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Acute asthma exacerbations in children: Emergency department managementAuthorRichard J Scarfone, MD, FAAPSection Editors

Robert A Wood, MDGregory Redding, MDDeputy EditorElizabeth TePas, MD, MS

All topics are updated as new evidence becomes available and ourpeer review processis complete.

Literature review current through: Jun 2014. | This topic last updated: Mar 25, 2014.

INTRODUCTIONClinical decision-making in the management of the child with an acute asthma exacerbation

includes the following questions:

How sick is the child?

Which drugs should be used for treatment?

What are the optimal doses and delivery routes?

When is more aggressive management necessary?

The approach to the outpatient management of the child with an acute asthma exacerbation is presented below.

Rescue medications for acute symptoms and inpatient management of asthma exacerbations in children are

discussed in detail separately. (See"Acute asthma exacerbations in children: Inpatient management"and"Acute

severe asthma exacerbations in children: Intensive care unit management"and"Asthma in children younger than 12

years: Rescue treatment for acute symptoms".)

The management of acute asthma exacerbations in adults is also discussed separately. (See"Treatment of acute

exacerbations of asthma in adults".)

OVERVIEW OF TREATMENTThe approach to the management of acute asthma exacerbations described below

is geared toward management in the emergency department (ED). Initial treatment (beta-agonist therapy and oral

glucocorticoids) is sometimes provided in the primary care setting or even at home [1]. However, children with

moderate to severe exacerbations require close observation for clinical deterioration, frequent treatments, and

repeated evaluation. Thus, most children with moderate or severe asthma exacerbations should be managed in an ED

setting. (See"Acute asthma exacerbations in children: Home/office management and severity assessment".)

We used the Pulmonary Index Score (PIS) (table 1)to determine the initial severity of the exacerbation and level of

treatment needed (ie, mild, moderate, or severe) [2]. Other scores are available and are reviewed separately.

GoalsThe goals of therapy for an acute asthma exacerbation include [1]:

Rapid reversal of airflow obstruction by repeated administration of inhaled bronchodilators and early institutionof systemic glucocorticoids. (See'Pharmacotherapy'below.)

Correction of hypoxemia and/or severe hypercapnia, if present; hypoxemia is alleviated by administration of

supplemental oxygen as necessary; hypercapnia usually improves with reversal of airflow obstruction.

(See'Oxygen therapy'below and'Pharmacotherapy'below.)

Reduction of likelihood of recurrence by intensifying baseline therapy. (See'Discharge meds'below.)

General approachThe general approach to treatment of an acute asthma exacerbation includes administration of

inhaled bronchodilators (eg,albuterol), as well as antiinflammatory agents (ie, glucocorticoids) in most patients

(algorithm 1andalgorithm 2). Supportive care for children with acute asthma exacerbations includes administration of

supplemental oxygen and fluids as necessary and frequent monitoring of response to therapy.

MedicationsInhaled, short-acting, selective beta-2 adrenergic agonists (beta agonists or SABA) are the mainstay

of emergent treatment of acute asthma exacerbations. For children with mild exacerbations, systemic glucocorticoids

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are usually added if the symptoms and signs of airway obstruction fail to resolve after the first treatment with inhaled

beta agonists. Children with moderate or severe exacerbations should receive systemic glucocorticoids as soon as

possible. Additional pharmacotherapeutic agents that may be indicated in children with moderate or severe asthma

include nebulizedipratropiumbromide, intravenousmagnesium sulfate,and parenteral beta agonists.

Oxygen therapyMany patients with moderate to severe acute asthma exacerbations have hypoxemia as a result

of ventilation-perfusion (V/Q) mismatch, although in most patients the hypoxemia is mild and does not require

treatment with supplemental oxygen. Beta agonists may worsen this mismatch by causing pulmonary vasodilation in

areas of the lung that are poorly ventilated. Humidified oxygen should be provided as needed to maintain an oxygen

saturation of 92 percent [3]. All nebulized medications should also be delivered with oxygen, generally at a flow rate

of 6 to 8 L/min. (See"Continuous oxygen delivery systems for infants, children, and adults".)

MonitoringThe clinical status of children who are being treated for acute asthma should be monitored frequently.

