mcg/ kg/min.92 In another study, children with acute severe asthma given 15 mcg/kg of intravenous albuterol over 10 minutes showed significant improvement compared to those who received nebulized albuterol.93

Oral Therapy
Oral administration of -agonists is generally discouraged.94 Short-acting oral agents such as oral albuterol do not improve quality of life when added to inhaled therapy and significantly increase side effects such as tremor and palpitations.95 Children with wheezing should receive home therapy using an MDI with spacer (and mask in the case of the younger child), not oral agents. In certain situations, long-acting oral agents such as bambuterol (not yet available in the United States) can be helpful in nocturnal asthma.96

Early administration (within one hour) of glucocorticoids in the treatment of acute reactive airway disease results in fewer hospital admissions and a lower rate of relapse after ED discharge.97-99 Therefore, steroids should be administered to all asthmatics whose acute exacerbation is not relieved by one nebulized bronchodilator aerosol and given urgently to those who appear in moderate to severe distress. While the exact mechanism of action is unclear, one theory proposes a reduction of airway inflammation, as well as restoration of -adrenergic responsiveness in the constricted airways. Accepted dosage regimens in adults include prednisone (40-60 mg PO), a 60-125 mg intravenous bolus of methylprednisolone, or a 60-125 mg intramuscular dose of methylprednisolone. No clear benefit has been demonstrated by using high-dose steroids (> 80 mg/d of methylprednisolone) for those patients requiring hospitalization for their exacerbation,100 though it is commonplace for adult patients to receive 120 mg of methylprednisolone in the ED. Oral, intravenous, and intramuscular routes of administration of steroids share equal efficacy and have an onset of action of approximately four hours.98,101 In prolonged ED stays or ED observation units, steroids should be re-administered every 6-8 hours, whether they are given orally or intravenously. In one study, 125 mg of intravenous methylprednisolone increased PEFR and percent-predicted PEFR over time compared to placebo.102 However, because no well-designed trial has demonstrated a head to head superiority of one route

over another, oral administration is the preferred route, particularly in children and even in moderately ill asthmatics if they are able to tolerate the drug (i.e., they do not regurgitate it within the hour). Intramuscular steroids have also been well studied in the treatment of asthma. Studies on the use of intramuscular depo steroids show they are as effective as a seven- to 10day course of oral prednisone.103 Side effects are rare. In one randomized study, a single intramuscular injection (approximately 1.7 mg/kg) of dexamethasone acetate (Decadron, Dexasone, Dexone, Hexadrol) was as effective as a five-day course of oral prednisone (approximately 2 mg/kg/day) in children with mild-to-moderate asthma exacerbations. In a similar study involving adults, a single 40 mg dose of intramuscular triamcinolone diacetate (Aristocort, Kenalog, Aristospan) proved equivalent to prednisone (40 mg/d PO for 5 days) after ED treatment of mild-to-moderate exacerbations of asthma.104 Intramuscular methylprednisolone sodium acetate (Depo-Medrol) is therapeutically equivalent to an eight-day course of oral prednisone.105 Inhaled corticosteroids are currently under investigation for the treatment of the acute exacerbation and may be beneficial for asthmatics who have a more severe exacerbation.101,106,107 Home use of inhaled budesonide and oral prednisone is equally effective in patients discharged from the ED after treatment with systemic corticosteroids for a severe acute exacerbation of asthma. In one study, patients randomized to receive either inhaled budesonide (Turbuhaler) 600 mcg QID (3 puffs QID) or prednisone 40 mg each morning for 7-10 days showed no difference in relapse rates.108 However, combining inhaled with oral steroids does not consistently provide an additive effect.109 In one study, the addition of high-dose inhaled flunisolide to standard therapy (including oral steroids) did not benefit inner-city patients with acute asthma in the first 24 days after ED discharge.110 Other studies have confirmed this finding.111 On the flip side, however, Rowe et al did show improved outcomes in patients who were prescribed inhaled corticosteroids at the time of discharge.112 In this study, patients with acute asthma who were discharged from the ED were prescribed inhaled budesonide (1600 mcg/d) or placebo added to a fixed course of oral prednisone. Those who received the inhaled budesonide had fewer relapses, fewer asthma symptoms, a decreased need for inhaled -agonists, and reported an improved quality of life over the next 21 days.

Anticholinergic therapy, including ipratropium bromide and glycopyrrolate, antagonizes the neuromuscular transmitter acetylcholine at the postganglionic parasympathetic receptor, which reduces vagally mediated bronchoconstriction in the larger central airways. Anticholinergic bronchodilation peaks within 1-2 hours. Simultaneous treatment with -adrenergic agents and anticholinergics may produce an additive effect.113,114 The pooled results of five randomized, controlled trials (RCTs) showed

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that the addition of ipratropium to standard therapy with steroids and -agonists results in fewer hospitalizations when compared to placebo (P = 0.007). The addition of ipratropium bromide also improves pulmonary function in the first 90 minutes of treatment.115 Rodrigo et al demonstrated the most benefit with those who present with severe asthma (FEV1 < 35% predicted ).115 The NIH guidelines recommend that ipratropium bromide (0.5 mg via either nebulizer or MDI) be administered to all patients with a PEFR or FEV1 less than 80% predicted. Ipratropium is useful in pediatric asthma as well. One study showed significant improvement in pulmonary function studies over 120 minutes in children with severe asthma who were given nebulized ipratropium (combined with albuterol and oral steroids) compared with children who received the albuterol and steroids alone.116 In a systematic review of 10 studies regarding the use of anticholinergic inhalations added to the -agonist regimen, children who received multiple-dose ipratropium had improved pulmonary function and a trend to reduced hospitalization. Single-dose ipratropium improved FEV1 but did not decrease hospitalizations. However, the single-dose studies tended to focus on children with less severe exacerbations, while the multiple-dose studies involved children with more severe attacks.117 When nebulized, ipratropium may be combined in the same holding chamber with the -agonist. It also is marketed as a single agent in an MDI (Atrovent) and as a combination inhaler with albuterol (Combivent). At present, ipratropium bromide is the only anticholinergic agent recommended for use during an acute asthma exacerbation.115 Other anticholinergics, such as aerosolized atropine sulfate and glycopyrrolate, have fallen out of favor.118 These medications have a high incidence of side effects, including tachycardia, restlessness, irritability, dry mouth, thirst, and difficulty swallowing.

magnesium over 10-15 minutes. Magnesium is now being used as a vehicle for nebulized albuterol. In acute asthma, nebulized magnesium-albuterol increases the peak flow when compared to albuterol plus normal saline.123

Controversies/Cutting Edge
Heliox, an 80:20 mixture of helium and oxygen, can be considered in patients with respiratory acidosis who fail conventional therapy. Helium is a low-density, inert gas that lowers airway resistance and decreases respiratory work.124 Significant improvement may be noted within 10-20 minutes of initiating therapy in the asthmatic with severe bronchospasm.125 Kass and Terregino compared the effect of heliox to 30% oxygen in asthmatics with severe symptoms. Patients who received heliox had significant improvement in PEFRs compared to controls.126 In contrast, Henderson et al did not demonstrate a difference in spirometry or admission rates for mild-to-moderate asthmatics treated with heliox.127 This disparity may relate to differences in disease severity between the study populations. Ultimately, further studies are necessary to determine the role of heliox in current asthma management.

Nitric Oxide
Inhaled nitric oxide (NO) may be valuable in status asthmaticus refractory to other therapies. In one series, it was administered to five consecutive children with life-threatening status asthmaticus who required mechanical ventilation. Four showed a greater than 20% decrease in baseline PaCO2 soon after the administration of inhaled NO.128

Certain anesthetic agents such as halothane and isoflurane are potent bronchodilators.129,130 These agents produce rapid bronchodilatation but are also myocardial depressants. Halothane can produce arrhythmias and intrapulmonary shunting of blood. Close monitoring of heart rate and blood pressure is essential when using anesthetics to treat status asthmaticus.129 Though general anesthetics have theoretical benefits in the acute treatment of an intubated asthmatic, it is unlikely that such agents will be available in the ED. They are most appropriate for an intensive-care setting in consultation with the anesthesiologist.

