eMedicine Specialties > Emergency Medicine > Pulmonary

Asthma: Treatment & Medication

Author: Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Contributor Information and Disclosures

Updated: Jul 2, 2009

Treatment

Prehospital Care

Therapy for acute asthma can be initiated in the prehospital setting consistent with EMS providers' legally authorized scope of practice and local medical direction. The primary treatment approach is administration of supplemental oxygen and inhaled bronchodilators. The latter treatment most often involves inhaled beta2-agonists given by hand-held nebulizer or using a metered-dose inhaler (MDI) with spacer (holding chamber). If these delivery devices are not available, subcutaneous epinephrine or terbutaline can be given for severe exacerbations.

When initiating bronchodilator use, EMS personnel should not delay patient transport to the appropriate medical facility—which remains a high priority. If necessary, and again consistent with the scope of practice and local medical direction, bronchodilator treatments may be repeated while transporting patients. Prolonged transport times (eg, in rural settings or during transport on congested urban streets) may necessitate multiple bronchodilator treatments before arrival to the medical facility. To improve prehospital care, ambulance services are encouraged to develop protocols for the management of acute asthma in children and adults. A model protocol was developed by a CDC-funded workgroup to help advance this process.5

Emergency Department Care

  • The mainstay of ED therapy for acute asthma is inhaled beta2-agonists. The most effective particle sizes are 1-5 µm. Larger particles are ineffective because they are deposited in the mouth and central airways. Particles smaller than 1 µm are too small to be effective since they move in the airways by Brownian motion and do not reach the lower airways.
  • Standard delivery systems and routes are as follows:
    • Albuterol 2.5-5 mg every 20 minutes for 3 doses, then 2.5-10 mg every 1-4 hours as needed. Dilution of 2.5 mg in 3-4 mL of saline or use of premixed nebules is standard. Oxygen or compressed air delivery of the inhaled beta-agonists should be at a rate of 6-8 L/min. For children, use 0.15 mg/kg (minimum dose 2.5 mg) every 20 minutes for 3 doses then 0.15-0.3 mg/kg up to 10 mg every 1-4 hours as needed.
    • An equivalent method of beta-agonist delivery in mild-to-moderate exacerbations is the MDI used in conjunction with a spacer or holding chamber. For severe exacerbations, it is less clear if nebulized versus MDI/spacer delivery is truly equivalent. Each puff delivers a standard 90 mcg of albuterol. The dose is 4-8 puffs every 20 minutes up to 4 hours, then every 1-4 hours as needed. A potential advantage of the MDI/holding chamber is that it requires little or no assistance from the respiratory therapist once the patient understand how to use administer the medication; the patient can be discharged from the ED with the same spacer and albuterol canister. This modality is especially effective in areas where patients may be unable to afford their inhaled beta-agonists.
    • Continuous nebulization may be superior to the MDI/holding chamber method in a patient with severe exacerbations (eg, PEF <200 L/min). The dose of albuterol is 10-15 mg in 70 mL of isotonic saline. For children, this method is reserved for severe asthma at an albuterol dose of 0.5 mg/kg/h. Based on meta-analyses, there is no advantage of intravenous albuterol over inhaled albuterol, even in severe asthma. However, the role of parenteral beta-agonists in addition to inhaled beta-agonist treatments is uncertain.
    • Side effects may include tremor and a slight tendency toward tachycardia. However, many patients who present with acute asthma and tachycardia actually decrease their heart rate with inhaled beta-agonist therapy. Also, inhaled beta-agonists decrease potassium by an average of 0.4 mEq/L.
    • Patients who respond poorly or not at all to an inhaled beta-agonist regimen may respond to parenteral beta 2-agonists, such as 0.25 mg terbutaline or 0.3 mg of 1:1000 concentration of epinephrine administered subcutaneously. This treatment should be reserved for patients who are seriously ill and not responding to serial treatments with inhaled beta-agonist/anticholinergic therapy and other more established therapies.
    • Ipratropium 0.5 mg has had variable benefit in controlled trials demonstrating most consistent efficacy in children and smokers with comorbid COPD. The 2002 and 2007 NAEPP guidelines recommend its use in severe exacerbations only.6,7 Ipratropium should be given in combination with albuterol every 20 minutes for 3 doses then as needed. The addition of ipratropium has not been shown to provide further benefit once the patient is hospitalized.
    • For severe asthma exacerbations, intravenous magnesium sulfate has been shown to be beneficial. The usual dose is 2 g over 20 minutes; the effect of higher and faster doses is uncertain. These larger doses have demonstrated safety for almost 50 years in the obstetrics literature, with rates as high as 1 g/min for 3 g. Intravenous magnesium sulfate has little (if any) value in mild-to-moderate exacerbations and should not be used in that setting.