Ongoing monitoring of respiratory rate, heart rate, oxygen saturation, degree of alertness, accessory muscle use, and

retractions is crucial to decisions regarding treatment and disposition [4].The frequency of monitoring varies

depending upon the severity of illness and response to initial therapy, but for most patients is typically every 20 to 30

minutes for the first hour of therapy. Patients who require continuous nebulizer therapy continue to be monitored every

20 to 30 minutes. Clinicians may also find it helpful to measure peak expiratory flow rate (PEFR). However,

assessment of PEFR may have limited utility in the assessment of sicker or younger children. It is optimal if the child

can make three attempts while standing (the best score is used) and is most useful when it can be compared with the

child's known personal best score.

Arterial blood gasIt is rarely necessary to obtain arterial blood gas (ABG) samples in children with acute asthma.

Oxyhemoglobin saturation can be assessed with pulse oximetry.

Many severely ill children have hypercapnia on arrival to ED, but this usually improves after therapy. In children who

require admission to the intensive care unit (ICU), measurement of PaCO2via ABG after a clinical plateau has been

reached provides an objective measure of disease severity. In moderately or severely ill children, ABG's obtained

before aggressive intervention often are abnormal, but rarely affect management. (See "Acute severe asthma

exacerbations in children: Intensive care unit management".)

Chest radiograph Chest radiographs (CXRs) rarely provide information that alters the management of children

with acute asthma exacerbation [5,6]. Viral upper respiratory tract infections are the most common trigger for

wheezing in children and the presence of low grade fever in children with acute asthma exacerbation often prompts

clinicians to obtain CXRs to exclude pneumonia. However, the rate of specific CXR findings in this setting is extremely

low, except in the presence of focal examination findings (eg, crackles or decreased breath sounds), fever (>39C), or

severe disease [5,7]. Consider obtaining CXRs to rule out pneumonia, atelectasis, and air leak if there are focal

examination findings (eg, crackles or decreased breath sounds), fever (>39C), severe disease, uncertainty about the

diagnosis, or tachypnea, hypoxemia, or chest pain that are present after initial therapy has been given.

Mild exacerbationFor children with mild asthma exacerbation (PIS

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Administration of supplemental oxygen if oxygen saturation 92 percent in room air. (See'Oxygen

therapy'above.)

Albuterolnebulization (0.15 mg/kg, maximum 5 mg) combined withipratropiumbromide (250 microgram/dose if

20 kg) every 20 to 30 minutes for three doses or continuously.

Many studies show comparable outcomes for patients who receivealbuterolvia SVN or MDI-S. However,

continuous delivery of the first three doses of albuterol via SVN in the first hour after ED arrival helps to ensure

compliance with national treatment guidelines. In addition, delivery via SVN also facilitates simultaneous

administration of albuterol andipratropium.Thus, many ED clinicians choose to treat moderately to severely ill

patients with albuterol delivered via SVN. (See'Nebulizer versus inhaler'below and'Continuous delivery'below.)

Patients who have received three doses of intermittent therapy and require additional albuteroltherapy may be

treated intermittently every 30 to 45 minutes or may be switched to continuous therapy. (See 'Inhaled short-

acting beta agonists'below and'Ipratropium bromide'below.)

Administration of systemic glucocorticoids soon after arrival in the ED or after the first inhalation therapy is

initiated (table 2). (See'Systemic glucocorticoids'below.)

Administration of intravenousmagnesium sulfate(75 mg/kg, maximum 2.5 g administered over 20 minutes) if

there is clinical deterioration despite treatment with beta agonists,ipratropiumbromide, and systemic

glucocorticoids. (See'Magnesium sulfate'below.)

Severe exacerbationFor children with severe asthma exacerbation (PIS 12, (table 1)), we suggest the following

approach (algorithm 2):

Administration of supplemental oxygen if oxygen saturation is 92 percent in room air. (See 'Oxygen

therapy'above.)

Albuterolnebulization (0.15 mg/kg, maximum 5 mg) combined withipratropiumbromide (250 microgram/dose if

20 kg), every 20 to 30 minutes for three doses or continuously.

Patients who have received three doses ofalbuterolin the first hour after ED arrival and require additional

albuterol therapy may be treated intermittently every 30 to 45 minutes or may be switched to continuous therapy.