Magnesium sulfate is efficacious for the relief of severe bronchoconstriction but adds little to the treatment of mildto-moderate bronchospasm.119-121 This medication regulates intracellular calcium flux, inhibits the release of histamine from mast cells, inhibits the action of acetylcholine, and directly inhibits bronchial smooth-muscle contraction. Bronchodilation is observed within 2-5 minutes after the initiation of therapy but disappears rapidly after termination of treatment. Side effects of magnesium therapy potentially include hypotension, malaise, and a warm, flushing sensation. Monitoring of cardiac rhythm, blood pressure, pulse, neurologic status, and renal function is prudent, but a recent systematic review demonstrated no clinically significant changes in vital signs or presence of side effects with the administration of magnesium.122 In a systematic review of 27 studies and seven trials, the authors found that magnesium reduced hospital admission rates and improved pulmonary function for patients with severe asthma. However, no difference was shown for patients with mild-to-moderate asthma.120 For patients with severe asthma, consider giving 2 g of

Leukotriene-Receptor Antagonists
Leukotriene modifiers result in improved lung function, diminished symptoms, and less need for short-acting -agonists over a wide spectrum of asthma severity. However, they are not currently indicated for acute exacerbations.131 In one ED study, patients were given either 10 mg chewable montelukast or placebo within 20 minutes of presentation (in addition to standard therapy). There were no significant differences in the final PEFR

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scores or the need for hospitalization.132

Airway Management
If the patient deteriorates or fails to improve despite intensive therapy, intubation and mechanical ventilation must be considered. Fortunately, fewer than 1% of asthmatics require mechanical ventilation. Although there are no absolute criteria other than respiratory arrest and coma, the following are indications for acute airway intervention: Worsening pulmonary function tests despite vigorous bronchodilator therapy Decreasing PaO2 Increasing PaCO2 Progressive respiratory acidosis Declining mental status Increasing agitation Many experienced emergency physicians believe that the decision to intubate is best made on clinical grounds (looks bad and not getting better) as opposed to using objective parameters such as PEFR or ABG. This contention is difficult to prove one way or another. Intubation of the asthmatic patient is a daunting task fraught with potential for serious complications. Rapidsequence intubation is the method of choice. (For a full discussion of airway management, please see the May 2000 issue of Emergency Medicine Practice, Emergency Endotracheal Intubations: An Update On The Latest Techniques.) Despite some advantages of the nasal route of intubation (minimal use of sedation), the oral route is the preferred route in asthmatics. Most asthmatics who are in enough distress to require intubation will not be able to readily cooperate with a nasal intubation; in addition, there is increased risk of trauma and bleeding with the nasal route, and it necessitates the use of a smaller endotracheal tube, thereby increasing airflow resistance.153 Some authors suggest pre-treating the asthmatic with lidocaine in the presumption that this will decrease the reflex bronchospasm associated with cord manipulation. While no study has directly evaluated pre-treating the moribund asthmatic with lidocaine, one interesting study suggests that this is unnecessary. In a group of asthmatics undergoing elective surgery, inhaled albuterol blunted airway response to tracheal intubation in asthmatic patients, whereas intravenous lidocaine did not.154 The use of inhalational lidocaine has been shown to worsen bronchoconstriction and does not have a role at this time in the rapid-sequence intubation of asthmatics.155,156 Consider the use of the dissociative agent ketamine for the induction agent. Ketamine indirectly stimulates catecholamine release and, in a dose of up to 2 mg/kg, will produce bronchodilation in the critically ill asthmatic.157,158 Ketamine is contraindicated in patients with ischemic heart disease, severe hypertension, preeclampsia, or increased intracranial pressure. Side effects of ketamine include hallucinations, increased secretions, and, on rare occasions, laryngospasm. Once intubation has been successfully performed, mechanical ventilation should be initiated. However,

Lidocaine And Anti-Hypertensives

Lidocaine surfaces in anecdotal reports as an agent that may succeed when conventional therapies fail.133 Despite these reports, prospective study into this choice of pharmacologic therapy is needed. Likewise, reports of improvement with calcium-channel blockers and clonidine should spur further investigation into their possible role in the acute treatment of asthma.134

TheophyllineThe Drug That Wont Die

Theophylline/aminophylline is not generally recommended therapy in the ED. The vast majority of studies show that it provides no additional benefit to short-acting inhaled -agonists and frequently causes adverse effects.135-140 In hospitalized patients, most data indicate that intravenous methylxanthines are not beneficial in children with severe asthma,141-143 and they remain controversial for adults.144,145 While the occasional study suggests some positive effect in severely ill children unresponsive to standard treatment,146 its marginal benefit and poor safety profile argue against routine use.

Therapies Not Recommended For Treating Exacerbations

Narcotics, sedatives, and tranquilizers should be avoided in an acute asthmatic because respiratory arrest may occur after their use. The combative asthmatic is more likely to need aggressive therapy or even intubation than sedation. Mucolytics, expectorants, and aggressive hydration do not aid in the treatment of asthma. A meta-analysis regarding the use of antihistamines in adult asthmatics showed that these agents increase side effects without improving pulmonary function. The literature does not generally support their use.147 While some physicians prescribe antihistamines for allergen- and exercise-induced asthma, the scientific basis for this remains thin. Nedocromil and cromolyn inhibit mast cell mediator release through the blockage of chlorine channels. Although efficacious in preventing the acute release of these pro-inflammatory cytokines, mast cell mediators play no role in the actively wheezing patient. Continuous infusions of ketamine have been occasionally used as an adjunct to treat status asthmaticus in the non-intubated patient.148 However, a randomized trial suggests ketamine infusion is not useful in this situation.149 Many alternative or complementary medicine therapies are used to treat asthma. Of note, manual therapy (performed by chiropractors, respiratory therapists, or osteopaths) is sometimes touted to improve lung function. There are no data or very poor data to suggest that any manual therapy is appropriate to treat patients with asthma.150 Likewise, no well-controlled trials support the use of other alternative therapies (acupuncture, homeopathy). Currently, these have no place in the acute or long-term treatment of asthma.151,152

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mechanical ventilation carries its own peculiar risks in the asthmatic. In the early phases of treatment, airflow obstruction results in larger tidal volumes secondary to air trapping. This produces auto-PEEP or increased residual volumes and may lead to barotrauma and possibly tension pneumothorax. Mechanical ventilation with rapid-flow rates, reduced respiratory frequency, combined with a prolonged expiratory phase, helps prevent this distressing condition. This pattern of mechanical ventilation is commonly referred to as controlled mechanical hypoventilation or permissive hypercapnia.159-162 Jain et al recommend initial ventilatory settings of a VT of 6-8 cc/kg, no extrinsic PEEP, a respiratory rate of 8-10 per minute, and an inspiratory flow of 80-100 L/min

with a square waveform.153 (See the clinical pathway Ventilatory Management Of The Asthmatic on page 16.) Once the initial ventilatory settings have been chosen, continued close monitoring of the patient is essential. According to Williams et al, the most sensitive indication of the patients ongoing risk for barotrauma or volutrauma is his end inspiratory volume, which is a measure of dynamic hyperinflation.163 Because this is difficult to measure, a practical substitute is the plateau pressure (Pplat), which reflects the pressure in the alveoli. The goal should be to keep Pplat less than 30 cmH2O; if the plateau pressure is consistently higher than this, lower the patients minute ventilation. As mentioned, this lowered minute ventilation to decrease hyperinflation often results in hypercapnia and

Ten Excuses That Dont Work In Court

1. Really, he wasnt wheezing when I discharged him. Its right there on the chart. Other things are on the chart as well. The nurse documented that the respiratory rate was 35 and the room air pulse oximetry was 90%. The patient wasnt wheezing because he still wasnt moving any air. No wheezing can be a very ominous sign in the asthmatic. Interpret a silent chest on initial evaluation or after pharmacologic interventions in the clinical context of the patientsomnolence with this physical exam finding necessitates immediate intervention, including the possibility of invasive ventilation. 2. Really, he wasnt wheezing when I first evaluated him. Ditto. 3. I thought I would let his primary doctor start him on steroids. Steroids play an integral role in the treatment of an acute asthma exacerbation, and nearly all asthmatics should be discharged with a pulse-course of oral steroids (except those with minimal symptoms who responded to a single inhalation treatment). Inhaled or intramuscular steroids remain other options. 4. He couldnt move the peak-flow meter, but I just assumed he wasnt cooperating. If the PEFR is documented, then be prepared to use the data. If a patient has a difficult time using this device, document other indicators of the patient s improvement (such as an ability to count to five or speak in full sentences). Documenting a smiling patient who states, I feel great, doc! may be as useful as a good peak flow. 5. He had just used his -agonists at home, so I thought I would wait to treat him. Let the patients presentation dictate the treatmentif he is in distress and wheezing, start therapy. No matter how much pharmacologic intervention he received at home, hes obviously in need of additional treatment or he wouldnt have come to the ED. 6. I didnt instruct him how to use the MDI because they are so simple to use. Every patient should be instructed on the proper use of the MDI and discharged with a spacer (or a prescription for a spacer) to accompany it. If the patient has the medication but cant use the delivery device properly, he is in a canoe without a paddleand possibly up some sort of creek. 7. After intubating him, I just figured a large tidal volume would open his airway. How was I supposed to know we were out of chest tubes? Intubating asthmatics is fraught with difficulty, and the emergency physician must be acutely aware of the possible complications, including high airway pressures leading to barotrauma. Consider lower tidal volumes (5-7 cc/kg) and monitor the plateau pressures. If they arrest on the ventilator, decompress the chest! 8. I reserve ipratropium for elderly COPD patients. Anticholinergics are indicated for moderate-to-severe asthma exacerbations. They are safe, effective, and offer at least some benefit to many asthmatics. 9. Of course Im sorry he died, but no one can predict who will have a fatal attack. Not quite true. The past may guide the future. Patients with a history of prior intubations or intensive care admissions are more likely to suffer fatal asthma in the future. Ask. 10. I thought a small dose of midazolam would help relax him. Make sure you arent making a patient permanently relaxed. Most asthmatics who are in distress are not breathing well. Their distress will resolve with treatment of their primary respiratory disease, not their anxiety. v

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respiratory acidosis. A PaCO2 as high as 80 mmHg, resulting in a pH of 7.15, is well within the acceptable limits for this type of ventilatory management. Indeed, multiple studies have shown minimal adverse effects from this hypoventilation and clearly improved outcomes resulting from a lower incidence of barotrauma.164-167 Few relative contraindications exist for permissive hypercapnia, but they include severe hypertension, severe metabolic acidosis, and severe hypoxemia.153 Any patient undergoing hypoventilation will require heavy sedation and at times the use of neuromuscular-

blocking agents, as this type of ventilatory management is usually poorly tolerated. Although corticosteroidtreated patients with severe asthma who undergo prolonged neuromuscular paralysis may develop protracted muscle weakness,233 this is not a concern in emergency management. Rarely, the use of buffer therapy to maintain pH is indicated; this decision should be undertaken in consultation with an intensivist and in the context of the patients comorbid medical conditions. Once a patient has been intubated and initial ventilatory management determined, -agonist therapy must be