    • Inhaled corticosteroids are a safe and effective treatment of persistent asthma. The inhaled corticosteroid can be used for short- or long-term treatment without the adverse side effects of oral corticosteroids.
    • Research studies suggest that inhaled corticosteroids may one day have a role in the management of acute asthma, in addition to the important role they play in preventing exacerbations in the first place. Randomized trials, including a 2008 study from Israel, demonstrate that corticosteroids in the ED can result in improved pulmonary function in approximately 2 hours and thereby decrease risk of hospital admission.8 This therapeutic approach is experimental and thought to work through nonspecific vasoconstriction in the airways. The time to pulmonary function benefit (90-120 min) is too short to support an anti-inflammatory effect mediated by the traditional effects of corticosteroids within a cell. The potential role of inhaled corticosteroids in acute asthma remains under investigation.
    • Heliox is a helium-oxygen (80:20 or 70:30) mixture that may provide dramatic benefit for ED patients with severe exacerbations.
      • Helium is about 25% as dense as room air and, consequently, it travels more easily down narrowed passages. This property makes heliox of particular value to patients at risk of intubation—by quickly decreasing the work of breathing and, when the gas mixture is used to drive the nebulizer, by better delivery of the inhaled bronchodilator.
      • Despite considerable promise, the literature shows mixed results. Potential explanations include the large number of small trials (low statistical power) and suboptimal delivery of albuterol to the patient. Briefly, heliox-driven nebulizer treatments should have the gas set at a rate of 8-10 L/min and with double the usual amount of albuterol. These adjustments result in the delivery of the appropriate amount of albuterol to the patient but with particles being delivered in the heliox mixture instead of oxygen or room air. When patients need supplemental oxygen, one can deliver it via nasal prong. Of course, as the supplemental oxygen is increased, the benefits of using heliox decrease. Oxygen requirements should determine the ideal mix. The role of heliox in acute asthma remains under investigation.
    • Intravenous leukotriene modifiers (such as montelukast 7 mg IV) provide rapid bronchodilation (within 10 min), but they are not yet available outside of phase II/III research trials. Montelukast 20 mg orally may produce an increase in FEV1 in severe asthma exacerbations, but, given the pharmacokinetics of the drug, this benefit may not be seen for approximately 30-75 minutes. The role of leukotriene modifiers in acute asthma is an active area of research.
    • In life-threatening exacerbations, to avoid intubation, many of these therapies (including inhaled albuterol, inhaled ipratropium, intravenous and inhaled corticosteroids, intravenous magnesium sulfate, parenteral terbutaline, heliox, and oral montelukast) may be administered simultaneously. Although the individual contribution of each treatment is uncertain, most of these agents contribute to bronchodilation in different ways, and each likely adds a little to what may be an important overall improvement.
    • Despite the best efforts of the ED, some patients will require endotracheal intubation. Approximately 5-10% of all asthma hospitalizations are to an intensive care unit—for further care of already intubated patients or for close supervision of patients at very high risk of intubation. Mechanical ventilation of patients with acute asthma presents special challenges, such as the risk of high pressures lowering systemic blood pressure (auto-PEEP) and less commonly, complications such as barotrauma, pneumothorax, or pneumomediastinum. The role of permissive hypercapnia goes beyond the scope of this article but is a ventilator strategy used in the ICU management of some patients with severe asthma exacerbations.
  • In general, 3-4 hours in the ED is adequate time to determine if a patient with acute asthma has improved symptomatically and demonstrates pulmonary flow rates sufficiently improved for safe discharge. To allow time for corticosteroids to take effect, extended treatment in a clinical holding area has been demonstrated to be effective. Such observation units have avoided 60% of admissions to the hospital for acute asthma by treating and observing the patient for as long as 12 hours. These units are appropriate if nursing care and monitoring are adequate. They provide an excellent site for specialized asthma education.
  • In one holding unit, asthma study patients were discharged within 12 hours at 50% of predicted PEF if they had no high-risk relapse factors (see list above) or at 60% of predicted PEF if they had one or more high-risk relapse factors. At time of discharge, patients were given albuterol inhalers and prednisone tablets, avoiding delay and inconvenience of filling the prescriptions and possible noncompliance. At 2 weeks following the ED visit, a 9% relapse rate was noted, considerably less than the 20% for most EDs.
  • Difficulty and inability to obtain medications due to socioeconomic and psychiatric factors should lower the threshold for hospital admission for patients who have asthma and PEF of 50-69% of predicted or personal best.