Children with poor inspiratory flow or children who cannot cooperate with nebulized therapy can be treated with

epinephrine orterbutaline(0.01 mL/kg of a 1 mg/mL solution; maximum dose of 0.4 mg or 0.4 mL) administered

intramuscularly or subcutaneously instead of inhaledalbuterolandipratropium. (See'Inhaled short-acting beta

agonists'below and'Ipratropium bromide'below and'Parenteral beta agonists'below.)

Subsequent management depends upon response to initial therapy:

For patients who improve after the initial treatment, the approach is as described above for moderate

exacerbations. (See'Moderate exacerbation'above.)

For patients with a poor response to initial treatment, we recommend:

Administration of intravenousmethylprednisolone(1 to 2 mg/kg, maximum 125 mg). (See'Systemic

glucocorticoids'below.)

Administration of intravenousmagnesium sulfate(75 mg/kg, maximum 2.5 g administered over 20

minutes). (See'Magnesium sulfate'below.)

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For patients who do not respond to these interventions, administration of intravenous terbutalinemay be indicated:

bolus with 10 microgram/kg over ten minutes, then 0.3 to 0.5 microgram/kg per minute; infusion may be increased by

0.5microgram/kg per minute every 30 minutes to a maximum of 5 microgram/kg minute. (See'Parenteral beta

agonists'below.)

PHARMACOTHERAPYThe two primary agents used in the treatment of acute asthma exacerbations are inhaled

beta agonists and systemic glucocorticoids. Additional agents are used as needed depending upon the severity of the

exacerbation.

Inhaled short-acting beta agonists Inhaled, short-acting, selective beta-2 adrenergic agonists (beta agonists or

SABA) are the mainstay of emergent treatment of acute asthma exacerbations [8-11].Albuterolis the most widely

used SABA in the acute setting.

Inhaled beta agonists are administered by intermittent nebulization, continuous nebulization, or metered-dose inhaler

with a spacer (MDI-S, preferably a valved holding chamber). These delivery systems are discussed in detail

separately. (See"Use of medication nebulizers in children"and"The use of inhaler devices in children".)

Nebulizer versus inhalerClinicians may use either small volume nebulizers (SVNs) or MDI-S when administering

inhaled beta agonists intermittently. These methods appear to be equally effective for children of all ages and with a

wide range of illness severity. Thus, the choice of one over the other mainly depends upon the frequency of dosing

required. (See'Moderate exacerbation'above and'Continuous delivery'below.)

Clinical trials and meta-analyses indicate that the administration of beta agonists via MDI-S (4 to 12 puffs) is at least

as effective, and possibly superior to, delivery of medication by SVN in reversing bronchospasm in infants and

children [1,12-14]. (See"The use of inhaler devices in children", section on 'Pressurized MDI or nebulizer?'.)

Advantages of SVN delivery compared with MDI-S include the ability to simultaneously deliver humidified oxygen

andipratropiumbromide and to passively administer drug therapy to a child in respiratory distress. However, when

using SVNs, up to 90 percent of drug remains in the machine or is lost to the atmosphere [15]. In addition, the

portability of SVNs is limited by the need for an external power source. (See"The use of inhaler devices in children",

section on 'Spacers and holding chambers'.)

Continuous deliveryStudies comparing continuous versus intermittent nebulized delivery of beta agonists have

found similar outcomes and side effect profiles with both methods [8,9,16-18]. We suggest continuous therapy over

intermittently nebulized or MDI-S therapy for children with moderate to severe exacerbations. (See "Use of medication

nebulizers in children", section on 'Continuous nebulization'.)

Continuous nebulizer therapy is less labor intensive than intermittent nebulizer therapy, resulting in reduced

respiratory therapy costs. In addition, it ensures that the goal of three treatments within the first hour of care for

moderately ill children is met. However, young children may not tolerate wearing a facemask for long periods of time.

(See'Moderate exacerbation'above and"Delivery of inhaled medication in children", section on 'Patient technique,

acceptance, and preference'.)

