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February 2001Volume 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

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 tosevere; and

3.identify the appropriate disposition for an asthmatic

presenting to the ED.

Dat e of o rigina l release: Februa ry 9, 2001.

Dat e of m ost recent review : Februar y 7, 2001.

See “Physician CME Inform atio n” on back p age.

EMERGENCY  MEDICINE PRACTICEAN EVIDENCE-BASED A PPROACH T O EMERGENCY MEDI CINE

Editor-in-Chief 

Stephen A. Colucciello, MD, FACEP,Assistant Chair, Director of Clinical Services, Department of Emergency Medicine, CarolinasMedical Center, Charlotte, NC;

Associate Clinical Professor,Department of EmergencyMedicine, University of NorthCarolina at Chapel Hill, ChapelHill, NC.

Associate Editor

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

Editorial Board

 Judith C. Brillman, MD,ResidencyDirector, Associate Professor,Department of Emergency

Medicine, The University of New Mexico Health SciencesCenter School of Medicine,Albuquerque, NM.

W. Richard Bukata, MD,AssistantClinical Professor, EmergencyMedicine, Los Angeles County/

USC Medical Center, Los Angeles,CA; Medical Director, EmergencyDepartment, San Gabriel ValleyMedical Center, San Gabriel, CA.

Francis M. Fesmire, MD, FACEP,Director, Chest Pain—StrokeCenter, Erlanger Medical Center;Assistant Professor of Medicine,UT College of Medicine,Chattanooga, TN.

Valerio Gai, MD,Professor and Chair,Department of EmergencyMedicine, University of Turin, Italy.

Michael J . Gerardi, MD, FACEP,Clinical Assistant Professor,Medicine, University of Medicineand Dentistry of New Jersey;Director, Pediatric EmergencyMedicine, Children’s Medical

Center, Atlantic Health System;Chair, Pediatric EmergencyMedicine Committee, ACEP.

Michael A. Gibbs, MD, FACEP,Residency Program Director;Medical Director, MedCenter Air,Department of Emergency

Medicine, Carolinas MedicalCenter; Associate Professor of Emergency Medicine, Universityof North Carolina at Chapel Hill,Charlotte, NC.

Gregory L. Henry, MD, FACEP,CEO, Medical Practice RiskAssessment, Inc., Ann Arbor,MI; Clinical Professor, Departmentof Emergency Medicine,University of Michigan MedicalSchool, Ann Arbor, MI; President,American Physicians AssuranceSociety, Ltd., Bridgetown,Barbados, West Indies; PastPresident, ACEP.

 Jerome R. Hoffman, MA, MD, FACEP,Professor of Medicine/Emergency Medicine, UCLA

School of Medicine; AttendingPhysician, UCLA EmergencyMedicine Center;Co-Director, The DoctoringProgram, UCLA School of Medicine, Los Angeles, CA.

 John A. Marx, MD,Chair and Chief,

Department of EmergencyMedicine, Carolinas MedicalCenter, Charlotte, NC; ClinicalProfessor, Department of Emergency Medicine, Universityof North Carolina at Chapel Hill,Chapel Hill, NC.

Michael S. Radeos, MD, MPH, FACEP,Attending Physician inEmergency Medicine, LincolnHospital, Bronx, NY; ResearchFellow in Emergency Medicine,Massachusetts General Hospital,Boston, MA; Research Fellow inRespiratory Epidemiology,Channing Lab, Boston, MA.

Steven G. Rothrock, MD, FACEP,FAAP, Associate Professorof Emergency Medicine,

University of Florida; OrlandoRegional Medical Center; MedicalDirector of Orange CountyEmergency Medical Service,Orlando, FL.

Alfred Sacchetti , MD, FACEP,Research Director, Our Lady of 

Lourdes Medical Center, Camden,NJ; Assistant Clinical Professorof Emergency Medicine, Thomas Jefferson University,Philadelphia, PA.

Corey M. Slovis, MD, FACP, FACEP,Department of EmergencyMedicine, Vanderbilt UniversityHospital, Nashville, TN.

Mark Smith, MD,Chairman,Department of EmergencyMedicine, Washington HospitalCenter, Washington, DC.

 Thomas E. Terndrup, MD, Professorand Chair, Department of Emergency Medicine, Universityof Alabama at Birmingham,Birmingham, AL.

Asthma: An Evidence-Based

Management Update

THE young man looks bad. The medics struggle to keep himupright as they wheel him past, but his skin is slippery from thetorrents 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 boy’s 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 relyon an ever-growing pharmacological armamentarium and continue to

expand our means of preventative care. Furthermore, as increasing

numbers of patients seek emergency care for the treatment of their

asthma, the role of the emergency physician also grows. Our task now

includes not only acute treatment, but also initiation of preventative and

maintenance care.

This issue of Emergency Medicine Practice addresses acute treatment

decisions involved with patients with an acute asthma exacerbation, as

well as their long-term care requirements.