Cost-Effective Strategies For Patients With Asthma

Strategies That Focus On ED Care
1. Increase the ED use of MDIs and spacers, as opposed to nebulizers. MDIs plus spacers are at least as effective and less expensive than nebulizer therapy. Risk-Management Caveat: These devices are less well studied in the moribund asthmatic. 2. Use oral instead of parenteral steroids. There is no convincing evidence that intravenous steroids are more effective than the less expensive oral route. In one pediatric study of severe asthma, there was no difference in length of hospital stay between asthmatic patients receiving oral prednisone and those receiving intravenous methylprednisolone.225 Risk-Management Caveat: Moribund patients as well as those who are vomiting may require intravenous steroids. Consider intramuscular steroids for non-compliant or indigent patients (see below). 3. Avoid unnecessary laboratory tests. Most asthmatics will not require bloodwork. The CBC is rarely helpful. If you suspect pneumonia, order a chest x-ray, not a CBC. Blood gases are seldom necessary. A pulse ox will detect hypoxia, and a patient with a PEFR above 25% of predicted will rarely (if ever) be hypercarbic. Risk-Management Caveat: Patients taking theophylline (especially those who are tremulous and vomiting) may be theophylline toxic and will require a blood level. 4. Avoid unnecessary x-rays. Most patients with a history of asthma who present with wheezing will not require chest film. Risk-Management Caveat: If you suspect pneumonia, foreign body, congestive heart failure, or other asthma mimics, get the film. 2. Give the patient a spacer. Only 40% of ED asthma patients own a spacer.208 Increase this number to 100% by dispensing them in the ED. Patients can even make their own spacer using a 500 mL plastic bottle. A sealed 500 mL soda bottle produces similar bronchodilation when compared to a conventional spacer in children with asthma.227 (Whether Coke or Pepsi bottles yield better PEFRs remains to be studied.) Even giving the patient a nebulizer can be cost-effective. In one study, providing home nebulizers for selected outpatients resulted in significant savings due to reduced ED and office visits.228 4. Avoid unnecessary antibiotics. Many healthy young adults with wheezing are given antibiotics for bronchitis. Most of these patients have a virus that results in reactive bronchospasm. Randomized, placebo-controlled trials do not support routine antibiotic treatment of uncomplicated acute bronchitis. However, RCTs do show that inhaled albuterol decreases the duration of cough in adults with uncomplicated acute bronchitis.229 Despite this fact, as many as 74% of patients with acute uncomplicated bronchitis are given antibiotics, while only about 17% receive bronchodilators.230 These numbers should be reversed. (Better yet, no antibiotics and 100% bronchodilators.) Risk-Management Caveat: Antibiotics are certainly indicated in asthmatics who suffer concurrent pneumonia. They also decrease the relapse rate for patients with an acute exacerbation of COPD.231

Strategies For Indigent Patients

1. Give the patient discharge medications such as an MDI and steroids. One study showed that providing medications and increasing the use of steroids decreased bounce-backs in patients with asthma.232 2. Consider the use of intramuscular steroids for noncompliant patients. Intramuscular steroids are therapeutically equivalent to a weeks therapy with oral steroids. v

Strategies That Focus On Preventing Relapse

1. Educate the patient. Patient education programs can decrease ED visits.226 This education ranges from the proper use of the MDI to developing an action plan for exacerbations.

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continued. Bronchodilators may be administered via an MDI or by nebulization. Both methods have been shown to be efficacious in the literature.168 The use of an MDI offers the advantages of ease of administration, lower cost, and ability to maintain ventilatory settings. Dhand et al documented good efficacy and safety with the use of four puffs of an albuterol MDI administered at the beginning of inspiration through an in-line spacer device.169 If a patient with severe asthma suddenly arrests while on the ventilator, quickly place bilateral chest tubes. (Okay, first auscultate the lungs, look for tracheal deviation, and evaluate the peak pressures on the ventilatorthen place bilateral chest tubes.) Tension pneumothorax is an important cause of sudden death in the intubated asthmatic. In patients with persistent and markedly elevated peak pressures, high-frequency jet ventilation may improve gas exchange.170 This, however, is rarely employed in the ED setting.

Non-Invasive Ventilation
Non-invasive ventilation (NIV) offers an attractive alternative to intubation in the patient with a severe asthma exacerbation. The trials evaluating this method of ventilatory support are small but promising; most involve bi-level positive airway pressure (BiPAP).171-173 Initial settings can begin at 8 or 10 cmH2O inspiratory positive airway pressure (IPAP), while the expiratory positive airway pressure (EPAP) can be set at 3 or 5 cmH2O. The settings are then adjusted according to clinical response. In one study, the authors suggested that for hypoxemic patients, EPAP should be raised in increments of 2 cmH2O while maintaining the IPAP at a fixed interval above EPAP (i.e., the difference between IPAP and EPAP is kept at 5 cmH2O). For hypercapnic patients, IPAP was raised in increments of 2 cmH2O with EPAP increased at a slower rate (1 cm increase in EPAP for every 2.5 cm increase in IPAP).172 -agonists given via BiPAP appear to be more effective than those administered by small-volume nebulizers.174 At this time, NIV represents a reasonable alternative to invasive ventilation for selected asthmatics.175 However, such patients must be monitored very closely, as some will ultimately require intubation. The cheeks are ruddy; eyes protuberant, as if from strangulationthey breathe standing, as if desiring to draw in all the air which they possibly can inhale. Aretaeus the Cappadocian (81-138?) on asthma176

will present to the ED one or more times for an acute exacerbation.179 Multiple factors may contribute to the change in a pregnant asthmatics disease, but the important lesson is that these patients require close monitoring and may present with worsening of their disease.177,180 Early therapy is vital to the prevention of fetal hypoxemia, and under-treatment can lead to increased perinatal mortality and prematurity, as well as low birth weight.181-184 Demissie et al also found an increased risk of preeclampsia in pregnant asthmatics as well as congenital malformations in their babies.185 The management of pregnant asthmatics is essentially the same as for non-pregnant asthmatics, but there are a few exceptions. Subcutaneous epinephrine should be avoided since it causes uterine artery constriction, whereas subcutaneous terbutaline probably does not. Inhaled -agonists and corticosteroids are considered safe in pregnancy.181-184,186,187 Ipratropium is also acceptable and is listed as category B (presumed safe) in pregnancy. Despite the data demonstrating the importance and safety of steroids in the pregnant asthmatic, Cydulka et al demonstrated that pregnant women were 30% less likely to receive this therapy when compared to their nonpregnant cohorts, despite similar symptomatology and PEFRs.178 Current guidelines can be found in the National Asthma Education and Prevention Program (NAEPP) expert panel guidelines for the treatment of acute asthma exacerbations.188

Elderly Patients
Elderly patients represent the fastest-growing segment of our population and therefore consume a relatively larger amount of the healthcare dollar. Skobeloff et al cited an asthma prevalence of 7%-10% in the elderly population.189 When hospitalized, the elderly have longer hospital stays and more are discharged to skilled facilities, rather than to home.189 Elderly patients also present a diagnostic dilemma how often do we hear, I have asthma, when the patient really means, I have emphysema? Fortunately, the acute treatment of these two disease entities is similar. Remember that elderly patients with new-onset wheezing may be in CHF. Be particularly aware of medication side effects in the elderlyfor example, steroids in the diabetic or theophylline in the patient with underlying coronary artery disease. Though the emergency physician didnt start the theophylline, consider that he or she might be treating a patient in multifocal atrial tachycardia with a theophylline level of 25 mg/dL! Likewise, consider the example of an asthmatic patient just placed on timolol for his glaucoma. Caution is the advisory in the elderly.

Special Circumstances: Pregnant Patients, The Elderly, And The Young

Pregnant Patients
Asthma affects approximately 4% of pregnant women. Of these, approximately one-third improve during pregnancy, one-third remain unchanged, and one-third become worse.177,178 Forty-two percent of pregnant asthmatics will require hospitalization, and up to 18%

Pediatric Patients
Children with asthma are treated in a similar manner to the adult: -agonists, anticholinergics, and systemic steroids. Assess fluid status and make appropriate corrections for infants and children, particularly in the
Continued on page 17

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Clinical Pathway: Management Of Patients With An Acute Asthma Exacerbation

ABCs IV/O2/Monitor* Physical exam Vital signs

Is the pa tient stable?

Is the pa tient impr oving?