LevalbuterolRacemicalbuterol(RA) is an equal mixture of two mirror-imaged enantiomers: the active R-albuteroland S-albuterol.Levalbuterol(LA), on the other hand, is pure R-albuterol. Data from animal studies and in vitro studies

with human cells suggest that S-albuterol may be a weak bronchoconstrictor [19-26]. Thus, in theory, pure active R-

albuterol could be more effective than RA because there is no bronchoconstricting effect from the S-isomer. However,

studies of LA for acute asthma in children have had conflicting results. In addition to its lack of proven superiority, LA

is substantially more expensive than RA. Thus, we suggest RA rather than LA as the drug of choice for children with

acute asthma exacerbations, except in patients with a known history of adverse affects from albuterol. Use of LA is

discussed in greater detail separately. (See"Beta agonists in asthma: Acute administration and prophylactic use",

section on 'Levalbuterol'.)

In the earliest trial, 547 children with acute asthma who were treated in the emergency department (ED) were

randomly assigned to treatment with 1.25 mg LA or 2.5 mg RA every 20 minutes for a maximum of six doses [27]. Thehospitalization rate was higher among children who received RA (45 versus 36 percent). Three subsequent studies

comparing RA with LA in the ED treatment of children with acute asthma found no differences in outcome measures

(changes from baseline clinical asthma score, changes in forced expiratory volume in one second [FEV1], number of

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treatments, length of ED care, rate of hospitalization) [28-30]. It is worth noting that the baseline admission rates in

these three studies [28-30]were substantially lower than in the first study [27].

Dosing and administrationThe doses of medications commonly used in the management of acute asthma

exacerbations in children are listed in the table (table 2).

Albuterol via MDI-SOptimal dosing foralbuteroladministered by MDI-S is not well established. The 2007 National

Asthma Education and Prevention Program (NAEPP) guidelines state that "equivalent bronchodilation can be

achieved either by high doses (4 to 12 puffs) of a short-acting beta agonist by MDI-S with a valved holding chamber orby nebulizer"; they suggest a dose of four to eight puffs [1].

One strategy is to administer one-quarter to one-third puff/kg (22.5 to 30 microgram/kg) with a maximum of eight puffs

(720 microgram). Thus, proportionately greater doses are provided for young children weighing less than 20 to 30 kg

(44 to 66 pounds), who are the least efficient users.

Another strategy is to use a dosing schedule, stratified by weight, as with continuousalbuterolnebulization:

For children who weigh 5 to 10 kg, the dose is four puffs

For children who weigh 10 to 20 kg, the dose is six puffs

For children who weigh >20 kg, the dose is eight puffs

The dose can be repeated every 20 to 30 minutes for three doses, then every one to four hours as needed.

To maximize drug delivery, a spacer (preferably a valved holding chamber [VHC]) should be employed by all patients,

and infants and young children should use a spacer with a facemask, low dead space, and a low resistance valve

(picture 1). Mouthpieces are preferable to facemasks for older children to avoid nasal filtering of drug, which may

reduce lung deposition. (See"The use of inhaler devices in children", section on 'Spacer devices'.)

Intermittent albuterol nebulization The standard dose for nebulizedalbuterolis 0.15 mg/kg (minimum 2.5 mg;

maximum 5 mg) (table 2)[1,31]. Nebulized albuterol can be administered every 20 to 30 minutes for three doses [1].Beyond that, frequency of therapy may be limited by side effects, such as tachycardia, hypertension, or tremors.

Patients who have shown little or no improvement after three doses and who are not experiencing significant adverse

effects may be treated every 30 to 45 minutes or switched to continuous therapy.

Drug delivery is maximized by having a total solution volume of 3 to 4 mL and an oxygen flow rate of 6 to 8 L/min [32-

35], tapping the sides of the reservoir to renebulize droplets, and having older children use a mouthpiece to avoid

nasal deposition of drug (picture 1).

Continuous albuterol nebulizationThe optimal dose for continuousalbuterolnebulization therapy has not been

determined. One dosing schedule, stratified by weight, is as follows:

For children who weigh 5 to 10 kg, the dose is 7.5 mg/hour

For children who weigh 10 to 20 kg, the dose is 11.25 mg/hour

For children who weigh >20 kg, the dose is 15 mg/hour

GlucocorticoidsThe antiinflammatory action of glucocorticoids effectively reduces the airway edema and

secretions associated with acute asthma exacerbations.

