Beruflich Dokumente
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A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
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.
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.
Editor-in-Chief
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
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
Infectious disease
Social
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.
History
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
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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
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
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.
Treatment
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.
-agonists
-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.
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
Dosage
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
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
Glucocorticoids
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.
Anticholinergics
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
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
Anesthetics
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
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
February 2001
Airway Management
Intubation
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,
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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
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11
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
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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.
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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13
No
Yes
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)
No
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)
* 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
Yes
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%
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)
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)
No
Yes
Yes
No
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
Yes
No
No
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.
Radiography
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.
Treatment
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
Disposition
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.
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February 2001
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!
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19
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
Education
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.
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
Smoking
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.
Summary
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
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References
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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
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26.
4.
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
February 2001
21
27.
28.
29. 30.
31.
32.
33. 34.
35. 36.
37. 38.
39.
40.
41.
42. 43.
44.
45.
46. 47.
48.
49.
50.
2000;117(4):935-943. (Cross-sectional; 32 patients) Gupta D, Aggarwal AN, Subalaxmi MV, et al. Assessing severity of asthma: spirometric correlates with visual analogue scale (VAS). Indian J Chest Dis Allied Sci 2000;42(2):95-100. (Comparative; 195 patients) Turner MO, Noertjojo K, Vedal S, et al. Risk factors for near-fatal asthma. A case-control study in hospitalized patients with asthma [see comments]. Am J Respir Crit Care Med 1998;157(6 Pt 1):18041809. (Prospective; 19 cases) McFadden ER Jr, Warren EL. Observations on asthma mortality. Ann Intern Med 1997;127(2):142-147. (Review; 93 references) Koury TG, Counselman FL, Huff JS, et al. Comparison of peak expiratory flow rate with speaking time in ED patients presenting with acute exacerbation of asthma. Am J Emerg Med 1998;16(6):572-575. (Prospective; 36 patients) Lin RY, Rehman A. Clinical characteristics of adult asthmatics requiring intubation. J Med 1995;26(5-6):261-277. (Retrospective; 58 admissions) Maitre B, Similowski T, Derenne JP. Physical examination of the adult patient with respiratory diseases: inspection and palpation. Eur Respir J 1995;8(9):1584-1593. (Review; 64 references) Stevens MW, Gorelick MH. Interrater agreement in the evaluation of pediatric asthma severity. Acad Emerg Med 1999;6:502. Cardin DL, Nowak RM, Sarkar D, et al. Vital signs including pulsus paradoxus in the assessment of acute bronchial asthma. Ann Emerg Med 1983;12:80-83. (Retrospective) McFadden ER Jr. Clinical physiologic correlates in asthma. J Allergy Clin Immunol 1986;77(1 Pt 1):1-5. (Review) Martin TG, Elenbaas RM, Pingleton SH. Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 1982;11:70. (Retrospective; 51 patients) Bishop J, Nolan T. Pulse oximetry in acute asthma [see comments]. Arch Dis Child 1991;66(6):724-725. (100 patients) Yamamoto LG, Wiebe RA, Rosen LM, et al. Oxygen saturation changes during the pediatric emergency department treatment of wheezing. Am J Emerg Med 1992;10(4):274-284. (Prospective; 785 patients) Rosen LM, Yamamoto LG, Wiebe RA. Pulse oximetry to identify a high-risk group of children with wheezing. Am J Emerg Med 1989;7(6):567-570. (1101 patients) Sole D, Komatsu MK, Carvalho KV, et al. Pulse oximetry in the evaluation of the severity of acute asthma and/or wheezing in children. J Asthma 1999;36(4):327-333. (Comparative; 174 patients) Wright RO, Santucci KA, Jay GD, et al. Evaluation of preand posttreatment pulse oximetry in acute childhood asthma. Acad Emerg Med 1997;4(2):114-117. (Prospective, double-blind, observational) Harden R. Oxygen saturation in adults with acute asthma. J Accid Emerg Med 1996;13:28-30. McGee SR. Physical examination of venous pressure: a critical review [see comments]. Am Heart J 1998;136(1):10-18. (Review; 78 references) Pearson MG, Spence DP, Ryland I, et al. Value of pulsus paradoxus in assessing acute severe asthma. British Thoracic Society Standards of Care Committee. BMJ 1993;307(6905):659. (Prospective; 314 patients) Jay GD, Onuma K, Davis R, et al. Analysis of physician ability in the measurement of pulsus paradoxus by sphygmomanometry. Chest 2000;118(2):348-352. (Comparative; 19 physicians) Flaherty KR, Kazerooni EA, Martinez FJ. Differential diagnosis of chronic airflow obstruction. J Asthma 2000;37:201-223. (Review) Centor RM, Yarborough B, Wood JP. Inability to predict relapse in acute asthma. N Engl J Med 1984;310:577-580. (Prospective; 114 patients) Fischl MA, Pitchenik A, Gardner LB. An index predicting relapse and need for hospitalization in patients with acute asthma. N Engl J Med 1981;305:783-789. (Prospective; 205 patients) Rose CC, Murphy JG, Schwartz JS. Performance of an index predicting the response of patients with acute bronchial asthma to intensive ED treatment. N Engl J Med 1983;310:573-577. (Prospective; 134 patients) Cotes JE. Structure, expansion and movement of the lung. In: Cotes JE. Lung Function: Assessment and Application in Medicine, 5th ed. Oxford, England: Blackwell Scientific Publications;