In general, it is best care to follow the NAEPP 2007 guidelines for acute asthma (EPR3).7 The flow charts for asthma care in the ED especially are an invaluable aid to clinicians and nurses. Other guidelines do exist; use of guidelines from the Global Initiative for Asthma (GINA) for acute and chronic care in patients with prior near-fatal asthma have shown remarkable reductions in asthma relapses after ED visits, hospitalizations, near-fatal attacks, and asthma mortality. Asthma mortality was reduced in patients already presenting with near fatal asthma, from 15% in historical controls over 4 years to 0% by following the GINA guidelines.9

On June 25, 2009, The American Thoracic Society and the European Respiratory Society jointly released new official standards on asthma evaluation for clinical trials and practice.The Medscape Medical News article, New Guidelines Issued for Asthma Assessment, has a more detailed discussion.10  

Medication

The goals of therapy are to maintain SaO2 greater than 92% and to treat dehydration only if it is clinically apparent. Routine hydration is not indicated.

Antibiotics should be administered only if bacterial sinusitis, bronchitis, or pneumonia is suspected clinically. Asthma exacerbation severity and therapeutic choices instituted should be evaluated according to the percent of predicted FEV1 or PEF. The 2002 National Asthma Education and Prevention Program (NAEPP) cutpoints are less than 50% (severe exacerbation), 50-79% (moderate exacerbation), and 80% or higher (mild exacerbation). Some experts believe that more appropriate cutpoints are less than 40% as "severe" (because that is the approximate percentage predicted where several adjunct therapies, such as continuous nebulization and intravenous magnesium, begin to work) and 70% or higher as "mild" (because that is the target PEF for discharge of patients from the ED).

Corticosteroids

These anti-inflammatory agents have myriad effects, including restoration of beta2-agonist receptors in the bronchial smooth muscles and, therefore, improved response to beta2-agonists.

Corticosteroids are indicated in all patients with severe exacerbations and in the vast majority of patients with moderate exacerbations. If response to the first or second beta2-agonist inhaler treatment is incomplete, this too is an indication for corticosteroids in most patients.

Additional high-risk patients for whom corticosteroids may be recommended are those who require frequent ED visits, have been admitted with asthma exacerbations, have been intubated, are already on outpatient steroids, or have been experiencing an episode for longer than 2-3 days.

The onset of action of corticosteroids is approximately 4-6 hours. The bioavailability of orally and parenterally administered steroids is the same, and numerous randomized double-blind trials have demonstrated this equivalence. A primary reason to use intravenous corticosteroids is the adage to avoid medications by mouth when intubation is imminent. However, for most ED patients with acute asthma, the use of oral corticosteroids obviates placement of an intravenous line.


Prednisone (Sterapred)

Useful in treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.

Adult

40-60 mg PO (often administered once in ED in place of IV/IM corticosteroids) followed by discharge from hospital with 40-50 mg/d for 5-10 d; 50-mg tab provides a very convenient and effective prescription: 1 tab, once daily for 5 d

Pediatric

1-2 mg/kg PO qd (maximum 60 mg/d) for 3-10 d

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, fungal, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation after >10 d of corticosteroid treatment may cause adrenal crisis; adverse effects include hyperglycemia, edema, myopathy, hypokalemia, euphoria, psychosis, myasthenia gravis, and infections


Methylprednisolone (Solu-Medrol, Depo-Medrol)

For treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Depo-Medrol is long-lasting and avoids compliance problems and financial issues that may affect patients' ability to obtain outpatient corticosteroids.