Prepare for intubation Continuous 2-agonists 0.1 mg/kg/h (Class IIb) OR Subcutaneous terbutaline 10 mcg/kg (Class IIb) OR Consider subcutaneous epinephrine 0.01 mg/kg (Class IIb) PLUS Ipratropium bromide 0.5 mg >10 kg < 0.25 mg (Class IIa) Systemic corticosteroids 1-2 mg/kg (Class IIa) Magnesium 2 g IV over 5-10 minutes (Class IIb)

Inhaled 2-agonists by MDI or nebulizer (Class IIa) O2 as needed to keep saturation > 90% Multiple-dose ipratropium for moderate-to-severe attacks (Class IIb) Systemic corticosteroids* (Class IIa)


Proceed with airway management Rapid-sequence intubation (Class IIb) BiPAP (Class indeterminate)

Repeat evaluation Clinical examination May include evaluation of PEFR or FEV1 (Class IIb)

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* Patients with very mild attacks may not require IV/O2 monitoring or systemic corticosteroids.
The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II a: Acceptable and useful. Very good evidence provides support. Class II b: Acceptable and useful. Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. Emergency Medicine Practice 14 February 2001


Clinical Pathway: Management Of Patients With An Acute Asthma Exacerbation

(continued) Mild to minimal exacerbation? Asymptomatic Normal physical examination PFTs > 70% Moderate exacerbation? Moderate symptoms present PFTs 50%-80% predicted/ personal best Severe exacerbation? Symptoms at rest, retractions, accessory muscle use No improvement FEV1 or PEFR < 50% predicted/ personal best

Good response Response sustained longer than 60 minutes Physical exam normal FEV1 or PEFR > 70%

Incomplete response Mild to moderate symptoms Persistent wheezing FEV1 or PEFR > 50% and < 70%

Poor response PCO2 > 42mmHg Drowsiness or confusion FEV1 or PEFR < 50%

Reassess need for in tubation

Discharge to home 2-agonist MDIs (Class IIa) Systemic corticosteroids (Class IIa) Patient education (Class indeterminate) Early outpatient follow-up Consider inhaled steroids (Class indeterminate)

Continued ED therapy (Class indeterminate) OR Admit to clinical observation unit (Class indeterminate) OR Admit to hospital floor (Class indeterminate) 2-agonists (Class IIa) Anticholinergics (Class IIa) Systemic corticosteroids (Class IIa) Monitor FEV1 and O2 saturations (Class IIb)

Admit to hospital ICU or stepdown unit (Class indeterminate) 2-agonists hourly or continuously (Class IIb) Anticholinergic agents (Class IIa) Systemic corticosteroids (Class IIa) Oxygen Chest x-ray (Class IIb) Consider ABG (Class IIb)

The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II a: Acceptable and useful. Very good evidence provides support. Class II b: Acceptable and useful. Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.

Consider need for alternative therapies if continued deterioration or failure to improve (Class indeterminate) Magnesium 2 g IV (Class IIb) Intravenous -agonists (continuous drip) (Class indeterminate) Heliox (Class indeterminate) Inhalation anesthesia (Class indeterminate) BiPAP if not intubated (Class indeterminate)

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. February 2001 15 Emergency Medicine Practice

Discharge to home 2-agonist MDIs (Class IIa) Systemic corticosteroids (Class IIa) Patient education (Class indeterminate) Early outpatient follow-up Consider inhaled steroids (Class indeterminate)

Continue treatment for 1-3 hours (Class indeterminate) 2-agonists (Class IIa) Anticholinergics (Class IIa) Corticosteroids (Class IIa)

How is the pa tient responding?

Continue treatments OR Continuous aerosols with 2-agonists (Class IIb) Multiple-dose anticholinergics (Class IIb) Intravenous corticosteroids (Class IIa) Consider magnesium 2 g IV (Class IIb)


Yes Proceed with RSI Low tidal volumes ABG

Clinical Pathway: Ventilatory Management Of The Asthmatic

Initial ventilator settings: Mode = Assist control, FiO2 = 1.0 RR = 8-10/min, VT = 80-100 L/min PEEP = 0, sensitivity = 1.0 cmH2O (Class indeterminate)

Physiological objectives: Pplat < 30 cmH2O (Class indeterminate)

Physiological objectives achieved?


Change ventilator mode to SIMV or pressure support (Class indeterminate)



LEGEND FiO2 = fraction of inspired oxygen VT = tidal volume RR = respiratory rate PEEP = positive end-expiratory pressure Pplat = plateau airway pressure SIMV = synchronized intermittent mandatory ventilation NMB = neuromuscular blockade Adapted from Figure 4 in: Jain S, Hanania NA, Guntupalli KK. Ventilation of patients with asthma and obstructive lung disease. Crit Care Clin 1998;14:685-705. The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II a: Acceptable and useful. Very good evidence provides support. Class II b: Acceptable and useful. Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. Emergency Medicine Practice 16 February 2001

Continue aggressive medical therapy (Class IIa)

Consider buffer therapy (Class indeterminate)

Measure pH (Class indeterminate) pH 7.15?


Reduce minute ventilation (may require heavy sedation/NMB) (Class indeterminate)

Physiological objective achieved?


Unconventional therapies Heliox, anesthetic agents (Class indeterminate)


Continued from page 13

face of notable tachypnea. Since they may be less dexterous than adults, be sure to prescribe a spacer or valved holding chamber for use with MDIs. Smaller children and infants will need a spacer with a mask. These devices are a necessity for children, as well as most adults. There are versions with holding chambers (with or without face masks) for both infants and older children alike. Even in very young children with acute wheezing, RCTs show that the MDI plus spacer is at least as effective as a nebulizer.80,190 In the child with asthma, consider inhaled steroids. In one RCT, children who received 1.5 mg/kg of nebulized dexamethasone in the ED had fewer short-term relapses than children treated with 2 mg/kg of oral prednisone.191 Though a concern about the long-term growth effects of inhaled steroids exists, their efficacy usually outweighs the potential risk. In fact, poorly

controlled asthma may result in poor growth.192,193 The majority of studies evaluating the use of inhaled beclomethasone (at dosages of 400-800 mcg/d) revealed no negative effect on growth,194-196 although several shortterm studies did demonstrate a dose-related phenomenon.197,198 At this time, the use of inhaled steroids is not only safe, but considered usual care.

As in adults, chest radiographs rarely influence the management of children with a history of asthma and should not be routine.199 Overall, fewer than 14% of films show significant findings (such as infiltrates, atelectasis, pneumothorax, or pneumomediastinum).200 When a wheezing child presents to the ED, a trial of inhaled agonists is appropriate before any imaging studies. Children who improve during ED observation rarely need a chest film.

Tool 1. Sample Discharge Instructions For The Patient With Asthma. Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. Asthma is a chronic disease of the breathing passages that affects about one in 10 peopleit is not an infection, and it cannot be cured. People of all ages and backgrounds can have asthma. There are more than 15 million Americans with asthmaincluding almost 5 million childrenand their numbers are increasing. Asthma can be well controlled with appropriate therapy. When you have an asthma attack, your airways become small in response to some form of irritation, or trigger, making breathing difficult. Asthma attacks can be mild or life-threatening. Common asthma triggers include pollen, molds, animal dander, dust mites, smoke, strong odors or fumes, respiratory infections, cold air, and sometimes exercise. By knowing what your triggers are, you may be able to reduce your daily risk of having an asthma attack.

What Are The Symptoms Of Asthma?

The main symptoms of asthma are shortness of breath, wheezing, tightness in the chest, and prolonged cough (greater than one week). Although wheezing is a hallmark of asthma, not all people with asthma wheeze. For some, coughing may be the only symptom of asthma. Coughing often occurs during the night or after exercise.

There are two basic categories of asthma medications. Long-term control medications are taken regularly (often every day) to prevent or reduce inflammation in the airways. Using these medications makes the asthma sufferer less likely to have an asthma attack. Quick-relief or rescue medications are designed to open the airways rapidly and are taken when symptoms of an asthma attack are first noticed. You can help prevent asthma attacks by taking the following steps: Take your asthma medication(s) exactly as directed by your doctor. Use a peak-flow meterto monitor your breathingas often as instructed by your doctor. Keep track of your condition and learn to recognize when your asthma symptoms are worsening. Know how to respond when an asthma attack is beginning. A severe asthma attack is a medical emergency. Untreated, it can be fatal. Asthma episodes rarely occur without warning. Most people with asthma have warming signs (physical changes) that occur hours before symptoms appear. Warning signs are not the same for everyone. You may have different signs at different times. By knowing your warning signs and acting on them, you may be able to avoid a serious episode of asthma. February 2001 17 Emergency Medicine Practice

However, there is considerable controversy regarding the need for routine chest radiography in children who present with a first-time episode of wheezing. Some authors suggest chest films for all children who have no prior history of bronchospasm in order to identify important mimics such as foreign body, pneumonia, CHF, or other cardiopulmonary disease. In one study of firsttime wheezing in children, the authors stated that they were unable to identify any individual or combination of clinical factors that could accurately predict a positive chest film. They suggested routine use of chest radiography for the initial episode of childhood bronchospasm.201 In contrast, another group found several clinical characteristics among children with first-time wheezing that were associated with a positive chest x-ray. These included elevated temperature (37.9C vs 37.5C; P = 0.04), absence of family history of asthma (72.6% vs 27.4%; P < 0.01), and the presence of localized wheezes (76.0% vs 24.0%; P = 0.02) or localized rales (76.0% vs 24.0%; P < 0.01).202 Chest x-rays may be worthwhile in asthmatic children with fever or those with persistent rales and rhonchi. The following are indications for chest x-rays in children with wheezing and a history of reactive airway disease:203 Toxicity Significant respiratory distress Persistent rales and rhonchi Fever with no obvious viral source Poor response to ED treatment Suspicion of pneumothorax, pneumonia, foreign

body, or heart failure

Numerous guidelines exist to help the emergency physician form an educated decision with regards to patient disposition. (See also the bottom part of the clinical pathway Management Of Patients With An Acute Asthma Exacerbation, which starts on page 14.) Response assessment should be based on subjective improvement of wheezing, air exchange, and dyspnea; objective criteria such as improvement in FEV1 or PEFR; and the patients risk for relapse and poor outcomes, in part predicted by his or her past history. Complete resolution of symptoms and a PEFR or FEV1 greater than 70% predicted signifies a good response to treatment.204 When determining improvement, one group suggests that a 12% (of predicted) improvement in PEFR and a 2 cm improvement on a 10 cm dyspnea visual analog scale may represent the minimum clinically significant response.205 Individuals who demonstrate significant improvement, as well as those with minimal symptoms, may be safely discharged home. An five- to 10-day course of oral corticosteroids and a 10-day regimen of intense -agonist therapy remain the mainstay of outpatient therapy. This seems to be true despite conflicting data on relapse rates of discharged patients.60 Even with the most aggressive of therapies, some asthmatics may fail to respond. Poor response to treat-

Tool 2. Your MDI: Guidelines To Proper Use. Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. The guidelines that follow will help you use the inhaler the right way. Ask your doctor or nurse to show you how to use the inhaler.