1993. (Textbook) Enright PL, Lebowitz MD, Cockroft DW. Physiologic measures: Pulmonary function tests: Asthma outcome. Am J Respir Crit Care Med 1994;149:S9-S18. (Review) 52. Vaughan TR, Weber RW, Tipton WR, et al. Comparison of PEFR and FEV1 in patients with varying degrees of lung obstruction: effect of modest altitude. Chest 1989;95:558-562. (Prospective, observational; 102 patients) 53. McCarthy DS, Craig DB, Cherniack RM. Intraindividual variability in maximum expiratory flow volume and closing volume in asymptomatic subjects. Am Rev Respir Dis 1975;112:407411. (Prospective) 54. Nickerson BG, Lemon RJ, Gerdes CB, et al. Within-subject variability and percent change for significance of spirometry in normal subjects and in patients with cystic fibrosis. Am Rev Respir Dis 1980;122:859-866. (Prospective; 30 patients) 55. Silverman R, Scharf SM. Pulmonary function testing in the emergency department. In: Brenner BE, ed. Emergency Asthma. New York: 1999:233-252. (Textbook) 56. Nowak RM, Pensler MI, Sarkar DD. Comparison of peak expiratory flow and FEV1, admission criteria for acute bronchial asthma. Ann Emerg Med 1982;11:64. (Retrospective) 57. Rodrigo G, Rodrigo C. A new index for early prediction of hospitalization in patients with acute asthma. Am J Emerg Med 1997;15:8-13. (Prospective, observational; 184 patients) 58.* Emerman CL, Woodruff PG, Cydulka RK, et al. Prospective multicenter study of relapse following treatment for acute asthma among adults presenting to the emergency department. MARC investigators. Multicenter Asthma Research Collaboration. Chest 1999;115:919-927. Prospective; 939 patients. 59. Diner B, Brenner BE, Camargo CA. Inaccuracy of personal best peak expiratory flow rate reported by inner city patients with acute asthma. Acad Emerg Med 2000;7:469. 60. Emerman CL, Cydulka RK. Factors associated with relapse following emergency department treatment for acute asthma. Ann Emerg Med 1995;26:6-11. (Prospective; 91 patients) 61. Martin TG, Elenbaas RM, Pingleton SH. Failure of peak expiratory flow rate to predict hospital admission in acute asthma. Ann Emerg Med 1982;11(9):466-470. (Prospective; 51 patients) 62. White CS, Cole RP, Lubetcky HW, et al. Acute asthma. Admission chest radiography in hospitalized adult patients. Chest 1991;100:14-16. (Retrospective; 54 patients) 63. Dalton AM. A review of radiological abnormalities in 135 patients presenting with acute asthma. Arch Emerg Med 1991;8:36. (Retrospective; 135 patients) 64. Findley LJ, Sahn SA. The value of chest roentgenograms in acute asthma in adults. Chest 1981;80:535. (Retrospective; 90 patients) 65. Tsai TW, Gallagher EJ, Lombardi G, et al. Guidelines for the selective ordering of admission chest radiography in adult obstructive airway disease. Ann Emerg Med 1993;22(12):1854-1858. (Retrospective; 128 patients) 66. Mills PJ, Karnik RS, Dillon E. L-selectin expression affects T-cell circulation following isoproterenol infusion in humans. Brain Behav Immun 1997;11(4):333-342. (12 patients) 67. Emerman CL, Cydulka RK, Effron DE, et al. A randomized, controlled comparison of isoetharine and albuterol in the treatment of acute asthma. Ann Emerg Med 1991;20:1090-1093. (Prospective, blinded; 103 patients) 68. Cydulka RK, Davison R, Granner L, et al. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med 1988;17:322-326. (Prospective; 95 patients) 69. Hargreave F, Dolovich J, Newhouse M. The assessment and treatment of asthma: A conference report. J Allergy Clin Immunol 1990;85:1098-1111. (Review) 70. Hartley D, Middlemiss D. Absolute configuration of the optical isomers of salbutamol. J Med Chem 1971;14:895-899. (Review) 71. Page CP, Morley J. Contrasting properties of albuterol stereoisomers. J Allergy Clin Immunol 1999;104:S31-S41. (Review) 72. Asmus MJ, Hendeles L. Levalbuterol nebulizer solution: is it worth five times the cost of albuterol? Pharmacotherapy 2000;20(2):123-129. (Review; 28 references) 73. Gawchik SM, Saccar CL, Noonan M, et al. The safety and efficacy of nebulized levalbuterol compared with racemic albuterol and placebo in the treatment of asthma in pediatric patients. J Allergy 51.
22
February 2001
