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7/28/2019 Asthma an Evidence Based Management Update
1/28
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.
Date of original release: February 9, 2001.
Date of most recent review: February 7, 2001.
See Physician CME Information on back page.
EMERGENCYMEDICINEPRACTICEAN EVIDENCE-BASED A PPROACH T O EMERGENCY MEDI CINE
Editor-in-Chief
Stephen A. Colucciello, MD, FACEP,Assistant Chair, Director ofClinical Services, Department ofEmergency Medicine, CarolinasMedical Center, Charlotte, NC;
Associate Clinical Professor,Department of EmergencyMedicine, University of NorthCarolina at Chapel Hill, ChapelHill, NC.
Associate Editor
Andy J agoda, 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 ofNew 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 PainStrokeCenter, 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, Childrens 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 ofEmergency 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 ofMedicine, Los Angeles, CA.
John A. Marx, MD,Chair and Chief,
Department of EmergencyMedicine, Carolinas MedicalCenter, Charlotte, NC; ClinicalProfessor, Department ofEmergency 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 ofEmergency 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 boys neck muscles strain, his chest heaves, but you
detect no breath sounds as you quickly listen to his lungs. As the team moves
him to the ED stretcher, the terrified light in his eyes begins to dim, and the
gasps start to quiet. This young asthmatic is slipping away.
In the past two decades, our knowledge and understanding of the
pathophysiology and treatment of asthma has steadily increased. We 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 ofEmergency 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
7/28/2019 Asthma an Evidence Based Management Update
2/28Emergency Medicine Practice 2 February 2001
Asthma is the third-leading cause of preventable
hospitalization in the United States7 and each year
accounts for approximately 2 million visits to the nations
EDs.8 The direct costs for the treatment of asthma are
projected to have been higher than $14.5 billion in the
year 2000, more than double the cost one decade ago.4
Although asthma is characterized by reversible airflow
obstruction, it is a chronic disease with long-term 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. (SeeTable 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 -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 ofpro-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
7/28/2019 Asthma an Evidence Based Management Update
3/283 Emergency Medicine PracticeFebruary 2001
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 patients appearance,
vital signs, and chest examination. If needed, aggressive
therapy directed at relieving airway obstruction must
begin as soon as the diagnosis is suspected.
HistoryThe patients history will not only help determine the
course of immediate treatment in the ED, but it will also
place the exacerbation in the context of the disease.
History Of Present IllnessEstablish 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 attackfeels 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 ExacerbationsThe patients history offers the backdrop for his current
exacerbation. Does the patient have a history of asthma?
Many patients will report no history of asthma but admit
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 asthmatics exacerbation
should guide the addition of extra tests, such as ABG
and chest radiography.
2.Always place the context of the asthmatics current
attack into his past historysignificant differences in
this presentation should spur consideration of
alternative or concomitant diagnoses.
3.Every asthmatic requiring more than one-agonist
treatment should receive corticosteroids in the ED and
should be discharged to home on a pulse regimen.
4.Suggest short-term follow-up (within 3-4 days of the ED
visit) to patients with asthma. Tell them to return to the
ED if they get worse.v
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they wheeze all the time or have lots ofbronchitis
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 Medical History, Social History, Medications
Obtaining a history of other medical problems, allergies,current medications, and social history is vital to the
course of medical management. The patient with a
history of asthma may also have a history of cardiovascu-
lar disease, pulmonary embolism, or DVT. Ignoring this
history could lead to misfortune ifshortness 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 patients asthma. For example, recently
prescribed timolol ophthalmic drops may have worsened
the disease due to their -blocking effect.
Physical ExaminationBe wary when performing the physical exam. A patients
ventilatory status can change rapidly. Remember that
patients with no wheezing may actually be in extremis;
they cannot move enough air to produce the turbulent
whistle of asthma. Such patients, however, will appear
dyspneic and will not be able to speak normally. Others
who are just holding their own may tire and rapidly
become acidotic and hypercarbic. Many experienced
physicians use their gestalt to rapidly assess the severity
of distress. They may overtly or subliminally incorporate
a variety of the clinical clues outlined below.