Epidemiology And Pathophysiology

Despite continuing advances in treatment and prevention, asthma isincreasing in prevalence worldwide,1 reaching 4%-5% in the developed

nations2,3 and affecting more than 15 million Americans.4 In the United

States, it is the most prevalent chronic disease among children. 4 The death

rate from asthma among those 19 years and younger has increased by

almost 80% since 1980.4 Asthma carries higher morbidity and is even more

lethal in the elderly, among whom 7%-10% are affected.5,6

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Asthma is the third-leading cause of preventable

hospitalization in the United States7 and each year

accounts for approximately 2 million visits to the nation’s

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 implica-

tions. 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, aller-

genic, 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 patienttraditionally has included pharmacological therapy that

works in one of two ways: by relaxing bronchial smooth

muscle (bronchodilation) or reducing airway inflamma-

tion (anti-inflammatory action).15 While pharmacologic

therapy is the mainstay of emergency treatment of 

asthma, we can improve long-term outcomes by recog-

nizing the genesis of the disease.

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 pneu-

monitis, and carcinoid syndrome. Even those with no

predisposition to asthma may develop wheezing after

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 masquerad-

ing as reactive airway disease.

“‘Healing,’ Papa would tell me, ‘is not a science,

but the intuitive art of wooing nature.’”

 —W.H. Auden

Clinical Practice GuidelinesAnd Systematic Reviews

The National Heart, Lung, and Blood Institute of the

National Institutes of Health (NIH) first published guide-

lines for the diagnosis and management of asthma in 1991

and updated these recommendations in 1997. However,

there is no consistent or widespread acceptance of these

guidelines.16 In fact, the management of asthma in many

EDs deviates significantly from published guidelines.17

Furthermore, there is little evidence that these (or other)

guidelines actually improve outcomes.18 As we will show in

the ensuing pages, many of the NIH guidelines are not

evidence-based. A number of recommendations are based

on the opinion of the panel, and unlike most evidence-based

guidelines, they did not use a ranking system to establish a

hierarchy of “best evidence.” (In such a hierarchical system,

a large, prospective, randomized, controlled trial free from

significant bias is specifically designated as more valid than

a case report.)

Nonetheless, as many as 40% of hospitals havedeveloped some critical pathways for asthma. Hospitals

that use asthma clinical guidelines are more likely to

engage in asthma-specific quality improvement efforts

than hospitals that do not use such guidelines.19 There is

some evidence that an acute asthma quality improvement

initiative can advance patient care. In one urban teaching

hospital, such an initiative decreased delays to β-agonist

and steroid therapy by approximately 16 minutes and 34

minutes, respectively. The program decreased median ED

length of stay by 58 minutes and resulted in fewer

inpatient admissions.20

In some hospitals, the triage or treatment area nurses

will initiate asthma protocols in order to speed interven-tions and decrease resource utilization. One study

prospectively examined 149 patients with asthma treated

 by a pathway protocol and compared them with a

historical cohort of 97 patients with asthma who were

treated by conventional means. Protocol patients had less

oxygen use, fewer handheld nebulizer treatments, fewer

saline locks, and received fewer intravenous steroids.

There was a significant increase in the use of metered-

dose inhalers with spacer and oral steroids in patients

treated by protocol.21

Even scientific reviews and meta-analysis regarding

 Table 1. Pathophysiology Of Asthma.

Etiology Relevance to treatment

Cellular Interaction of mast cells with IgE

molecules leading to the flood of pro-inflammatory molecules in thepulmonary system10,13

Infectious disease Connection between viralrespiratory infections and thedevelopment of asthma14

Social Psychological and emotional factorsthat act via modification of vagalefferent activity

Public health Influence of other precipitants likeenvironmental pollutants andpharmacologic agents

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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 subcuta-

neous terbutaline significantly reduces respiratory

distress.23 In this study, albuterol provided greater

subjective improvement.

Some limited data suggest that 125 mg of intrave-

nous 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 patient’s appearance,

vital signs, and chest examination. If needed, aggressive

therapy directed at relieving airway obstruction must

 begin as soon as the diagnosis is suspected.

HistoryThe patient’s 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.

History O f Present Illness 

Establish any precipitants of the attack and its duration.

Be aware of attacks that are prolonged, as they may not

respond as rapidly to therapy. In one study, patients with

sudden-onset asthma were less likely to report an upper-

respiratory-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 mythol-

ogy 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. Acute-

onset chest pain may denote potential pneumothorax,

pneumomediastinum, pneumonia, or pulmonary

embolism (in addition to possible cardiac disease). New-

onset 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 asthma-

related bronchospasm more likely.)

There appear to be significant differences in the waydifferent 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 thepatient how the current attack compares to prior epi-

sodes. 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 Exacerba tions 

The patient’s 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

Key Points In Treating The Asthmatic Patient1.Most asthmatics can be appropriately assessed

with a history and physical, vital signs, PEFR, or

spirometry and ongoing clinical evaluation. Specific

signs and the severity of the asthmatic’s exacerbation

should guide the addition of extra tests, such as ABG

and chest radiography.