Adult

80-125 mg IV, then 40-80 mg IV in 1 or 2 divided doses until PEF reaches 70% of predicted or personal best

Pediatric

2 mg/kg IV, then 1 mg/kg/dose IV in 2 divided doses (maximum 60 mg/d) until PEF 70% of predicted or personal best

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia if taking concurrent diuretics

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, hypokalemia, euphoria, psychosis, myopathy, and infections are possible complications


Triamcinolone (Aristocort)

Decreases inflammation by suppressing migration of PMNs and reversing capillary permeability.

Adult

60 mg IM, followed by additional doses of 20-100 mg IM; doses given when signs and symptoms recur

Pediatric

<6 years: Not recommended
6-12 years: 0.03-0.2 mg/kg IM at 1- to 7-d intervals
>12 years: Administer as in adults

Coadministration with barbiturates, phenytoin, or rifampin decreases effects

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation after >10 d of corticosteroid treatment may cause adrenal crisis

Bronchodilators

Their primary action is to decrease muscle tone in both small and large airways in lungs, thus increasing airflow and ventilation. This category includes beta-adrenergic, methylxanthine, and anticholinergic medications.


Albuterol (Proventil, Ventolin)

Bronchodilator in reversible airway obstruction due to asthma. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on heart rate.

Adult

2.5-5 mg via hand-held nebulizer or metered-dose inhaler (MDI) with spacer (holding chamber) q20min for 3 doses, then 2.5-10 mg q1-4h prn; dilute 2.5 mg in 3-4 mL of saline or use premixed nebules

Pediatric

0.15 mg/kg (minimum dose 2.5 mg) via hand-held nebulizer or using a metered-dose inhaler (MDI) with spacer (holding chamber) q20min for 3 doses, then 0.15-0.3 mg/kg up to 10 mg q1-4h prn

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, or sympathomimetic agents

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism; excessive use may result in tolerance and hypokalemia and hypomagnesemia; adverse reactions may occur more frequently in children aged 2-5 y


Epinephrine (EpiPen, TwinJect)

Alpha-agonist effects increase peripheral vascular resistance and reverse peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist activity of epinephrine produces bronchodilatation. IM route (outer thigh) probably provides faster and more consistent epinephrine delivery than SC route.

Adult

0.3-0.5 mg IM q20min for up to 3 doses

Pediatric

0.01 mg/kg up to 0.3-0.5 mg IM q20min for up to 3 doses

Increases toxicity of halogenated inhalational anesthetics

Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; use as local anesthetic in areas such as fingers or toes (vasoconstriction may produce sloughing of tissue); use during pregnancy (decreases uterine blood flow causing uteroplacental insufficiency)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias; caution in elderly persons and hyperthyroidism


Terbutaline (Brethaire, Bricanyl)

Selective beta2-agonist acts directly on beta2-receptors, relaxing bronchial smooth muscle, relieving bronchospasm, and reducing airway resistance.

Adult

0.25 mg SC q20min for up to 3 doses
2 puffs MDI q4-6h
5 mg PO tid; not to exceed 15 mg/d

Pediatric

<12 years: 0.25 mg SC q20min for up to 3 doses; 2 puffs MDI q4-6h; 0.05 mg/kg/dose PO tid, not to exceed 5 mg/d
>12 years: Administer as in adults

Concomitant beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects of beta-agonists; concomitant MAOIs may result in hypertensive crisis; concurrent oxytocic drugs such as ergonovine may result in severe hypotension

Documented hypersensitivity; tachycardia resulting from cardiac arrhythmias

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Through intracellular shunting, terbutaline may decrease serum potassium levels, which can produce adverse cardiovascular effects; decrease is usually transient and may not require supplementation


Ipratropium (Atrovent)

Anticholinergic agent with antisecretory properties. When applied locally, inhibits secretions from serous and seromucous glands lining nasal mucosa. Ipratropium has been found effective in severe asthma exacerbations only. The addition of ipratropium has not been shown to provide further benefit once the patient is hospitalized.