No one fakes diaphoresis.
Ancient ED saying
General AppearanceThe patients general appearance will often determine the
pace of subsequent interventions. Upon entering the room,
assess for the general level of distress. A patient who is
sweating and unable to speak in full sentences is in trouble.
The number of seconds a patient can spend counting
correlates well with pulmonary function.30 In the first
several moments, quickly appraise the patients mental
status. Both lethargy and agitation presage respiratory
failure. Cyanosis is a very late finding in asthma. By the
time it appears, it is likely that the patient is moribund.31
While these suggestions are considered common
knowledge, studies that focus on clinical examination
show that inter-observer agreement regarding respiratory
signs in adults is low.32 However, one study indicates that
inter-observer agreement may be better in the assessment
of acute asthma in children.33
Vital SignsTachycardia and tachypnea do not always correlate with
the degree of airway obstruction.34,35 Tachycardia will
often resolve with appropriate -agonist therapy, not
worsen. A decreasing respiratory rate can simply mean
the patient is tiring, rather than improving.
There is little research that examines the relationship
of blood pressure to respiratory distress. However, if the
blood pressure is extremely high (or extremely low),
consider cardiac etiologies such as CHF or cardiogenic
shock in the differential diagnosis of wheezing.
If the determination of fever is important, consider
obtaining a rectal temperature. Oral temperatures arenotoriously inaccurate in patients with tachypnea.
Pulse OximetryPulse oximetrythe fifth vital signis often useful in
the assessment of asthma. It will rapidly alert the ED staff
to hypoxia and the need for supplemental oxygen.
Hypoxemia generally reflects the extent of ventilation/
perfusion mismatch.36 Remember, however, that pulse
oximetry does not reflect ventilation status. Patients with
near-normal saturations while on oxygen may be
hypercarbic and in danger of incipient respiratory failure.
Pulse oximetry may also predict the need for
admission in children. Children with initial low 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
7/28/2019 Asthma an Evidence Based Management Update
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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 NeckA careful cardiopulmonary evaluation is central to the ED
evaluation. Findings such as increased jugular venous
pressure, lymphadenopathy, and carotid bruits may
signal alternative diagnoses. Pay special attention to the
patients neck veins. If they distend during inspiration
(Kussmauls sign), then the patient has a significant
increase in right-sided venous pressure that might
possibly be due to right ventricular infarction, tension
pneumothorax, pulmonary embolism, or pericardial
tamponade.43 In the unlikely event of a deviated trachea,
consider the possibility of a tension pneumothorax on the
side opposite the deviation. The strap muscles of the
anterior neck will bulge when the patient is in significant
distress in an attempt to pull air into the lungs. Those in
respiratory distress may breathe with pursed lips.
Pulmonary And Cardiac ExamThe chest exam is, of course, central to the evaluation ofan 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 patients 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
patients overall airway obstruction, as well as the
patients ability to ventilate.51 In addition, FEV1 is much
less dependent on patient effort, making it more reliable
than PEFR. However, FEV1 requires a more involved
maneuver and significant patient cooperation.52-55 A 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
scoresa value that the asthma guidelines champion as
an important benchmark for ED managementamong
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 patients history
or physical exam suggests the possibility of additional or
7/28/2019 Asthma an Evidence Based Management Update
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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.62Major 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 Laboratory EvaluationBlood 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 -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 -agonists
(e.g., subcutaneous terbutaline or epinephrine) may
replace or be combined with aerosolized treatments.
Assess the improvement of that patient with several
measures: mental status, air exchange, oxygenation, and
ventilation. Progressive deterioration or failure to
improve with maximal therapy may require intubation.
Thankfully, the majority of asthmatics who present to the
ED will not require such extreme measures.
The most standard therapies can be grouped
into three primary categories: -adrenergic agonists,
glucocorticoids, and anticholinergics. A fourth category
of drugs, the methylxanthines, has no significant role in
emergency management, while a fifth and sixth category
of drugs, the cromones and leukotriene modifiers, aregenerally reserved for maintenance therapy. Magnesium
is emerging as a treatment for very severe asthma
exacerbations. The role of other agents, including -
agonist isomers (e.g., levalbuterol), heliox, anesthetics,
and anti-hypertensive agents are currently the topics of
intensive clinical research in the management of acute
asthma exacerbations.