2.Always place the context of the asthmatic’s current

attack into his past history—significant differences in

this presentation should spur consideration of 

alternative or concomitant diagnoses.

3.Every asthmatic requiring more than oneβ-agonist

treatment should receive corticosteroids in the ED and

should be discharged to home on a pulse regimen.

4.Suggest short-term follow-up (within 3-4 days of the ED

visit) to patients with asthma. Tell them to return to the

ED if they get worse.

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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 discontinua-

tion 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 near-

fatal episode of asthma is a risk factor for future life-

threatening attacks; approximately 10% of such patients

die in the year after the event.29

Past M edical History, Social History, Med icat ions 

Obtaining a history of other medical problems, allergies,current medications, and social history is vital to the

course of medical management. The patient with a

history of asthma may also have a history of cardiovascu-

lar disease, pulmonary embolism, or DVT. Ignoring this

history could lead to misfortune if “shortness of breath”

is automatically attributed to asthma. This is especially

important if the patient states that the current problem is

not similar to previous attacks.

Ask patients whether they are using an inhaler, and in

particular whether they are using it with a spacer chamber.

How many puffs a day are they using? Many patients may

list albuterol as one of their medications without informing

the physician that their inhaler is empty. Because propertechnique is critical to the efficacy of an MDI, have them

demonstrate how they use their inhaler. This simple

intervention may have a dramatic impact on their disease if 

they are able to learn the proper technique.

Questioning the patient about tobacco use or exposure

may lead to an explanation for the asthmatic who seems to

 be on the right pharmacologic regimen but continues to

have frequent exacerbations. Finally, the ubiquitous “list of 

meds” can offer insight into both this exacerbation and the

severity of the patient’s asthma. For example, recently

prescribed timolol ophthalmic drops may have worsened

the disease due to their β-blocking effect.

Physical ExaminationBe wary when performing the physical exam. A patient’s

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

a variety of the clinical clues outlined below.

“No one fakes diaphoresis.”

 —  Ancient ED saying

General Appeara nce 

The patient’s 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 patient’s 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

Vita l Signs 

Tachycardia and tachypnea do not always correlate with

the degree of airway obstruction.34,35 Tachycardia will

often resolve with appropriate β-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 arenotoriously inaccurate in patients with tachypnea.

Pulse Oximet ry Pulse oximetry—the “fifth vital sign”—is 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 oxygensaturation (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-than-

sixfold 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

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treatment intervention in adults (if low) or provide reassur-

ance (if high). However, the initial oxygen saturation has

little prognostic utility in the adult asthmatic.42

Head And N eck 

A careful cardiopulmonary evaluation is central to the ED

evaluation. Findings such as increased jugular venous

pressure, lymphadenopathy, and carotid bruits may

signal alternative diagnoses. Pay special attention to the

patient’s neck veins. If they distend during inspiration

(Kussmaul’s sign), then the patient has a significant

increase in right-sided venous pressure that might

possibly be due to right ventricular infarction, tension

pneumothorax, pulmonary embolism, or pericardial

tamponade.43 In the unlikely event of a deviated trachea,

consider the possibility of a tension pneumothorax on the

side opposite the deviation. The strap muscles of the

anterior neck will bulge when the patient is in significant

distress in an attempt to pull air into the lungs. Those in

respiratory distress may breathe with pursed lips.

Pulmonary And Cardiac Exam The chest exam is, of course, central to the evaluation of an asthmatic. Look for intercostal retractions and

accessory muscle use. Next, careful auscultation of the

lungs may reveal wheezing, rhonchi, rales, or a silent

chest. The latter can be ominous, as wheezing can be

absent when airflow is minimal.34

The presence of unilateral wheezing or rales should

lead one to consider the possibility of pneumonia or

other causes of obstruction. Unequal breath sounds

suggest a variety of diagnoses. While this finding may be

present in asthma, it also occurs with pneumothorax,

pulmonary embolism, pneumonia, pleural effusion, or

foreign body. Stridor should be distinguished fromwheezing. When listening with a stethoscope, stridor is

most prominent over the glottis, while wheezing is

louder in the chest fields. Stridor is associated with

tracheal or laryngeal obstruction and is usually more

distinct upon inspiration.

A complete cardiac exam includes evaluation of the

heart sounds. A gallop rhythm, in particular an S3, is

evidence of cardiac failure.

Pulsus paradoxus (> 20 mmHg) is associated with

severe obstruction in some individuals, although it is absent

in up to one-third of severe asthmatics.34 It is not clear that

this finding is useful in clinical practice. No study proves

that it adds any further information to that provided byroutine clinical assessment. In one British trial, pulsus

paradoxus did not correlate with either the severity of acute

asthma in individuals or with peak flow. The authors

suggested that it be abandoned as an indicator of asthma

severity.44 Furthermore, physicians differ widely in their

ability to measure pulsus paradoxus.45

Diagnostic Studies

The therapeutic quandary with asthma is not usually in

the diagnosis, but in the treatment and disposition of the

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

Asthma Index Scores And Pulmonary Function TestsScoring systems are usually employed to help with

management and triage decisions. Asthma index scores,

once commonly used for predicting emergency disposi-

tion and treatment, have proven to be no better than

clinical judgment in predicting outcome.47-49

The peak expiratory flow rate (PEFR) measures the

obstruction in larger airways.50 Beware of the patient

making a poor effort with his peak flow; peak flow data

alone should not dictate disposition but should be used

in the context of the patient’s overall clinical picture.