Adult

Nebulizer: 0.5 mg q20min for 3 doses then prn
MDI: 8 puffs q20min prn up to 3 h

Pediatric

Nebulizer: 0.25-5 mg q20min for 3 doses, then prn
MDI: 4-8 puffs q20min up to 3 h

Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not indicated for single-agent treatment of acute bronchospasm given its relatively slow onset (20 min); caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction


Ipratropium and albuterol (Combivent)

Anticholinergic agent with anti-secretory properties. When applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa. Ipratropium has been found effective in severe asthma exacerbations only. The addition of ipratropium has not been shown to provide further benefit once the patient is hospitalized.
Albuterol is a beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility.
Recommended to "test spray" 3 times before using first time and in cases where aerosol has not been used for >24 h.

Adult

Nebulizer: 3 mL q20min for 3 doses, then prn
MDI: 4-8 puffs q20min prn up to 3 h

Pediatric

Nebulizer: 1.5 mL q20min for 3 doses, then prn
MDI: 4-8 puffs q20min prn up to 3 h

Drugs with anticholinergic properties (eg, dronabinol) may increase toxicity; albuterol increases effects of ipratropium
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction


Theophylline (Theo-Dur, Theo-24, Aminophylline)

Purported efficacy thought to be due to potentiation of exogenous catecholamines, stimulation of endogenous catecholamine release, and diaphragmatic muscular stimulation.
Effects as bronchodilator are mild, and toxicity (levels >20 mg/dL) is common.

Adult

Loading dose: 6 mg/kg lean body weight IV over 20-30 min
Drip (1 g in 250 mL D5W): 0.5-0.7 mg/kg/h IV

Pediatric

1 mg/kg/h IV

Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects; effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon

Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism; do not inject IV solution faster than 25 mg/min; patients with pulmonary edema or liver dysfunction at greater risk of toxicity because of reduced drug clearance


Ketamine (Ketalar)

Acts on cortex and limbic system, decreasing bronchospasm. A dissociative anesthetic agent.

Adult

Initial dose: 1-4.5 mg/kg IV
Maintenance dose: One third to one half initial dose IV

Pediatric

Initial dose: 0.5-2 mg/kg IV
Maintenance dose: One third to one half initial dose

Increases CNS effects of narcotics, barbiturates, and hydroxyzine; thyroid hormones and muscle relaxants increase toxicity

Documented hypersensitivity; thyrotoxicosis

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with intracranial hypertension; may increase bronchial secretions, prompting some practitioners to administer concomitant antisecretory agent (ie, glycopyrrolate) routinely as preventive measure
Resuscitative equipment should be immediately available when administering this medication

Inhaled volatile anesthetics

These agents may aid in smooth muscle relaxation.


Halothane (1-2%)

Leads to moderate effects on bronchial muscular relaxation and causes bronchodilation.

Adult

24 years: 0.84 MAC
42 years: 0.76 MAC
81 years: 0.64 MAC

Pediatric

Infants: 1.08 MAC
3 years: 0.91 MAC
10 years: 0.87 MAC
15 years: 0.92 MAC

Simultaneous use with epinephrine or norepinephrine may induce ventricular tachycardia or fibrillation (use caution)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hepatic dysfunction may occur

More on Asthma

Overview: Asthma
Differential Diagnoses & Workup: Asthma
Treatment & Medication: Asthma
Follow-up: Asthma
References
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Further Reading

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Keywords

asthma, asthma attack, asthma symptoms, asthma treatment, asthma evaluation, asthma assessment, asthma causes, airway obstruction, asthma management, asthma exacerbation, airway inflammation, bronchial asthma, asthma triggers, dyspnea, wheezing, shortness of breath, asthmatic, reactive airway disease, wheeze, bronchiolitis, acute asthma, asthma prevention, allergies, bronchial airways, bronchial airway narrowing, inflammation of the bronchi, bronchial smooth muscle contraction, airway narrowing, noisy breathing, difficult breathing, difficulty breathing, inhalers, lung disease

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Contributor Information and Disclosures

Author

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Paul Blackburn, DO, FACOEP, FACEP, Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona
Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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