-agonists-adrenergic agonists are the mainstays in the treatment
of acute bronchospastic disease. They exert their effects
by increasing cyclic adenosine monophosphate (cAMP).
A series of interactions cause intracellular calcium to 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 AgentsThe older catecholamine bronchodilators include
isoproterenol, isoetharine, and epinephrine. Isoproterenol
is a more selective -adrenergic agent than epinephrine,
but a number of deaths were associated with 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 2-selective agent than
epinephrine and is as effective a bronchodilator as
albuterol.67 It is available as a metered-dose inhaler or as
an aerosol solution. Doses may be repeated every 20-30
minutes during an acute attack.
Epinephrine is a nonselective - and -adrenergic
agonist. While it can be nebulized, it is usually 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 -agonists. Despite its popularity, researchers
have not consistently validated its clinical superiority.69
Other -agonists include metaproterenol, terbutaline,
fenoterol, and carbuterol. They are similar to albuterol in
that they all share greater 2-specificity and longer
duration of action than the catecholamines.
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 AdministrationAerosol 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
DosageThe most effective dose of inhaled -agonist remains
unknown. Standard doses of albuterol for adults range from
2.5-5.0 mg per treatment; however, continuous nebulization
may involve administering 20 mg or more per hour. In one
study, two 5.0 mg treatments of aerosolized albuterol at a
40-minute interval were more effective than three 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).85-agonist doses may be administered nebulized
every 15-20 minutes or as a continuous aerosol.86 Recent
literature has failed to demonstrate the superiority of
either method.87 Continuous nebulization has a 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 TherapyParenteral-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
-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 TherapyOral administration of-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 nebulizedbronchodilator aerosol and given urgently to those who
appear in moderate to severe distress.
While the exact mechanism of action is unclear, one
theory proposes a reduction of airway inflammation, as
well as restoration of-adrenergic responsiveness in the
constricted airways. Accepted dosage regimens in adults
include prednisone (40-60 mg PO), a 60-125 mg 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 -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 -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 -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 -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 -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
-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
TheophyllineThe Drug That Wont 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 -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 marginalbenefit 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 ofEmergency 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 patients ongoing risk for barotrauma or
volutrauma is his end inspiratory volume, which is a
measure of dynamic hyperinflation.163 Because this is
difficult to measure, a practical substitute is the plateau
pressure (Pplat), which reflects the pressure in the alveoli.
The goal should be to keep Pplat less than 30 cmH2O; if the
plateau pressure is consistently higher than this, lower
the patients minute ventilation.
As mentioned, this lowered minute ventilation to
decrease hyperinflation often results in hypercapnia and
Ten Excuses That Dont Work In Courthes obviously in need of additional treatment or he
wouldnt have come to the ED.
6. I didnt instruct him how to use the MDI because they
are so simple to use.
Every patient should be instructed on the proper use
of the MDI and discharged with a spacer (or a prescription
for a spacer) to accompany it. If the patient has the
medication but cant use the delivery device properly,
he is in a canoe without a paddleand possibly up some
sort of creek.
7. After intubating him, I just figured a large tidal volume
would open his airway. How was I supposed to know we
were out of chest tubes?Intubating asthmatics is fraught with difficulty, and the
emergency physician must be acutely aware of the possible
complications, including high airway pressures leading to
barotrauma. Consider lower tidal volumes (5-7 cc/kg) and
monitor the plateau pressures. If they arrest on the
ventilator, decompress the chest!
8. I reserve ipratropium for elderly COPD patients.
Anticholinergics are indicated for moderate-to-severe
asthma exacerbations. They are safe, effective, and offer at
least some benefit to many asthmatics.
9. Of course Im sorry he died, but no one can predict 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 arent making a patient permanently
relaxed. Most asthmatics who are in distress are not
breathing well. Their distress will resolve with treatment of
their primary respiratory disease, not their anxiety.v
1. Really, he wasnt wheezing when I discharged him. Its
right there on the chart.