Despite its shortcomings, PEFRs are easy to obtain,

inexpensive, and less time-consuming than FEV1 mea-

surements. In the appropriate setting, with good patient

cooperation, many emergency physicians consider them

useful. In addition, PEFRs may be used to avoid other

invasive tests (see the “Arterial Blood Gas” section laterin this article).

The forced expiratory volume in the first second

(FEV1) tends to be a more sensitive reflection of the

patient’s overall airway obstruction, as well as the

patient’s ability to ventilate.51 In addition, FEV1 is much

less dependent on patient effort, making it more reliable

than PEFR. However, FEV1 requires a more involved

maneuver and significant patient cooperation.52-55 A pre-

treatment PEFR or FEV1 of less than 50% predicted

indicates severe obstruction.56

The National Guidelines recommend PEFR or FEV1measurements to assist in ED management decisions.

While pulmonary function tests such as PEFR may bevaluable in the home management of asthma, there is

considerable controversy regarding their utility in the

ED. Only one study shows that the use of PEFR initially

and at 30 minutes (combined with assessment of acces-

sory muscle use) might help predict which patients may

require hospitalization.57

However, a better-designed large prospective trial

demonstrated that peak flow rates could not predict

which patients would return to the ED with a relapse.58

Another study looked at the “personal best” PEFR

scores—a value that the asthma guidelines champion as

an important benchmark for ED management—among

inner-city ED patients with acute asthma. The authorsfound that the “personal best” PEFR was inaccurate and

argue that “in contradistinction to NAEPP guidelines,

these values should not be used routinely (or preferen-

tially) as part of the ED discharge decision.”59

Other studies confirm that PEFRs do not correlate well

with need for admission or with return visits to the ED.60,61

Chest RadiographyChest radiography should not be routine in the ED

evaluation of acute asthma. Unless the patient’s 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 asthmat-

ics that identified a “major” abnormality in 34% of chest

radiographs in patients requiring admission for acute

asthma.62 “Major abnormality” included infiltrate, pneu-

mothorax, 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, pneumo-

nia, or foreign body

• Failure to improve in the ED

• Compromised host

• Unexplained fever

Patients with COPD are more likely to have abnor-

malities on chest film, and their need for chest radiogra-

phy depends on a variety of factors.65

Arterial Blood GasMeasurement of arterial blood gases is expensive,

painful, and is occasionally associated with significant

morbidity (arterial thrombosis). It is also unnecessary in

the vast majority of patients who are suffering an acute

exacerbation. ABG may be useful in patients experiencing

severe or prolonged attacks, those with a PEFR or FEV1less than 25% of predicted who appear in significant

distress,56 or in those with altered mental status.

Pulmonary function tests can usually exclude the

possibility of respiratory failure. Martin et al demonstrated

that PEFR accurately predicted hypercarbia or acidosis. Inhis study, no patient with a PEFR greater than 25% pre-

dicted had a PaCO2 greater than 45 or a pH less than 7.35.36

When an ABG is obtained, some pitfalls await the

unwary physician. In the patient with significant tachyp-

nea, a “normal” PaCO2 is actually a worrisome finding,

since the tachypneic patient is expected to be hypocarbic.

A near-normal value reflects the fact that the patient is

tiring and should warn of impending ventilatory failure.

Electrocardiography And Cardiac MonitoringCardiac monitoring and ECG testing are not indicated in

the evaluation of the acute asthmatic unless co-existing

cardiac conditions are suspected. When present, typicalECG patterns include findings consistent with pulmo-

nary disease, including right ventricular strain, right

atrial enlargement or nonspecific ST-T wave abnormali-

ties that resolve with treatment.

Routine Labora tory Evaluation Blood tests, including a complete blood count, are rarely

indicated in the evaluation of acute asthma exacerba-

tions. Again, the exceptions may include those patients in

whom other diagnoses are being considered.

If a CBC is obtained, note that β-agonist therapy and

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 asthmaticshould 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 β-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: β-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, aregenerally reserved for maintenance therapy. Magnesium

is emerging as a treatment for very severe asthma

exacerbations. The role of other agents, including β-

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.

β-agonistsβ-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 bindto 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 Agen ts The older catecholamine bronchodilators include

isoproterenol, isoetharine, and epinephrine. Isoproterenol

is a more selective β-adrenergic agent than epinephrine,

 but a number of deaths were associated with isoproter-

enol inhalation in England in the 1960s. Use of this agent

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is not generally warranted.