Using The Inhaler

1. Remove the cap and hold the inhaler upright. 2. Shake the inhaler; attach the inhaler to your spacer. 3. Tilt your head back slightly and breathe out. 4. Place your lips around the spacer. 5. Press down on the inhaler to release the medicine as you start to breathe in slowly. 6. Breathe in slowly for 3-5 seconds. 7. Hold your breath for 10 seconds to allow the medicine to reach deeply into your lungs. 8. Repeat puffs as prescribed. Waiting one minute between puffs may permit the second puff to go deeper into the lungs. Note: Dry powder capsules are used differently. To use a dry powder inhaler, close your mouth tightly around the mouthpiece and inhale very quickly.
Adapted with permission from: National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97-4051. Bethesda, MD, 1997: Figure 4-3.

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ment is defined as an FEV1 or PEFR of less than 50% predicted and persistent wheezing. Hospital admission or continued observation and ongoing aggressive therapy are warranted for these patients. An incomplete response or an FEV1 or PEFR that lingers between 50% and 70% predicted presents a clinical problem for even the most experienced emer-

gency physician. Consideration of concomitant risk factors (see Table 2 on page 20), as well as patient input, should help guide disposition.206 For all patients with an acute asthma exacerbation who are discharged from the ED, close follow-up is key. Encourage them to see or call their physician within several days of their ED visit.

Tool 3. Asthma Action Plan. Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. It is important to keep track of your symptoms, medications, and peak expiratory flow rates (PEFRs) in order to best treat your asthma. The relative severity of your asthma can be divided into three zonesgreen, yellow, and red. At any time, call your doctor if your symptoms worsen while on oral steroids, your inhaled bronchodilator medication is not lasting four hours, or your peak flow number remains or falls below ______ in spite of following the plan!

Green Zone: GO!

1. PEFR is _____________ (80%-100% of your personal best). 2. Breathing is good with no cough, wheeze, or chest tightness during work, school, exercise, or play. ACTION: Continue the medications prescribed in your daily plan.

Yellow Zone: CAUTION!

1. PEFR is _____________ (50%-79% of your personal best). 2. Asthma symptoms are present, including cough, wheeze, or chest tightness. 3. You have increased need for your quick-relief medications, you have increased asthma symptoms when you wake, or you are waking at night with symptoms. ACTIONS: Take ______ puffs of your quick-relief (bronchodilator) medication _____________ Repeat ______ times. Take ______ puffs of _____________ (anti-inflammatory) _____________ times per day. Begin or increase treatment with oral steroids. Take ______ mg of _____________ every a.m. ______ p.m. ______ Call your doctor (phone) _____________

Red Zone: DANGER!

1. PEFR is _____________ (< 50% of your personal best). 2. You continue to get worse despite treatments started in the yellow zone. ACTIONS: Take ______ puffs of your quick-relief (bronchodilator) medicine _____________ Repeat ______ times. Begin/increase treatment with oral steroids: Take ______ mg now. Call your doctor (phone) _____________ now. If you cannot contact your doctor, go directly to the emergency department.
Adapted with permission from: National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97-4051. Bethesda, MD, 1997: Figure 4-3.

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Discharge Medications
Patients will need to obtain medications that will prevent a relapse. Providing indigent patients with medications may avoid an ED bounce-back. The best outpatient strategy for administering -agonists is unclear. Many physicians prescribe -agonists every 4-6 hours. However, some studies show that PRN use (on-demand inhalation) of shortacting 2-agonists in moderate-to-severe asthma is safe and effective. In severe asthma, a reduction from regular to ondemand 2-agonist inhalation can even improve asthma control.207 Make sure that the patient either has or can get a spacer. Only 40% of ED asthma patients own a spacer.208 Increase this number to 100% by dispensing them in the ED. Give corticosteroids. Corticosteroids have multiple positive effects in the patient treated in the ED for acute asthma. They decrease the need for -agonists and reduce both the relapse rate and need for subsequent hospitalization in the ensuing 7-10 days.103 When giving oral steroids, there is no evidence that a taper is necessary.209 Prescribe prednisone (30-50 mg/d) for anywhere from five to 10 days and stop them without a taper.

followed are successfully treated and discharged.213,214 Choosing which patients to place in an observation unit is an inexact science. Fortunately, the literature supplies some guidance. In one study, the change in peak flow in response to treatment provided clues to the need for admission or further observation. In this trial, patients with 40% or higher PEFR after the third treatment had an 89% probability of reaching 50% predicted in 12 hours and were thus good candidates for an observation unit. Those with a third-treatment PEFR lower than 32% predicted had only a 22% probability of reaching 50% predicted in 12 hours and were more likely to ultimately require admission.215

Asthma education in the ED may decrease future emergency visits. One successful education program included topics such as prevention of asthma, decreasing inflammation as a means of improving asthma control (stressing inhaled corticosteroids), self-monitoring with a peak flow meter, and demonstrating the correct inhalation technique with metered-dose inhalers and a spacer device.216 In another study, ED asthma education using a nurse educator led to reduced symptoms, improved lung function, less time off work, and fewer consultations with health professionals.217 Despite some evidence that self-management programs with a written action plan reduce hospitalizations,218 only 28% of the adult patients hospitalized for asthma had written action plans that defined how to manage their asthma and control an exacerbation.219 Furthermore, Emond et al recently surveyed 77 emergency departments to assess the presence of formal asthma education programs. Only 16% of the sites had asthma education programs, and the majority of those were at pediatric facilities.220 This is an arena in which emergency physicians could play a greater role. Simple handouts including an Asthma Action Plan (see the sample on page 19) should be dispensed at discharge or at admission. Patients should be taught to monitor their peak flows: A drop in peak flow below 80% of personal best indicates need for added medications, while a drop below 50% indicates a severe exacerbation. In addition, provide handouts with written information about the symptoms and treatment of asthma, as well as instructions on the use of an MDI. (See Tool 1: Sample Discharge Instructions For The Patient With Asthma on page 17 and Tool 2: Your MDI: Guidelines To Proper Use on page 18.) This last strategy of proper MDI use is deceptively simple yet profoundly important. Only about 20% of asthmatics use their MDI correctly.221 The physician or respiratory therapist should critically observe the patients technique before discharge. Many asthmatics casually use their inhaler as if it were a breath freshener.

Peak-Flow Meters And Pulmonologists

In one large study, prescribing peak-flow meters and giving self-management guidelines to all asthma patients did not improve mortality or morbidity.210 This study, however, did not focus on ED patients with asthma. Patients whose asthma is severe may benefit from these interventions. Emergency physicians often act as the gatekeepers for referral to specialized carepatients may come to us just to get a referral. Studies show that physicians differ widely in their opinions as to which patients need specialty consultation.211,212 Some physicians consider suggesting a pulmonologist for patients with more than two bursts of oral steroids in one year, patients younger than 3 years of age, or patients with multiple ED visits for acute exacerbations. Again, while this recommendation seems reasonable, there is little to no evidence to show that it improves outcomes.

Observation Units
Observation units are an option for incomplete responders. Recent studies indicate that as many as 59% of asthmatics admitted to observation units where strict care protocols are

Table 2. Risk Factors For Asthma.

Prior intubation Prior intensive care unit hospitalization Chronic glucocorticoid use Comorbidity Two or more hospitalizations in the past year Recent ED care Psychosocial problems Poor compliance Poor follow-up
Adapted from Table 4 in: Brenner B, Kohn MS. The acute asthmatic patient in the ED: To admit or discharge. Am J Emerg Med 1998;16:69-75.

Ask the parents of wheezing children if they or anyone else smokes inside the house. Cigarette smoke in the home is an important modifiable risk factor in reactive airway disease among children.222,223 People who will not

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stop smoking despite their own respiratory agonies may at least smoke outside in deference to their children.

Numerous myths and pitfalls of asthma management are perpetuated despite modern medicine. Withholding agonist therapy in the ED because of recent use at home is unwarranted, has no scientific basis, and is extremely dangerous. Likewise, failing to start corticosteroids, lack of effort toward patient education, and failure to arrange prompt outpatient follow-up are also concerning. (For suggestions on how to avoid these pitfalls, see the Ten Excuses That Dont Work In Court on page 11.) No established treatment regimen is completely efficacious. Numerous drugs and drug combinations can be used in the acute asthmatic to achieve optimal and maximum bronchodilatory effect. Treatment should begin with inhaled -agonists and, if the patient is hypoxic, oxygen as well. Additional therapy may include anticholinergic agents and corticosteroids. Objective measures of treatment responsiveness, such as pulmonary function tests, vital signs, chest and heart exams, as well as the patients subjective assessment of dyspnea, may guide ED intervention. On discharge, all patients requiring systemic steroids in the ED should be prescribed steroid therapy equivalent to oral prednisone 40-60 mg in a non-tapering burst.224 The steroids may be given by mouth, by inhalation, or by injection. The best duration of therapy remains unclear; recommendations range from five to 10 days. Long-acting intramuscular steroids offer the advantage of foregoing outpatient oral steroids, thereby ensuring full patient compliance. v


6. 7.