Other things are on the chart as well. The nurse
documented that the respiratory rate was 35 and the room
air pulse oximetry was 90%. The patient wasnt wheezing
because he still wasnt moving any air.
No wheezing can be a very ominous sign in the
asthmatic. Interpret a silent chest on initial evaluation or
after pharmacologic interventions in the clinical context of
the patientsomnolence with this physical exam finding
necessitates immediate intervention, including the
possibility of invasive ventilation.
2. Really, he wasnt wheezing when I first evaluated him.
Ditto.
3. I thought I would let his primary doctor start him
on steroids.
Steroids play an integral role in the treatment of an acute
asthma exacerbation, and nearlyallasthmatics should be
discharged with a pulse-course of oral steroids (except
those with minimal symptoms who responded to a single
inhalation treatment). Inhaled or intramuscular steroids
remain other options.
4. He couldnt move the peak-flow meter, but I just
assumed he wasnt cooperating.
If the PEFR is documented, then be prepared to use thedata. If a patient has a difficult time using this device,
document other indicators of the patients 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 agoodpeak flow.
5. He had just used his-agonists at home, so I thought I
would wait to treat him.
Let the patients presentation dictate the treatmentif he
is in distress and wheezing, start therapy. No matter how
much pharmacologic intervention he received at home,
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respiratory acidosis. A PaCO2 as high as 80 mmHg, resulting
in a pH of 7.15, is well within the acceptable limits for this
type of ventilatory management. Indeed, multiple studies
have shown minimal adverse effects from this
hypoventilation and clearly improved outcomes resulting
from a lower incidence of barotrauma.164-167 Few relative
contraindications exist for permissive hypercapnia, but they
include severe hypertension, severe metabolic acidosis, and
severe hypoxemia.153
Any patient undergoing hypoventilation will require
heavy sedation and at times the use of neuromuscular-
blocking agents, as this type of ventilatory management
is usually poorly tolerated. Although 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 patients comorbid medical conditions.
Once a patient has been intubated and initial ventila-
tory management determined, -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 forbronchitis.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.230These
numbers should be reversed. (Better yet, no antibiotics and
100% bronchodilators.)
Risk-Management Caveat:Antibiotics are certainly indicated
in asthmatics who suffer concurrent pneumonia. They also
decrease the relapse rate for patients with an acute
exacerbation of COPD.231
Strategies For Indigent Patients
1. Give the patient discharge medications such as an MDI
and steroids.
One study showed that providing medications and
increasing the use of steroids decreasedbounce-backsin
patients with asthma.232
2. Consider the use of intramuscular steroids for non-
compliant patients.
Intramuscular steroids are therapeutically equivalent to a
weeks therapy with oral steroids.v
Strategies That Focus On ED Care
1. Increase the ED use of MDIs and spacers, as opposed to
nebulizers.
MDIs plus spacers are at least as effective and less expensive
than nebulizer therapy.
Risk-Management Caveat:These devices are less 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-Management Caveat:Moribund patients as well as
those who are vomiting may require intravenous steroids.
Consider intramuscular steroids for non-compliant or
indigent patients (see below).
3. Avoid unnecessary laboratory tests.
Most asthmatics will not require bloodwork. The CBC is rarely
helpful. If you suspect pneumonia, order a chest x-ray, not a
CBC. Blood gases are seldom necessary. A pulse ox will detect
hypoxia, and a patient with a PEFR above 25% of predicted
will rarely (if ever) be hypercarbic.
Risk-Management Caveat:Patients taking theophylline
(especially those who are tremulous and vomiting) may be
theophylline toxic and will require a blood level.
4. Avoid unnecessary x-rays.
Most patients with a history of asthma who present with
wheezing will not require chest film.
Risk-Management Caveat:If you suspect pneumonia,
foreign body, congestive heart failure, or other asthma
mimics, get the film.
Strategies That Focus On Preventing Relapse
1. Educate the patient.
Patient education programs can decrease ED visits.226This
education ranges from the proper use of the MDI to
developing an action plan for exacerbations.