Isoetharine is also a more β2-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 β- and α-adrenergic

agonist. While it can be nebulized, it is usually adminis-

tered 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 subcuta-

neous 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 bynewer, 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 β-agonists. Despite its popularity, researchers

have not consistently validated its clinical superiority.69

Other β-agonists include metaproterenol, terbutaline,

fenoterol, and carbuterol. They are similar to albuterol in

that they all share greater β2-specificity and longer

duration of action than the catecholamines.

Levalbuterol And Its Isomer CounterpartsLevalbuterol is the R-isomer of racemic albuterol (a

mixture of 50:50 R- and S-albuterol). The bronchodilatoreffects of racemic albuterol depend on the R-isomer; for

many years, the S-isomer was felt to be biologically

inert.70 However, a more in-depth evaluation of the

S-isomer indicates that it may have pharmacological

properties separate from its R counterpart.71 Theoretically,

levalbuterol could provide equivalent bronchodilatation

to albuterol with fewer side effects. It costs significantly

more than albuterol, and its therapeutic effects have not

 been directly compared to albuterol in patients with acute

exacerbations.72 Even when used on a non-emergent

 basis, the current literature does not uniformly support

the use of levalbuterol over its racemic counterpart.73-75

Routes Of Adm inistra tion 

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

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 compo-

nent 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 β-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 treat-

ments 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).85β-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 theoreti-

cal 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 puffsof albuterol at 10-minute intervals (24 puffs per hour).

Although patients in the MDI and nebulizer group

showed similar improvement, nebulizer therapy pro-

duced greater adverse side effects.88 Other studies have

employed 6-12 puffs per treatment using an albuterol

MDI, even in children.89

Parenteral Therapy 

Parenteralβ-agonist therapy usually involves subcutaneous

injections of epinephrine or terbutaline. These are some-

times 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 advan-

tages of this approach remains unproven.

The evidence regarding the utility of intravenous

β-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 β-agonists is generally discour-

aged.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 astremor 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

GlucocorticoidsEarly 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 β-adrenergic responsiveness in the

constricted airways. Accepted dosage regimens in adults

include prednisone (40-60 mg PO), a 60-125 mg intrave-

nous 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 exacerba-

tion,100 though it is commonplace for adult patients toreceive 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 pla-

cebo.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 10-

day 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 (approxi-

mately 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 investiga-tion 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 standardtherapy (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 β-agonists, and reported an improved

quality of life over the next 21 days.

AnticholinergicsAnticholinergic therapy, including ipratropium bromide

and glycopyrrolate, antagonizes the neuromuscular

transmitter acetylcholine at the postganglionic parasympa-

thetic receptor, which reduces vagally mediated

 bronchoconstriction in the larger central airways. Anticho-

linergic bronchodilation peaks within 1-2 hours. Simulta-

neous treatment with β-adrenergic agents and anticholin-

ergics 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 β-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 demon-

strated 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 β-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-dosestudies 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 β-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 aero-

solized 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.

MagnesiumMagnesium sulfate is efficacious for the relief of severe

 bronchoconstriction but adds little to the treatment of mild-

to-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 

magnesium over 10-15 minutes.

Magnesium is now being used as a vehicle for

nebulized albuterol. In acute asthma, nebulized magne-

sium-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 beconsidered 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 OxideInhaled 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 me-

chanical ventilation. Four showed a greater than 20%

decrease in baseline PaCO2 soon after the administration

of inhaled NO.128

AnestheticsCertain 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 inconsultation with the anesthesiologist.

Leukotriene-Receptor AntagonistsLeukotriene modifiers result in improved lung function,

diminished symptoms, and less need for short-acting

β-agonists over a wide spectrum of asthma severity.

However, they are not currently indicated for acute

exacerbations.131 In one ED study, patients were given

either 10 mg chewable montelukast or placebo within 20

minutes of presentation (in addition to standard therapy).

There were no significant differences in the final PEFR

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scores or the need for hospitalization.132

Lidocaine And Anti-HypertensivesLidocaine surfaces in anecdotal reports as an agent that

may succeed when conventional therapies fail.133 Despite

these reports, prospective study into this choice of 

pharmacologic therapy is needed. Likewise, reports of 

improvement with calcium-channel blockers and

clonidine should spur further investigation into their

possible role in the acute treatment of asthma.134

 Theophylline—The Drug That Won’t DieTheophylline/aminophylline is not generally recom-

mended therapy in the ED. The vast majority of studies

show that it provides no additional benefit to short-acting

inhaled β-agonists and frequently causes adverse

effects.135-140 In hospitalized patients, most data indicate

that intravenous methylxanthines are not beneficial in

children with severe asthma,141-143 and they remain

controversial for adults.144,145 While the occasional study

suggests some positive effect in severely ill children

unresponsive to standard treatment,146

 its marginal benefit and poor safety profile argue against routine use.

 Therapies Not RecommendedFor Treating ExacerbationsNarcotics, sedatives, and tranquilizers should be avoided in

an acute asthmatic because respiratory arrest may occur

after their use. The combative asthmatic is more likely to

need aggressive therapy or even intubation than sedation.