13. 14. 15.

16. 17.



Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.
1. Mannino DM, Homa DM, Pertowski CA, et al. Surveillance for asthmaUnited States, 1960-1995. MMWR Morb Mortal Wkly Rep 1998;47:1-28. (Retrospective) Centers for Disease Control and Prevention. Asthma mortality and hospitalization among children and young adults United States, 1980-93. MMWR Morb Mortal Wkly Rep 1966;45:5053. (Retrospective) Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Lancet 1998;351:1225-1232. (Review) Centers for Disease Control and Prevention. Forecasted











state-specific estimates of self-reported asthma prevalence United States, 1998. MMWR Morb Mortal Wkly Rep 1998;47:10221025. (Retrospective) Cydulka RK, McFadden ER, Emerman CL, et al. Patterns of hospitalization in elderly patients with asthma and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997;156:1807-1812. (Retrospective; 124,450 patients) McFadden ER, Gilbert IA. Asthma. N Engl J Med 1992;327: 1928. (Commentary) Pappas G, Hadden WC, Kozak LJ, et al. Potentially avoidable hospitalizations: inequalities in rates between US socioeconomic groups. Am J Public Health 1997;87:811-816. (Retrospective; 192,734 hospitalizations) Weiss KB, Gergen PG, Hodgson TA. An economic evaluation of asthma in the United States. N Engl J Med 1992;326: 862-866. (Retrospective) Fabbri LM, Caramori G, Beghe B, et al. Physiologic consequences of long-term inflammation. Am J Respir Crit Care Med 1998;157:S195-S198. (Review) Lange P, Parner J, Vestbo J, et al. A 15-year follow-up study of ventilatory function in adults with asthma. N Engl J Med 1998;339:1194-1200. (Retrospective; 17,506 patients) Centers for Disease Control and Prevention. Surveillance for asthmaUnited States, 1960-1995. MMWR Morb Mortal Wkly Rep 1998;47(no SS-1):1-28. (Retrospective) Weiss KB, Gergen PJ, Wagener DK. Breathing better or wheezing worse? The changing epidemiology of asthma morbidity and mortality. Ann Rev Public Health 1993:14:491-513. (Review) Barbee RA, Dodge R, Lebowitz MI, et al. The epidemiology of asthma. Chest 1985; 87(suppl):21S-25S. (Review) McDowell KM. Pathophysiology of asthma. Respir Care Clin North Am 2000;6:15-26. (Review) Burt CW, Knapp DE. Ambulatory care visits for asthma: United States, 1993-94. Advance Data. Centers for Disease Control and Prevention, National Center for Health Statistics. 1996;277:1-19. (Retrospective) Crim C. Clinical practice guidelines vs actual clinical practice: the asthma paradigm. Chest 2000;118(2 Suppl):62S-64S. (Review) Milks CJ, Oppenheimer JJ, Bielory L. Comparison of emergency room asthma care to national guidelines. Ann Allergy Asthma Immunol 1999;83(3):208-211. (Comparative; 1858 records) Worrall G, Chaulk P, Freake D. The effects of clinical practice guidelines on patient outcomes in primary care: a systematic review [see comments]. CMAJ 1997;156(12):1705-1712. (Evaluation; 91 trials) Grant EN, Li T, Lyttle CS, et al. Characteristics of asthma care provided by hospitals in a large metropolitan area: results from the Chicago Asthma Surveillance Initiative. Chest 1999;116(4 Suppl 1):162S-167S. (Survey; 59 respondents) Emond SD, Woodruff PG, Lee EY, et al. Effect of an emergency department asthma program on acute asthma care [see comments]. Ann Emerg Med 1999;34(3):321-325. (Retrospective; 196 patients) Goldberg R, Chan L, Haley P, et al. Critical pathway for the emergency department management of acute asthma: effect on resource utilization. Ann Emerg Med 1998;31(5):562-567. (Prospective, 149 patients; Retrospective, 97 patients) Jadad AR, Moher M, Browman GP, et al. Systematic reviews and meta-analyses on treatment of asthma: critical evaluation [published erratum appears in BMJ 2000;320(7240):984]. BMJ 2000;320(7234):537-540. (Meta-analysis) Zehner WJ Jr, Scott JM, Iannolo PM, et al. Terbutaline vs. albuterol for out-of-hospital respiratory distress: randomized, double-blind trial. Acad Emerg Med 1995;2(8):686-691. (Randomized, controlled trial; 83 patients) Stead L, Whiteside T. Evaluation of a new EMS asthma protocol in New York City: a preliminary report. Prehosp Emerg Care 1999;3(4):338-342. (Retrospective; 219 patients) Woodruff PG, Emond SD, Singh AK, et al. Sudden-onset severe acute asthma: clinical features and response to therapy. Acad Emerg Med 1998;5(7):695-701. (Retrospective; 225 patients) Hardie GE, Janson S, Gold WM, et al. Ethnic differences: word descriptors used by African-American and white asthma patients during induced bronchoconstriction [see comments]. Chest

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29. 30.



33. 34.

35. 36.

37. 38.




42. 43.



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151. Linde K, Jobst KA. Homeopathy for chronic asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 152. Linde K, Jobst K, Panton J. Acupuncture for chronic asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 153. Jain S, Hanania NA, Guntupalli KK. Ventilation of patients with asthma and obstructive lung disease. Crit Care Clin 1998;14:685705. (Review) 154. Maslow AD, Regan MM, Israel E, et al. Inhaled albuterol, but not intravenous lidocaine, protects against intubation-induced bronchoconstriction in asthma. Anesthesiology 2000;93(5):11981204. (Randomized, controlled; 60 patients) 155. McAlpine LG, Thomson NC. Lidocaine-induced bronchoconstriction in asthmatic patients. Chest 1989; 96:10121015. (Prospective; 20 patients) 156. Miller WC, Awe R. Effect of nebulized lidocaine on reactive airways. Am Rev Respir Dis 1975;111:739-741. (Prospective; 14 patients) 157. LHommedieu CSA, Arens JJ. The use of ketamine for the emergency intubation of patients with status asthmaticus. Ann Emerg Med 1987;16:568-571. (Retrospective; 5 patients) 158. Sarma V. Ketamine and asthma. Acta Scand 1992;36:15071510. (Review) 159. Pepe PE, Marini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Resp Dis 1982;126:166-170. (Review) 160. Leatherman JW. Mechanical ventilation in obstructive lung disease. Clin Chest Med 1996;17:577-590. (Review) 161. Werner C. Ventilatory management of respiratory failure in asthma. JAMA 1993;269:2128-2131. (Review) 162. Tuxen DV. Permissive hyercapnic ventilation. Am J Respir Crit Care Med 1994;150:870-874. (Review) 163. Williams TJ, Tuxen DV, Scheinkestel CD, et al. Risk factors for morbidity in mechanically ventilated patients with acute severe asthma. Am Rev Respir Dis 1992;146:607. (Retrospective; 88 ICU admissions) 164. Darioli R, Perret C. Mechanical controlled hypoventilation in status asthmaticus. Am Rev Respir Dis 1984;129:385. (Retrospective; 159 admissions) 165. Feihl F, Perret C. Permissive hypercapnia: How permissive should we be? Am J Respir Crit Care Med 1994;150:1722. (Review) 166. Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med 1990;16:372. (Evaluation; 50 patients) 167. Hickling KG, Walsh J, Henderson S, et al. Low volume ventilation in adult respiratory distress syndrome using low volume, pressure limited ventilation with permissive hypercapnia: A prospective study. Crit Care Med 1994;22:1568. (Prospective; 53 patients) 168. Dhand R, Tobin MJ. Inhaled bronchodilator therapy in mechanically ventilated patients. Am J Respir Crit Care Med 1997;156:3. (Review) 169. Dhand R, Duarte AG, Jubran A, et al. Dose-response to bronchodilator delivered by metered-dose inhaler in ventilator-supported patients. Am J Respir Crit Care Med 1996;154:388. (Comparative; 12 patients) 170. Goto E, Okamoto I, Tanaka K. The clinical characteristics at the onset of a severe asthma attack and the effects of high frequency jet ventilation for severe asthmatic patients. Eur J Emerg Med 1998;5(4):451-455. (Retrospective; 37 patients) 171. Meduri GU, Cook TR, Turner RE, et al. Noninvasive positive pressure ventilation in status asthmaticus. Chest 1996;110:767-774. (Prospective; 26 patients) 172. Pollack CV, Torres, MT, Alexander L. Feasibility study of the use of bilevel positive airway pressure for respiratory support in the emergency department. Ann Emerg Med 1996;151:1799-1806. (Prospective) 173. Patrick W, Webster K, Ludwig L, et al. Noninvasive positivepressure ventilation in acute respiratory distress without prior chronic respiratory failure. Am J Respir Crit Care Med