Clin Immunol 1999;103:615-621. (Prospective; 33 patients) Nelson HS. Clinical experience with levalbuterol. J Allergy Clin Immunol 1999;104:S77-S84. (Review) 75. Nelson HS, Bensch G, Pleskow WW, et al. Improved therapeutic ratio with levalbuterol versus racemic albuterol in patients with asthma. J Allergy Clin Immunol 1998;102:943-952. (Prospective; 424 patients) 76. Hindle M, Chrystyn H. Relative bioavailability of salbutamol to the lung following inhalation using metered dose inhalation methods and spacer devices [see comments]. Thorax 1994;49(6):549-553. (10 patients) 77. Amirav I, Newhouse MT. Metered-dose inhaler accessory devices in acute asthma: efficacy and comparison with nebulizers: a literature review. Arch Pediatr Adolesc Med 1997;151(9):876-882. (Review; 60 patients) 78. Hughes DA, Woodcock A, Walley T. Review of therapeutically equivalent alternatives to short acting beta (2) adrenoreceptor agonists delivered via chloroflurocarbon-containing inhalers. Thorax 1999;54:1087-1092. (Review) 79.* Cates CJ, Rowe BH. Holding chambers versus nebulisers for beta-agonist treatment of acute asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 80. Leversha AM, Campanella SG, Aickin, RP, et al. Costs and effectiveness of spacer versus nebulizer in young children with moderate and severe acute asthma. J Pediatr 2000;136:497-502. (Prospective, blinded; 60 patients) 81. Bowton DL, Goldsmith WM, Haponik EF. Substitution of metered-dose inhalers for hand-held nebulizers. Success and cost-savings in a large, acute care hospital. Chest 1992;101: 305-308. (Prospective) 82. Idris AH, McDermott MF, Raucci JC, et al. Emergency department treatment of severe asthma. Metered-dose inhaler plus holding chamber is equivalent in effectiveness to nebulizer. Chest 1993;103:665-672. (Prospective; 35 patients) 83. Turner JR, Corkery KJ, Eckman D, et al. Equivalence of continuous flow nebulizer and metered-dose inhaler with reservoir bag for treatment of acute airflow obstruction. Chest 1988;93:476-481. (Prospective, blinded; 75 patients) 84. Rubilar L, Castro-Rodriguez JA, Girardi G. Randomized trial of salbutamol via metered-dose inhaler with spacer versus nebulizer for acute wheezing in children less than 2 years of age. Pediatr Pulmonol 2000;29(4):264-269. (Randomized, controlled; 123 patients) 85. McFadden ER Jr, Strauss L, Hejal R, et al. Comparison of two dosage regimens of albuterol in acute asthma. Am J Med 1998;105(1):12-17. (Prospective; 160 patients) 86. Rudnitsky GS, Eberlein RS, Schoffstall JM, et al. Comparison of intermittent and continuously nebulized albuterol for treatment of asthma in an urban emergency department. Ann Emerg Med 1993;22:1842-1846. (Prospective; 99 patients) 87. Besbes-Ouanes L, Nouira S, Elatrous S, et al. Continuous versus intermittent nebulization of salbutamol in acute severe asthma: a randomized, controlled trial. Ann Emerg Med 2000;36:198-203. (Prospective; 42 patients) 88. Rodrigo C, Rodrigo G. Salbutamol treatment of acute severe asthma in the ED: MDI versus hand-held nebulizer. Am J Emerg Med 1998;16(7):637-642. (Randomized, double-blind) 89. Robertson CF, Norden MA, Fitzgerald DA, et al. Treatment of acute asthma: salbutamol via jet nebuliser vs spacer and metered dose inhaler. J Paediatr Child Health 1998;34(2):142-146. (Randomized, controlled; 160 patients) 90. Van Renterghem D, Lamont H, Elinck W, et al. Intravenous versus nebulized terbutaline in patients with acute severe asthma: a double-blind randomized study. Ann Allergy 1987;59(4):313-316. (Randomized, controlled; 23 patients) 91. OConnell MB, Iber C. Continuous intravenous terbutaline infusions for adult patients with status asthmaticus. Ann Allergy 1990;64(2 Pt 2):213-218. (5 patients) 92. Stephanopoulos DE, Monge R, Schell KH, et al. Continuous intravenous terbutaline for pediatric status asthmaticus [see comments]. Crit Care Med 1998;26(10):1744-1748. (Retrospective; 18 children) 74.