Systemic glucocorticoidsSystemic glucocorticoids are indicated for most children who present to the ED with an

acute asthma exacerbation, and their effects may be noted within two to four hours of administration [2,36]. Systemic

glucocorticoids are not indicated in children with mild exacerbations who have not received beta-agonist therapy within

a few hours of presenting for medical care and who respond promptly to a singlealbuteroltreatment. When indicated,

we recommend administering systemic glucocorticoids as soon as possible after arrival in the ED. Oral administration

is suitable for most patients. The dosing of systemic glucocorticoids is reviewed in the table (table 2).

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A study examined outcomes before and after initiation of a medical directive that allowed triage nurse-initiated

glucocorticoids before clinician assessment in 644 consecutive children presenting with a moderate to severe asthma

exacerbation [37]. Nursing initiation of glucocorticoids was associated with a reduced likelihood of admission (odds

ratio [OR], 0.56; 95% CI, 0.36-0.87), as well as significantly decreased times to clinical improvement and discharge.

The NAEPP guidelines suggest that oral administration of glucocorticoids is preferred to intravenous administration

because oral administration is less invasive and the effects are equivalent [1]. Intramuscular administration of

glucocorticoids (eg,dexamethasone)may be warranted in patients who vomit orally-administered glucocorticoids, yet

do not require an intravenous line for other purposes [38-40].

Orally-administeredprednisoneordexamethasoneare each a reasonable choice for ED therapy. A meta-analysis

comparing a five-day course of oralprednisoloneor prednisone with dexamethasone given as a single intramuscular

dose or one to two daily oral doses for asthma exacerbations managed in the ED found that the treatments were

equivalent with regard to rate of relapse, defined as an unplanned clinic visit, return ED visit, or unplanned

hospitalization related to the initial asthma exacerbation [41]. Lower rates of vomiting, both in the ED and at home,

were seen in the groups treated with dexamethasone via either route of administration compared

with prednisone/prednisolone. However, newer and more palatable prednisone/prednisolone liquid formulations and

oral dissolving tablets are far better tolerated with less frequent episodes of emesis compared with older prednisone

formulations.

It is not necessary to deliver glucocorticoids via the intravenous route, even among the subset of patients being

hospitalized. However, for severely ill patients, intravenous access should be established and

intravenousmethylprednisolonemay be administered (table 2).

The benefit of early administration (within one hour) of systemic glucocorticoids versus placebo in patients presenting

to the ED with acute asthma exacerbation was evaluated in a meta-analysis of 12 trials involving 863 patients [42].

The following results were reported:

Early administration of systemic glucocorticoids reduced admission rates (pooled OR 0.40, 95% CI 0.21-0.78);

eight patients (95% CI 5-21) would need to be treated to prevent one admission.

The benefit was more pronounced in those not receiving systemic glucocorticoids before ED presentation (OR

0.37, 95% CI 0.19-0.7) and in those with more severe asthma (OR 0.35, 95% CI 0.21-0.59).

Oral glucocorticoids were effective in reducing hospital admission (OR 0.24, 95% CI 0.11-0.53) compared with

placebo in the three trials included in the meta-analysis that evaluated oral glucocorticoids in children with an

acute asthma exacerbation.

Inhaled glucocorticoidsThe use of inhaled glucocorticoids to treat children with acute asthma is an area of

ongoing clinical research. Studies comparing the use of oral with inhaled glucocorticoids in the ED management of

children with acute asthma have thus far had mixed results. Until more conclusive data are available, we do not

suggest the routine use of inhaled glucocorticoids in addition to, or instead of, systemic glucocorticoids in themanagement of acute asthma exacerbation in children.

The following studies are illustrative:

Some studies have found benefits of inhaled glucocorticoids compared with oral glucocorticoids (eg, earlier

discharge from the ED, less vomiting, decreased relapse rate, improved clinical parameters, improved

pulmonary function) [43,44].

Other studies have found oral glucocorticoids and inhaled glucocorticoids to have similar outcomes [45-47].

One study found improved pulmonary function and a lower relapse rate with oralprednisonecompared withinhaledfluticasone[48].

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