1996;153:1005-1011. (Prospective; 11 patients) 174. Pollack CV Jr, Fleisch KB, Dowsey K. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995;26(5):552-557. (Randomized, controlled; 100 patients) 175. Hotchkiss JR, Marini JJ. Noninvasive ventilation: An emerging supportive technique for the emergency department. Ann Emerg Med 1998;32:470-479. (Review) 176. Huth EJ, Murray TJ, eds. Medicine in Quotations. Philadelphia; American College of Physicians: 2000. (Textbook) 177. Schatz M. Interrelationships between asthma and pregnancy: A literature review. J Allergy Clin Immunol 1999;103:S330S336. (Review) 178.* Cydulka RK, Emerman CL, Schreiber D, et al. Acute asthma among pregnant women presenting to the emergency department. Am J Respir Crit Care Med 1999;160:887-892. (Prospective, cohort; 551 patients) 179. Schatz M, et al. Asthma and allergy in pregnancy. Clin Perinatol 1997;24:407-432. (Review) 180. Schatz M. Asthma and pregnancy. Lancet 1999;353:12021204. (Commentary) 181. Nelson HS, Weber RW. Endocrine aspects of allergic diseases. In: Bierman CW, Pearlman DS, eds. Allergic Diseases from Infancy to Adulthood. Philadelphia: WB Saunders; 1988. (Textbook) 182.* Schatz M, Zeiger RS, Harden KM, et al. The safety of inhaled betaagonist bronchodilators during pregnancy. J Allergy Clin Immunol 1988;82:686-695. (Prospective, observational; 655 patients) 183. Federal Register. 21 CFR Parts 201, 202. 1979;44:37434-37467. 184. Briggs GG, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation: A Reference Guide to Fetal and Neonatal Risk, 2nd ed. Baltimore: Williams & Wilkins; 1986. (Textbook) 185. Demissie K, Breckenridge MB, Rhoads GG. Infant and maternal outcomes in the pregnancies of asthmatic women. Am J Respir Crit Care Med 1998;158:1091-1095. (Retrospective; 11,445 patients) 186. Schatz M, Zeiger RS, Harden K, et al. The safety of asthma and allergy medications during pregnancy. J Allergy Clin Immunol 1997;100:301-306. (Prospective; 1502 patients) 187. Stenius-Aarnial BSM, Hedman J, Teramo KA. Acute asthma during pregnancy. Thorax 1996;51:411-414. (Prospective; 504 patients) 188. National Asthma Education and Prevention Program Expert Panel 2: Report of the working group on asthma and pregnancy. Management of asthma during pregnancy. National Institute of Health publication no 93-3279, Bethesda, MD: National Institutes of Health; 1993. (Expert guidelines) 189. Skobeloff EM, Spivey WH, St. Clair SS, et al. The influence of age and sex on asthma admissions. JAMA 1992;268:3437-3440. (Retrospective; 33,269 patients) 190. Mandelberg A, Tsehori S, Houri S, et al. Is nebulized aerosol treatment necessary in the pediatric emergency department? [see comments]. Chest 2000;117(5):1309-1313. (Randomized, controlled; 42 children) 191. Scarfone RJ, Loiselle JM, Wiley JF, et al. Nebulized dexamethasone versus oral prednisone in the emergency treatment of asthmatic children. Ann Emerg Med 1995;26(4):480-486. (Randomized, controlled; 111 children) 192. Spock A. Growth patterns in 200 children with bronchial asthma. Ann Allergy 1965;23:608-615. (Comparative; 200 patients) 193. Ninan TK, Russel G. Asthma, inhaled corticosteroid treatment and growth. Arch Dis Chil 1992;67:703-705. (Review) 194. Wolthers OD. Long-, intermediate- and short-term growth studies in asthmatic children treated with inhaled glucosteroids. Eur Respir J 1996;9:821-827. (Review) 195. Kamada AK, Szefler SJ, Martin RJ, et al, and the Asthma Clinical Research Network. Issues in the use of inhaled glucocorticoids. Am J Respir Crit Care Med 1996;153:1739-1748. (Review) 196. Barnes PJ, Pedersen S. Efficacy and safety of inhaled steroids in asthma. Am Rev Respir Dis 1993;148:S1-S26. (Review) 197. Tinkelman DG, Reed CE, Nelson HS, et al. Aerosol beclomethasone dipropionate compared with theophylline as primary treatment of chronic, mild to moderately severe asthma in children. Pediatrics 1993;92:64-77. (Prospective, blinded; 195 patients) 198. Doull IJM, Freezer NJ, Holgate ST. Growth of pre-pubertal

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children with mild asthma treated with inhaled beclomethasone dipropionate. Am J Respir Crit Care Med 1995;151:1715-1719. (Prospective; 94 patients) 199. Brooks LJ, Cloutier MM, Afshani E. Significance of roentgenographic abnormalities in children hospitalized for asthma. Chest 1982;82:31-35. (Retrospective; 128 patients) 200. Zieverink SE, Harper AP, Holden RW, et al. Emergency room radiography of asthma: an efficacy study. Radiology 1982;145:27. (Retrospective; 997 patients) 201. Walsh-Kelly CM, Kim MK, Hennes HM. Chest radiography in the initial episode of bronchospasm in children: can clinical variables predict pathologic findings? Ann Emerg Med 1996;28(4):391-395. (Prospective; 633 patients) 202. Roback MG, Dreitlein DA. Chest radiograph in the evaluation of first time wheezing episodes: review of current clinical practice and efficacy [see comments]. Pediatr Emerg Care 1998;14(3):181-184. (Retrospective; 198 patients) 203. Colucciello SA. In: Cantrill SV, Karas S, eds. Cost-Effective Diagnostic Testing in Emergency Medicine: Guidelines for Appropriate Utilization of Clinical Laboratory and Radiology Studies. Dallas: American College of Emergency Physicians; 2000:135-141. (Textbook) 204. National Institutes of Health. Global strategy for asthma management and prevention NHLBI/WHO Workshop report. Bethesda, MD: National Heart, Lung, and Blood Institute; 1995, NIH Publication No. 95-3659. (Expert guidelines) 205. Karras DJ, Sammon ME, Terregino CA, et al. Clinically meaningful changes in quantitative measures of asthma severity. Acad Emerg Med 2000;7(4):327-334. (Prospective; 156 patients) 206. Brenner BE, Powell KA. The acute asthmatic in the emergency department. To admit or discharge? In: Brenner BE, ed. Emergency Asthma. New York: 1999:489-504. (Textbook) 207. Richter B, Bender R, Berger M. Effects of on-demand beta 2agonist inhalation in moderate-to-severe asthma. A randomized controlled trial. J Intern Med 2000;247(6):657. (Randomized, controlled; 80 patients) 208. Emond SD, Reed CR, Graff LG IV, et al. Asthma education in the emergency department. On behalf of the MARC Investigators. Ann Emerg Med 2000;36(3):204-211. (Survey; 77 participants) 209. ODriscoll BR, Kalra S, Wilson M, et al. Double-blind trial of steroid tapering in acute asthma. Lancet 1993;341:324-327. (Randomized, double-blind; 35 patients) 210. Grampian Asthma Study of Integrated Care (GRASIC). Effectiveness of routine self monitoring of peak flow in patients with asthma. BMJ 1994;308:564-567. (Randomized, controlled) 211. Li JT, Sheeler RD, Offord KP, et al. Consultation for asthma: results of a generalist survey [see comments]. Ann Allergy Asthma Immunol 1999;83(3):203-206. (Questionnaire; 37 participants) 212. Kljakovic M, Salmond C. The pattern of consultations for asthma in a general practice over 5 years. N Z Med J 1996;109(1016):48-50. (Retrospective; 1173 patients) 213.* Brillman JC, Tandberg D. Observation unit impact on ED admission for asthma. Am J Emerg Med 1994;12:11-14. (Prospective, observational; 1224 patients) 214. Rydman RJ, Isola ML, Roberts RR, et al. Emergency department observation unit versus hospital inpatient care for a chronic asthmatic population: a randomized trial of health status outcome and cost. Med Care 1998;36:599-609. (Prospective; 113 patients) 215. McCarren M, Zalenski RJ, McDermott M, et al. Predicting recovery from acute asthma in an emergency diagnostic and treatment unit. Acad Emerg Med 2000;7(1):28-35. (Cohort; 269 patients) 216. Kelso TM, Self TH, Rumbak MJ, et al. Educational and long-term therapeutic intervention in the ED: effect on outcomes in adult indigent minority asthmatics. Am J Emerg Med 1995;13(6):632-637. (30 patients) 217. Levy ML, Robb M, Allen J, et al. A randomized controlled evaluation of specialist nurse education following accident and emergency department attendance for acute asthma. Respir Med 2000;94(9):900-908. (Randomized, controlled; 211 patients) 218. Gibson PG, Coughlan J, Wilson AJ, et al. Self-management education and regular practitioner review for adults with asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update