Browne GJ, Penna AS, Phung X, et al. Randomised trial of intravenous salbutamol in early management of acute severe asthma in children [see comments]. Lancet 1997;349(9048):301-305. (Randomized, controlled; 37 patients) 94. Nathan RA. Beta 2 agonist therapy: oral versus inhaled delivery. J Asthma 1992;29(1):49-54. (Review; 13 references) 95. Thomas K, Peter JV, Cherian AM, et al. Cost-effectiveness of inhaled beta-agonists v. oral salbutamol in asthma: a randomized double-blind cross-over study [see comments]. Natl Med J India 1996;9(4):159-162. (Randomized, controlled) 96. Wallaert B, Brun P, Ostinelli J, et al. A comparison of two longacting beta-agonists, oral bambuterol and inhaled salmeterol, in the treatment of moderate to severe asthmatic patients with nocturnal symptoms. The French Bambuterol Study Group. Respir Med 1999;93(1):33-38. (Randomized, controlled; 117 patients) 97. Chapman KR, Verbeek PR, White JG, et al. Effect of a short course of prednisone in the prevention of early relapse after the emergency room treatment of acute asthma. N Engl J Med 1991;324:788. (Prospective, blinded; 93 patients) 98.* Rowe BH, Spooner CH, Ducharme FM, et al. Corticosteroids for preventing relapse following acute exacerbations of asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 99.* Rowe BH, Spooner C, Ducharme FM, et al. Early emergency department treatment of acute asthma with systemic corticosteroids. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 100.* Manser R, Reid D, Abramson M. Corticosteroids for acute severe asthma in hospitalised patients. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 101.* Rodrigo C, Rodrigo, G. Corticosteroids in the emergency department therapy of acute adult asthma. An evidence-based evaluation. Chest 1999;116:285-295. (Systematic review) 102. Lin RY, Pesola GR, Bakalchuk L, et al. Rapid improvement of peak flow in asthmatic patients treated with parenteral methylprednisolone in the emergency department: A randomized controlled study [see comments]. Ann Emerg Med 1999;33(5):487-494. (Randomized, controlled; 56 patients) 103. Rowe BH, Spooner CH, Ducharme FM, et al. The effectiveness of corticosteroids in the treatment of acute exacerbations of asthma: a meta-analysis of their effect on relapse following acute assessment. In: The Cochrane Library, The Cochrane Collaboration, Cochrane Database of Systematic Reviews, Issue 3. Oxford: Update Software; 1997. 104. Schuckman H, DeJulius DP, Blanda M, et al. Comparison of intramuscular triamcinolone and oral prednisone in the outpatient treatment of acute asthma: a randomized controlled trial [published erratum appears in Ann Emerg Med 1998;31(6):795]. Ann Emerg Med 1998;31(3):333-338. (Randomized, controlled; 168 patients) 105. Green SS, Lamb GC, Schmitt S, et al. Oral versus repository corticosteroid therapy after hospitalization for treatment of asthma. J Allergy Clin Immunol 1995;95(1 Pt 1):15-22. (Randomized, controlled; 26 patients) 106. Rodrigo G, Rodrigo C. Inhaled flunisolide for acute severe asthma. Am J Respir Crit Care Med 1998;157:698-703. (Prospective, blinded; 94 patients) 107.* Edmonds ML, Camargo CA Jr, Pollack CV Jr, et al. Early use of inhaled corticosteroids in the emergency department treatment of acute asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 108. FitzGerald JM, Shragge D, Haddon J, et al. A randomized, controlled trial of high dose, inhaled budesonide versus oral prednisone in patients discharged from the emergency department following an acute asthma exacerbation [see comments]. Can Respir J 2000;7(1):61-67. (Randomized, controlled; 185 patients) 109.* Edmonds ML, Camargo CA Jr, Saunders LD, et al. Inhaled steroids in acute asthma following emergency department discharge. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford:
93.