Mucolytics, expectorants, and aggressive hydration do not

aid in the treatment of asthma. A meta-analysis regarding

the use of antihistamines in adult asthmatics showed that

these agents increase side effects without improving

pulmonary function. The literature does not generallysupport their use.147 While some physicians prescribe

antihistamines for allergen- and exercise-induced asthma,

the scientific basis for this remains thin.

Nedocromil and cromolyn inhibit mast cell mediator

release through the blockage of chlorine channels.

Although efficacious in preventing the acute release of 

these pro-inflammatory cytokines, mast cell mediators

play no role in the actively wheezing patient.

Continuous infusions of ketamine have been

occasionally used as an adjunct to treat status

asthmaticus in the non-intubated patient.148 However, a

randomized trial suggests ketamine infusion is not useful

in this situation.149

Many alternative or complementary medicine

therapies are used to treat asthma. Of note, manual

therapy (performed by chiropractors, respiratory thera-

pists, or osteopaths) is sometimes touted to improve lung

function. There are no data or very poor data to suggest

that any manual therapy is appropriate to treat patients

with asthma.150 Likewise, no well-controlled trials

support the use of other alternative therapies (acupunc-

ture, homeopathy). Currently, these have no place in the

acute or long-term treatment of asthma.151,152

Airway Management

IntubationIf the patient deteriorates or fails to improve despite

intensive therapy, intubation and mechanical ventilation

must be considered. Fortunately, fewer than 1% of asthmat-

ics 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 vigor-ous 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 conten-

tion is difficult to prove one way or another.

Intubation of the asthmatic patient is a daunting task

fraught with potential for serious complications. Rapid-

sequence intubation is the method of choice. (For a full

discussion of airway management, please see the May 2000

issue of Emergency Medicine Practice, “Emergency Endotra-

cheal 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.155,156Consider 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 is-

chemic 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 pro-

longed 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 patient’s 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 patient’s minute ventilation.

As mentioned, this lowered minute ventilation to

decrease hyperinflation often results in hypercapnia and

 Ten Excuses That Don’t Work In Courthe’s obviously in need of additional treatment or he

wouldn’t have come to the ED.

6. “I didn’t instruct him how to use the MDI because they

are so simple to use.”

Every patient should be instructed on the proper use

of the MDI and discharged with a spacer (or a prescription

for a spacer) to accompany it. If the patient has the

medication but can’t use the delivery device properly,

he is in a canoe without a paddle—and possibly up some

sort of creek.

7. “After intubating him, I just figured a large tidal volume

would open his airway. How was I supposed to know we

were out of chest tubes?”Intubating asthmatics is fraught with difficulty, and the

emergency physician must be acutely aware of the possible

complications, including high airway pressures leading to

barotrauma. Consider lower tidal volumes (5-7 cc/kg) and

monitor the plateau pressures. If they arrest on the

ventilator, decompress the chest!

8. “I reserve ipratropium for elderly COPD patients.”

Anticholinergics are indicated for moderate-to-severe

asthma exacerbations. They are safe, effective, and offer at

least some benefit to many asthmatics.

9. “Of course I’m sorry he died, but no one can predict whowill have a fatal attack.”

Not quite true. The past may guide the future. Patients with

a history of prior intubations or intensive care admissions

are more likely to suffer fatal asthma in the future. Ask.

10. “I thought a small dose of midazolam would help

relax him.”

Make sure you aren’t making a patient permanently

relaxed. Most asthmatics who are in distress are not

breathing well. Their distress will resolve with treatment of 

their primary respiratory disease, not their anxiety.

1. “Really, he wasn’t wheezing when I discharged him. It’s

right there on the chart.”

Other things are on the chart as well. The nurse

documented that the respiratory rate was 35 and the room

air pulse oximetry was 90%. The patient wasn’t wheezing

because he still wasn’t moving any air.

No wheezing can be a very ominous sign in the

asthmatic. Interpret a silent chest on initial evaluation or 

after pharmacologic interventions in the clinical context of 

the patient—somnolence with this physical exam finding

necessitates immediate intervention, including the

possibility of invasive ventilation.

2. “Really, he wasn’t wheezing when I first evaluated him.”

Ditto.

3. “I thought I would let his primary doctor start him

on steroids.”

Steroids play an integral role in the treatment of an acute

asthma exacerbation, and nearlyall  asthmatics should be

discharged with a pulse-course of oral steroids (except

those with minimal symptoms who responded to a single

inhalation treatment). Inhaled or intramuscular steroids

remain other options.

 4. “He couldn’t move the peak-flow meter, but I just

assumed he wasn’t cooperating.”

If the PEFR is documented, then be prepared to use thedata. If a patient has a difficult time using this device,

document other indicators of the patient’s improvement

(such as an ability to count to five or speak in full

sentences). Documenting a smiling patient who states,“I

feel great, doc!”may be as useful as a“good”peak flow.

5. “He had just used hisβ-agonists at home, so I thought I

would wait to treat him.”