Software. (Systematic review) 219. Hartert TV, Windom HH, Peebles RS Jr, et al. Inadequate outpatient medical therapy for patients with asthma admitted to two urban hospitals. Am J Med 1996;100:386-394. (Cross-sectional survey; 101 patients) 220. Emond, SD, Reed CR, Graff LG. Asthma education in the emergency department. Ann Emerg Med 2000;36:204-211. (Survey) 221. Shrestha M, Parupia H, Andrews B, et al. Metered-dose inhaler technique of patients in an urban ED: prevalence of incorrect technique and attempt at education. Am J Emerg Med 1996;14(4):380-384. (Observational; 125 patients) 222. Ehrlich RI, Du Toit D, Jordaan E, et al. Risk factors for childhood asthma and wheezing. Importance of maternal and household smoking. Am J Respir Crit Care Med 1996;154(3 Pt 1):681-688. (Questionnaire; 368 cases, 294 controls) 223. Siroux V, Pin I, Oryszczyn MP, et al. Relationships of active smoking to asthma and asthma severity in the EGEA study. Epidemiological study on the Genetics and Environment of Asthma. Eur Respir J 2000;15(3):470-477. (Case-control; 1051 patients) 224. Cydulka RK, Emerman CL. A pilot study of steroid therapy in the prevention of early relapse after emergency department treatment of acute asthma: Is a taper needed? J Emerg Med 1998;16:15-19. (Prospective, blinded; 15 patients) 225. Becker JM, Arora A, Scarfone RJ, et al. Oral versus intravenous corticosteroids in children hospitalized with asthma. J Allergy Clin Immunol 1999;103(4):586-590. (Randomized, controlled; 66 patients) 226. Gibson PG, Coughlan J, Wilson J, et al. The effects of limited (information only) patient education programs on the health outcomes of adults with asthma (Cochrane Review). In: The Cochrane Library, Cochrane Database of Systematic Reviews, Issue 4, 1998. Oxford: Update Software. (Systematic review) 227. Zar HJ, Brown G, Donson H, et al. Home-made spacers for bronchodilator therapy in children with acute asthma: a randomized trial [see comments]. Lancet 1999;354(9183):979-982. (Randomized, controlled; 88 patients) 228. Yamamoto LG, Okamura D, Nagamine J, et al. Dispensing home nebulizers for acute wheezing from the hospital is cost-effective. Am J Emerg Med 2000;18(2):164-167. (232 patients) 229. Gonzales R, Sande MA, Gillock MR, et al. Uncomplicated acute bronchitis. Ann Intern Med 2000;133(12):981-991. (Review) 230. Gonzales R, Steiner JF, Lum A, et al. Decreasing antibiotic use in ambulatory practice: impact of a multidimensional intervention on the treatment of uncomplicated acute bronchitis in adults. JAMA 1999;281(16):1512-1519. (Prospective; 2027 patients) 231. Adams SG, Melo J, Luther M, et al. Antibiotics are associated with lower relapse rates in outpatients with acute exacerbations of COPD. Chest 2000;117(5):1345-1352. (Retrospective; 362 patient visits) 232. Low RB, Bielory L, Tejani N, et al. Bounce back asthma visits: the effect of ED medication management and airborne irritants. Acad Emerg Med 2000;7:468. 233. Leatherman JW, Fluegel WL, David WS, et al. Muscle weakness in mechanically ventilated patients with severe asthma. Am J Respir Crit Care Med 1996;153(5):1686-1690.

Physician CME Questions

17. Despite your best efforts, a patient suffering an acute asthma attack becomes more anxious and progresses to respiratory failure. Your next step in management includes: a. morphine to ease patient anxiety. b. a benzodiazepine to calm and relax this patient. c ketamine followed by rapid-sequence intubation. d. blind nasotracheal intubation. e. inserting a nasogastric tube to prevent gastric distension.

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18. Increased airway resistance in an acute asthma attack is produced by: a. constriction of airway smooth muscle. b. mucus secretion. c. inflammatory changes in the bronchioles. d. all of the above. 19. A patient has a rapid onset of wheezing and difficulty breathing after she enters a dust-filled room and presents to the ED in moderate distress. Which medication has no role in her management at this time? a. Terbutaline b. Epinephrine c. Methylprednisolone d. Cromolyn sodium e. Albuterol 20. All of the following are appropriate first-line agents in the treatment of a moderate asthma exacerbation except: a. inhaled 2-agonists. b. inhaled anticholinergics. c. systemic corticosteroids. d. inhaled lidocaine. e. supplemental oxygen. 21. When evaluating a patients pulmonary function, its important to keep in mind that: a. PEFR is a more sensitive measure of patients overall airway obstruction than FEV1. b. FEV1 measures the obstruction in larger airways. c. FEV1 is more dependent on patient effort. d. PEFR requires less patient cooperation. 22. Which of the following ancillary diagnostic tests should be ordered for the asthmatic presenting to the ED? a. Chest radiography in asthmatics being discharged from the ED b. ABG in asthmatics with a PEFR less than 25% c. CBC in asthmatics being admitted to the hospital d. Glucose test 23. Which of the following has shown some promise in the treatment of severe asthma exacerbations? a. Isoetharine b. Inhaled lidocaine c. Magnesium d. Calcium-channel blockers 24. Asthmatics presenting to the ED should receive which of the following therapies? a. Systemic steroids, except in pregnant asthmatics b. Epinephrine as first-line therapy on presentation for mild-to-moderate asthma attacks c. No additional -agonist therapy if the patient has received three nebulized treatments at home d. Anticholinergic therapy for moderate-tosevere exacerbations

25. All of the following concerning the physical examination are true except: a. No wheezing is always a good signit means that bronchoconstriction cannot be occurring. b. The number of seconds a patient can spend counting correlates well with pulmonary function. c. A patients ventilatory status can change rapidly, so caution is advised. d. Both lethargy and agitation presage respiratory failure. 26. Which of the following findings may suggest a diagnosis other than (or in addition to) asthma? a. Increased jugular venous pressure, lymphadenopathy, or carotid bruits b. Unilateral wheezing or rales c. Extremely high or extremely low blood pressure d. All of the above 27. Indications for chest radiography include: a. asthma severe enough to require hospitalization. b. clinical suspicion of pneumothorax, CHF, pneumonia, or foreign body. c. an immunocompromised host. d. unexplained fever. e. all of the above. 28. Early administration (within one hour) of glucocorticoids in the treatment of acute reactive airway disease: a. results in fewer hospital admissions and a lower rate of relapse after ED discharge. b. is rarely helpful. c. has not been proven to be effective. d. is only useful in asthmatic children. 29. Which of the following is an indication for discharge in acute asthma? a. Two ED visits in the past three days for an acute exacerbation b. The patient has improved subjectively but is still wheezing c. The peak expiratory flow rate after treatment is 40% predicted d. A PEFR greater than 70% predicted with a clear lung exam and subjective patient improvement e. Lack of wheezing 30. The addition of ipratropium to standard therapy with steroids and -agonists: a. decreases pulmonary function in the first 90 minutes of treatment. b. is least beneficial in those with severe asthma. c. results in fewer hospitalizations when compared to placebo. d. is contraindicated in patients with a PEFR or FEV1 less than 80% predicted.

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31. What proportion of asthmatics use their inhalers correctly? a. About one in five b. About half c. About four in five d. Virtually all adults and about 70% of children 32. An asthma attack that differs from a patients prior attacks: a. is no cause for concern. b. may indicate a concomitant or even alternative diagnosis. c. is only relevant if the patient has a history of other illnesses. d. presages respiratory failure.

Physician CME Information

This CME enduring material is sponsored by Mount Sinai School of Medicine and has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education. Credit may be obtained by reading each issue and completing the post-tests administered in December and June. Target Audienc e: This enduring material is designed for emergency medicine physicians. Needs A ssessmen t: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians. Date of O riginal R elease: This issue of Emergency Medicine Practice was published February 9, 2001. This activity is eligible for CME credit through February 9, 2004. The latest review of this material was February 7, 2001. Discussion of I nvestiga tional I nformation: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Disclosure of Off-Label Usage: Clinical trials of -agonists and anticholinergics use far higher doses that those approved by the FDA. Conversely, dosages approved by the FDA are not well-studied in moderate-to-severe asthma. Facult y Disclosur e: In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Cydulka reports research funding for Phase III trials from Sepracor and Merck. Dr. Reilly, Dr. Kaufmann, Dr. Sacchetti, and Dr. Mann report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians. Credit D esigna tion: Mount Sinai School of Medicine designates this educational activity for up to 4 hours of Category 1 credit toward the AMA Physicians Recognition Award. Each physician should claim only those hours of credit actually spent in the educational activity. Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category 1 credit (per annual subscription). Earning C redit: Physicians with current and valid licenses in the United States, who read all CME articles during each Emergency Medicine Practice six-month testing period, complete the CME Evaluation Form distributed with the December and June issues, and return it according to the published instructions are eligible for up to 4 hours of Category 1 credit toward the AMA Physicians Recognition Award (PRA) for each issue. You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates will be mailed to each participant scoring higher than 70% at the end of the calendar year.
Publisher : Robert Williford. Vice Presiden t/General Manager : Connie Austin. Executiv e Editor : Heidi Frost.

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives an alpha-numerical score based on the following definitions.
Class I Always acceptable, safe Definitely useful Proven in both efficacy and effectiveness Must be used in the intended manner for proper clinical indications Level of Evidence: One or more large prospective studies are present (with rare exceptions) Study results consistently positive and compelling Class IIa Safe, acceptable Clinically useful Considered treatments of choice Level of Evidence: Generally higher levels of evidence Results are consistently positive Class IIb Safe, acceptable Clinically useful Considered optional or alternative treatments Level of Evidence: Generally lower or intermediate levels of evidence Generally, but not consistently, positive results Class III: Unacceptable Not useful clinically May be harmful Level of Evidence: No positive high-level data Some studies suggest or confirm harm Indeterminate Continuing area of research No recommendations until further research Level of Evidence: Evidence not available Higher studies in progress Results inconsistent, contradictory Results not compelling Adapted from: The Emergency Cardiovascular Care Committees of the American Heart Association and representatives from the resuscitation councils of ILCOR: How to Develop Evidence-Based Guidelines for Emergency Cardiac Care: Quality of Evidence and Classes of Recommendations; also: Anonymous. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part IX. Ensuring effectiveness of community-wide emergency cardiac care. JAMA 1992;268(16):2289-2295.

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Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by Pinnacle Publishing, Inc., 1000 Holcomb Woods Parkway, Building 200, Suite 280, Roswell, GA 30076-2587. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of Pinnacle Publishing, Inc. Copyright 2001 Pinnacle Publishing, Inc. All rights reserved. No part of this publication may be reproduced in any format without written consent of Pinnacle Publishing, Inc. Subscription price: $249, U.S. funds. (Call for international shipping prices.)

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