February 2001
23
Update Software. (Systematic review) 110. Brenner BE, Chavda KK, Camargo CA Jr. Randomized trial of inhaled flunisolide versus placebo among asthmatic patients discharged from the emergency department. Ann Emerg Med 2000;36(5):417-426. (Randomized, controlled; 104 patients) 111. Guttman A, Afilalo M, Colacone A, et al. The effects of combined intravenous and inhaled steroids (beclomethasone dipropionate) for the emergency treatment of acute asthma. The Asthma ED Study Group. Acad Emerg Med 1997;4(2):100-106. (Randomized, controlled; 60 patients) 112. Rowe BH, Bota GW, Fabris L, et al. Inhaled budesonide in addition to oral corticosteroids to prevent asthma relapse following discharge from the emergency department: a randomized controlled trial. JAMA 1999;281:2119-2126. (Prospective, blinded; 188 patients) 113.* Karpel JP, Schacter EN, Fanta C, et al. A comparison of ipratropium and albuterol vs albuterol alone for the treatment of acute asthma. Chest 1996;110:611-616. (Prospective, blinded; 384 patients) 114. ODriscoll BR, Taylor RJ, Horsley MG, et al. Nebulized salbutamol with and without ipratropium bromide in acute airflow obstruction. Lancet 1989;1:1418-1420. (Prospective) 115.* Rodrigo G, Rodrigo C, Burschtin O. A meta-analysis of the effects of ipratropium bromide in adults with acute asthma. Am J Med 1999;107:363-370. (Systematic review) 116. Qureshi F, Zaritsky A, Lakkis H. Efficacy of nebulized ipratropium in severely asthmatic children. Ann Emerg Med 1997;29:205-211. (Prospective, randomized, controlled; 90 patients) 117. Plotnick LH, Ducharme FM. Efficacy and safety of combined inhaled anticholinergics and beta-2-agonists in the initial management of acute pediatric asthma. In: The Cochrane Library, Cochrane Database of Systematic Reviews, Issue 2, 1997. Oxford: Update Software. (Systematic review) 118. Gilman MJ, Meyer L, Carter J, et al. A comparison of aerosolized glycopyrrolate and metaproterenol in acute asthma. Chest 1990;98:1095-1098. (Prospective, blinded; 46 patients) 119. Bloch H, Silverman R, Mancherje N, et al. Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma. Chest 1995;107:1576-1581. (Prospective, blinded; 135 patients) 120.* Rowe BH, Bretzlaff JA, Bourdon C, et al. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review) 121.* Rowe BH, Bretzlaff JA, Bourdon C, et al. Intravenous magnesium sulfate treatment for acute asthma in the emergency department: a systematic review of the literature. Ann Emerg Med 2000;36:181190. (Systematic review) 122. Rodrigo G, Rodrigo C, Burschtin O. Efficacy of magnesium sulfate in acute adult asthma: a meta-analysis of randomized trials. Am J Emerg Med 2000;18:216-21. (Systematic review) 123. Nannini LJ Jr, Pendino JC, Corna RA, et al. Magnesium sulfate as a vehicle for nebulized salbutamol in acute asthma. Am J Med 2000;108(3):193-197. (Randomized, controlled; 35 patients) 124. Manthous CA, Hall JB, Caputo MA, et al. Heliox improves pulsus paradoxus and peak expiratory flow in non-intubated patients with severe asthma. Am J Respir Crit Care Med 1995;151:310-314. (Prospective; 27 patients) 125. Gluck EH. Helium-oxygen mixtures in intubated patients with status asthmaticus and respiratory acidosis. Chest 1990;98:693-698. (Review) 126. Kass JE, Terregino CA. The effect of heliox in acute severe asthma. A randomized controlled trial. Chest 1999;116:296-300. (Prospective; 23 patients) 127. Henderson SO, Acharya P, Kilaghbian T, et al. Use of helioxdriven nebulizer therapy in the treatment of acute asthma. Ann Emerg Med 1999;33:141-146. (Prospective; 205 patients) 128. Nakagawa TA, Johnston SJ, Falkos SA, et al. Life-threatening status asthmaticus treated with inhaled nitric oxide. J Pediatr 2000;137(1):119-122. (Case report; 5 children) 129. ORourke P, Crone R. Halothane in status asthmaticus. Crit Care Med 1982;10:341-343. (Case report) 130. Johnston RG, Noseworthy TW, Friesen EG, et al. Isoflurane
131. 132.
133. 134.
135.
136.
137.
138.
139.
140.
141.
142.
143.
144.
145.
146.
147.
148.
149.