Let the patient’s presentation dictate the treatment—if he

is in distress and wheezing, start therapy. No matter how

much pharmacologic intervention he received at home,

8/9/2019 Emp Asthma

12/28Emergency Medicine Practice 12 February 2001

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 corticosteroid-

treated 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 patient’s comorbid medical conditions.

Once a patient has been intubated and initial ventila-

tory management determined, β-agonist therapy must be

Cost-Effective Strategies For Patients With Asthma2. Give the patient a spacer.

Only 40% of ED asthma patients own a spacer.208 Increase this

number to 100% by dispensing them in the ED. Patients can

even make their own spacer using a 500 mL plastic bottle. A

sealed 500 mL soda bottle produces similar bronchodilation

when compared to a conventional spacer in children with

asthma.227 (Whether Coke or Pepsi bottles yield better PEFRs

remains to be studied.)

Even giving the patient a nebulizer can be cost-effective.

In one study, providing home nebulizers for selected

outpatients resulted in significant savings due to reduced ED

and office visits.228

4. Avoid unnecessary antibiotics.

Many healthy young adults with wheezing are given

antibiotics for“bronchitis.”Most of these patients have

a virus that results in reactive bronchospasm. Randomized,

placebo-controlled trials do not support routine antibiotic

treatment of uncomplicated acute bronchitis. However,

RCTs do show that inhaled albuterol decreases the

duration of cough in adults with uncomplicated acute

bronchitis.229 Despite this fact, as many as 74% of patients

with acute uncomplicated bronchitis are given antibiotics,

while only about 17% receive bronchodilators.230 These

numbers should be reversed. (Better yet, no antibiotics and

100% bronchodilators.)

Risk-Man agem ent Caveat: Antibiotics are certainly indicated

in asthmatics who suffer concurrent pneumonia. They also

decrease the relapse rate for patients with an acute

exacerbation of COPD.231

Strategies For Indigent Patients

1. Give the patient discharge medications such as an MDI

and steroids.

One study showed that providing medications and

increasing the use of steroids decreased“bounce-backs”in

patients with asthma.232

2. Consider the use of intramuscular steroids for non-

compliant patients.

Intramuscular steroids are therapeutically equivalent to a

week’s therapy with oral steroids.

Strategies That Focus On ED Care

1. Increase the ED use of MDIs and spacers, as opposed to

nebulizers.

MDIs plus spacers are at least as effective and less expensive

than nebulizer therapy.

Risk-Mana gem ent Caveat: These devices are less wellstudied in the moribund asthmatic.

2. Use oral instead of parenteral steroids.

 There is no convincing evidence that intravenous steroids

are more effective than the less expensive oral route. In

one pediatric study of severe asthma, there was no

difference in length of hospital stay between asthmatic

patients receiving oral prednisone and those receiving

intravenous methylprednisolone.225

Risk-Mana gem ent Caveat: Moribund patients as well as

those who are vomiting may require intravenous steroids.

Consider intramuscular steroids for non-compliant or

indigent patients (see below).

3. Avoid unnecessary laboratory tests.

Most asthmatics will not require bloodwork. The CBC is rarely

helpful. If you suspect pneumonia, order a chest x-ray, not a

CBC. Blood gases are seldom necessary. A pulse ox will detect

hypoxia, and a patient with a PEFR above 25% of predicted

will rarely (if ever) be hypercarbic.

Risk-Mana gem ent Caveat: Patients taking theophylline

(especially those who are tremulous and vomiting) may be

theophylline toxic and will require a blood level.

4. Avoid unnecessary x-rays.

Most patients with a history of asthma who present with

wheezing will not require chest film.

Risk-Mana gem ent Caveat: If you suspect pneumonia,

foreign body, congestive heart failure, or other asthma

mimics, get the film.

Strategies That Focus On Preventing Relapse

1. Educate the patient.

Patient education programs can decrease ED visits.226 This

education ranges from the proper use of the MDI to

developing an action plan for exacerbations.

8/9/2019 Emp Asthma

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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 docu-

mented 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

ventilator—then 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 em-

ployed in the ED setting.

Non-Invasive Ventilation

Non-invasive ventilation (NIV) offers an attractivealternative 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 hypercapnicpatients, 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 β-agonists given

via BiPAP appear to be more effective than those admin-

istered 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

strangulation…they breathe standing, as if desiring to draw in

all the air which they possibly can inhale.” —  Aretaeus the Cappadocian (81-138?) on asthma 176

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

Pregnant PatientsAsthma affects approximately 4% of pregnant women. Of 

these, approximately one-third improve during preg-

nancy, one-third remain unchanged, and one-third

 become worse.177,178 Forty-two percent of pregnant

asthmatics will require hospitalization, and up to 18%

will present to the ED one or more times for an acute

exacerbation.179 Multiple factors may contribute to the

change in a pregnant asthmatic’s disease, but the impor-

tant 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 essen-

tially 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 β-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 likelyto receive this therapy when compared to their non-

pregnant 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 PatientsElderly 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 staysand 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 wheez-

ing may be in CHF.