7/28/2019 Asthma an Evidence Based Management Update
13/2813 Emergency Medicine PracticeFebruary 2001
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
ventilatorthen place bilateral chest tubes.) Tension
pneumothorax is an important cause of sudden death in
the intubated asthmatic.
In patients with persistent and markedly elevated
peak pressures, high-frequency jet ventilation may
improve gas exchange.170 This, however, is rarely 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-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
strangulationthey 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 asthmatics 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 -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 elderlyfor example, steroids in the diabetic or
theophylline in the patient with underlying coronary
artery disease. Though the emergency physician didnt
start the theophylline, consider that he or she might 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: -agonists, anticholinergics, and systemic
steroids. Assess fluid status and make appropriate
corrections for infants and children, particularly in theContinued on page 17
7/28/2019 Asthma an Evidence Based Management Update
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 IIa: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 clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon apatients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber 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
Inhaled2-agonists by MDI or nebulizer (Class IIa)
O2as needed to keep saturation > 90%
Multiple-dose ipratropium for moderate-to-severeattacks (Class IIb)
Systemic corticosteroids* (Class IIa)
Prepare for intubation Continuous
2-agonists 0.1 mg/kg/h (Class IIb) OR
Subcutaneous terbutaline 10 mcg/kg (Class IIb)OR Consider subcutaneous epinephrine 0.01 mg/kg (Class
IIb)PLUS
Ipratropium bromide 0.5 mg >10 kg
7/28/2019 Asthma an Evidence Based Management Update
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 IIa: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 clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon apatients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber 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
FEV1or PEFR < 50% predicted/
personal best
Discharge to home
2-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)
2-agonists (Class IIa)
Anticholinergics (Class IIa)
Corticosteroids (Class IIa)
Continue treatmentsOR Continuous aerosols with
2-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
1or PEFR > 70%
Incomplete response Mild to moderate symptoms
Persistent wheezing FEV
1or PEFR > 50% and < 70%
Reassess need
for intubation
Discharge to home
2-agonist MDIs (Class IIa)
Systemic corticosteroids
(Class IIa) Patient education (Class
indeterminate) Early outpatient follow-up Consider inhaled steroids
(Class indeterminate)
Continued ED
therapy (Classindeterminate)
OR Admit to clinical
observation unit
(Class indetermi-nate)OR
Admit to hospital
floor (Classindeterminate)
2-agonists
(Class IIa) Anticholinergics
(Class IIa)
Systemic
corticosteroids(Class IIa)
Monitor FEV1and
O2saturations
(Class IIb)
Admit to hospital ICU or stepdown unit (Class indeterminate)
2-agonists hourly or continuously (Class IIb)
Anticholinergic agents (Class IIa) Systemic corticosteroids (Class IIa) Oxygen Chest x-ray (Class IIb)
Consider ABG (Class IIb)
Consider need for alternative therapies if continued deterio-
ration or failure to improve (Class indeterminate) Magnesium 2 g IV (Class IIb)
Intravenous-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
1or PEFR < 50%
Proceedwith RSI
Low tidal
volumes ABG
7/28/2019 Asthma an Evidence Based Management Update
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 IIa: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 clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon apatients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limitedcopying privileges for educational distribution within your facility or program. Commercial distribution topromote any product or service is strictly prohibited.
Physiological
objectives achieved?
Physiological objective achieved?
LEGENDFiO
2= fraction of inspired oxygen
VT
= tidal volumeRR = respiratory ratePEEP = positive end-expiratory pressureP
plat= plateau airway pressure
SIMV = synchronized intermittent mandatory ventilationNMB = neuromuscular blockade
Initial ventilator settings:
Mode = Assist control, FiO2= 1.0
RR = 8-10/min, VT
= 80-100 L/minPEEP = 0, sensitivity = 1.0 cmH
2O (Class indeterminate)
Physiological objectives:
Pplat
< 30 cmH2O (Class indeterminate)
NoYes
Reduce minute ventilation
(may require heavy sedat
Recommended