150.
therapy for status asthmaticus in children and adults. Chest 1990;97(3):698-701. (Case report; 2 adults, 2 children) Lipworth BJ. Leukotriene-receptor antagonists. Lancet 1999;353:5762. (Review) Sageman S, Knight VL, Mahon R. The effect of a leukotriene D4 receptor inhibitor on acute asthma exacerbations. Acad Emerg Med 1999;6:501. Rabold M, Tintinalli J. Tracheal lidocaine stops airway hyper responsiveness. Ann Emerg Med 1995;25:432. (Letter, case report) Panacek EA, Pollack CV. Medical management of severe acute asthma. In: Brenner BE, ed. Emergency Asthma, New York: 1999:395-418. (Textbook) Fanta CH, Rossing TH, McFadden ER Jr. Treatment of acute asthma: is combination therapy with sympathomimetics and methylxanthines indicated? Am J Med 1986;80:5-10. (Retrospective; 157 patients) Rossing TH, Fanta CH, Goldstein DH, et al. Emergency therapy of asthma: comparison of the acute effects of parenteral and inhaled sympathomimetics and infused aminophylline. Am Rev Respir Dis 1980;122:365-371. (Prospective; 48 patients) Murphy DG, McDermott MF, Rydman RJ, et al. Aminophylline in the treatment of acute asthma when beta-2 -adrenergics and steroids are provided. Arch Intern Med 1993;153:1784-1788. (Prospective, blinded; 44 patients) Rodrigo C, Rodrigo G. Treatment of acute asthma. Lack of therapeutic benefit and increase of the toxicity from aminophylline given in addition to high doses of salbutamol delivered by metered-dose inhaler with a spacer. Chest 1994;106:1071-1076. (Prospective, blinded; 94 patients) Coleridge J, Cameron P, Epstein J, et al. Intravenous aminophylline confers no benefit in acute asthma treated with intravenous steroids and inhaled bronchodilators. Aust N Z J Med 1993;23:348354. (Prospective; 59 patients) Bone R, Calverley P, Chapman K, et al. The international clinical respiratory group; special report. Chest 1992;101: 1420-1424. (Review) Strauss RE, Wertheim DL, Bonagura VR, et al. Aminophylline therapy does not improve outcome and increases adverse effects in children hospitalized with acute asthmatic exacerbations. Pediatrics 1994;93:205-210. (Prospective, blinded; 26 patients) Carter E, Cruz M, Chesrown S, et al. Efficacy of intravenously administered theophylline in children hospitalized with severe asthma. J Pediatr 1993;122:470-476. (Prospective, blinded; 21 patients) DiGiulio GA, Kercsmar CM, Krug SE, et al. Hospital treatment of asthma: lack of benefit from theophylline given in addition to nebulized albuterol and intravenously administered corticosteroid. J Pediatr 1993;122:464-469. (Prospective; 29 patients) Huang D, OBrien RG, Harman E, et al. Does aminophylline benefit adults admitted to the hospital for an acute exacerbation of asthma? Ann Intern Med 1993;119:1155-1160. (Prospective; 21 patients) Self TH, Abou-Shala N, Burns R, et al. Inhaled albuterol and oral prednisone therapy in hospitalized adult asthmatics. Does aminophylline add any benefit? Chest 1990;98:1317-1321. (Prospective, blinded; 39 patients) Yung M, South M. Randomised controlled trial of aminophylline for severe acute asthma. Arch Dis Child 1998;79(5):405-410. (Randomized, controlled; 163 patients) Van Ganse E, Kaufman L, Derde MP, et al. Effects of antihistamines in adult asthma: a meta-analysis of clinical trials. Eur Respir J 1997;10(10):2216-2224. (Meta-analysis) Rock MJ, Reyes de la Rocha S, LHommedieu CS, et al. Use of ketamine in asthmatic children to treat respiratory failure refractory to conventional therapy. Crit Care Med 1986;14(5):514516. (Case report; 2 children) Howton JC, Rose J, Duffy S, et al. Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma. Ann Emerg Med 1996;27(2):170-175. (Randomized, controlled; 53 patients) Hondras MA, Linde K, Jones AP. Manual therapy for asthma. In: The Cochrane Library, Cochrane Airways Group, Cochrane Database of Systematic Reviews, Issue 3, 2000. Oxford: Update Software. (Systematic review)
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February 2001
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.
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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.
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