Be particularly aware of medication side effects in

the elderly—for example, steroids in the diabetic or

theophylline in the patient with underlying coronary

artery disease. Though the emergency physician didn’t

start the theophylline, consider that he or she might betreating 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 PatientsChildren with asthma are treated in a similar manner to

the adult: β-agonists, anticholinergics, and systemic

steroids. Assess fluid status and make appropriate

corrections for infants and children, particularly in theCont inued on page 17 

8/9/2019 Emp Asthma

14/28Emergency Medicine Practice 14 February 2001

Clinical Pathway: Management Of PatientsWith An Acute Asthma Exacerbation

 Theevidence for recommendations 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 IIb:Acceptable and useful.

Fair-to-good evidence provides support.Class III: Not acceptable, not useful, may be harmful. Indeterminate:Continuing area of research.

This cl inical path way is intended to supplement, rather tha n subst i tute, professional judg ment and may b e changed depending u pon a 

pat ient  ’ s individual needs. Fai lure to com ply w i th t his pathw ay does not represent a breach of th e stand ard of care.

Copyright © 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limitedcopying privileges for educational distribution within your facility or program. Commercial distribution topromote any product or service is strictly prohibited.

Is the patient stable?

Is the patient improving?

• ABCs• IV/O

2/Monitor*

• Physical exam

• Vital signs    →   

• Inhaledβ2-agonists by MDI or nebulizer (Class IIa)

• O2 as needed to keep saturation > 90%

• Multiple-dose ipratropium for moderate-to-severeattacks (Class IIb)

• Systemic corticosteroids* (Class IIa)

Prepare for intubation• Continuousβ

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

8/9/2019 Emp Asthma

15/2815 Emergency Medicine PracticeFebruary 2001

Clinical Pathway: Management Of PatientsWith An Acute Asthma Exacerbation(continued)

 Theevidence for recommendationsis graded using the following scale. Forcomplete definitions, see back page.Class I: Definitely recommended.Definitive, excellent evidence providessupport.Class II a:Acceptable and

useful. Very good evidence providessupport.Class IIb:Acceptable anduseful. Fair-to-good evidence providessupport.Class III: Not acceptable, notuseful, may be harmful.Indetermi-

nate:Continuing area of research.

This cl inical pat hwa y is intended to supplement, rather than subst i tute, professional judg ment and may be changed depending u pon a 

pat ient  ’ s indiv idua l needs. Failure to com ply wit h th is pat hw ay does not repr esent a breach of th e stan dard o f care.

Copyright © 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limitedcopying privileges for educational distribution within your facility or program. Commercial distribution topromote any product or service is strictly prohibited.

No

    →   

  → Yes

   →       →   

Mild to minimal exacerbation?• Asymptomatic

• Normal physical examination• PFTs > 70%

Moderate exacerbation?• Moderate symptoms present

• PFTs 50%-80% predicted/personal best

Severe exacerbation?• Symptoms at rest, retractions,

accessory muscle use• No improvement

• FEV1 or PEFR < 50% predicted/

personal best

Discharge to home

• β2-agonist MDIs (Class IIa)

• Systemic corticosteroids (Class IIa)• Patient education (Class indeter-

minate)• Early outpatient follow-up• Consider inhaled steroids (Class

indeterminate)

• Continue treatment for 1-3 hours(Class indeterminate)

• β2-agonists (Class IIa)

• Anticholinergics (Class IIa)

• Corticosteroids (Class IIa)

Continue treatmentsOR 

• Continuous aerosols withβ2-agonists

(Class IIb)• Multiple-dose anticholinergics

(Class IIb)

• Intravenous corticosteroids (Class IIa)• Consider magnesium 2 g IV (Class IIb)

      →   

     →        

 →   

How isthe patient

responding?  →

                        →

   →   

Good response• Response sustained longer

than 60 minutes• Physical exam normal• FEV

1 or PEFR > 70%

Incomplete response• Mild to moderate symptoms

• Persistent wheezing• FEV

1 or PEFR > 50% and < 70%

Reassess need

for intubation

Discharge to home• β

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 (Classindeterminate)

OR • Admit to clinical

observation unit

(Class indetermi-nate)OR 

• Admit to hospital

floor (Classindeterminate)

• β2-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)• β

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)

• Consider need for alternative therapies if continued deterio-

ration or failure to improve (Class indeterminate)• Magnesium 2 g IV (Class IIb)

• Intravenousβ-agonists (continuous drip) (Class indetermi-nate)

• Heliox (Class indeterminate)• Inhalation anesthesia (Class indeterminate)• BiPAP if not intubated (Class indeterminate)

Poor response

• PCO2 > 42mmHg

• Drowsiness or confusion• FEV

1 or PEFR < 50%

• Proceedwith RSI

• Low tidal

volumes• ABG

8/9/2019 Emp Asthma

16/28Emergency Medicine Practice 16 February 2001

Clinical Pathway: Ventilatory Management Of The Asthmatic

 Theevidence for recommendations 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 IIb:Acceptable and useful.

Fair-to-good ev