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Acute asthma exacerbations in children younger than 12 years: Emergency department management

Acute asthma exacerbations in children younger than 12 years: Emergency department management
Literature review current through: Jan 2024.
This topic last updated: Nov 16, 2022.

INTRODUCTION — Initial treatment (beta-agonist therapy and oral glucocorticoids) of acute asthma exacerbations 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 emergency department (ED) setting. The general approach to treatment of an acute asthma exacerbation includes administration of inhaled bronchodilators (eg, albuterol), as well as systemic glucocorticoids in most patients.

The approach to ED management of the child with an acute asthma exacerbation is presented here. Management of acute asthma exacerbations in the home, office/outpatient clinic, and inpatient/intensive care unit (ICU) settings are discussed in detail separately:

(See "Acute asthma exacerbations in children younger than 12 years: Overview of home/office management and severity assessment".)

(See "Acute asthma exacerbations in children younger than 12 years: Inpatient management".)

(See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management".)

Rescue medications for acute symptoms are also reviewed elsewhere. (See "Asthma in children younger than 12 years: Quick-relief (rescue) treatment for acute symptoms".)

The management of acute asthma exacerbations in adolescents and adults is also discussed separately. (See "Acute exacerbations of asthma in adults: Home and office management".)

TREATMENT GOALS — The goals of therapy for an acute asthma exacerbation include [1]:

Rapid reversal of airflow obstruction (see 'Initial treatment' below and 'Management of bronchospasm' below)

Correction of hypoxemia and/or severe hypercapnia, if present (see 'Management of hypoxemia and hypercapnia' below)

Reduction of the likelihood of hospitalization and recurrence after discharge (see 'Management of inflammation' below and 'Discharge medications' below and 'Discharge education' below)

ASSESSMENT OF SEVERITY — The severity of an asthma exacerbation is primarily determined by assessment of clinical findings, occasionally supplemented by objective tests (table 1):

Mild – A mild exacerbation is characterized by normal alertness, slight tachypnea, expiratory wheezing only, a mildly prolonged expiratory phase (inspiratory-to-expiratory ratio of 1:1 rather than the normal 2:1), minimal accessory muscle use, and an oxygen saturation of >95 percent.

Moderate – A moderate exacerbation is characterized by normal alertness, tachypnea, wheezing throughout expiration with or without inspiratory wheezing, an inspiratory-to-expiratory ratio of approximately 1:2, significant use of accessory muscles, and an oxygen saturation that is typically 92 to 95 percent.

Severe – A severe exacerbation is characterized by inability to repeat a short phrase, extreme tachypnea, inspiratory and expiratory wheezing, an inspiratory-to-expiratory ratio exceeding 1:2, very poor aeration, significant use of accessory muscles, and an oxygen saturation that is typically <92 percent. Signs of impending respiratory failure include cyanosis, inability to maintain respiratory effort (respiratory rate may be inappropriately normal to low), depressed mental status (lethargy or agitation), pulse oxygen saturation (SpO2) <90 percent, and respiratory acidosis (elevated partial pressure of carbon dioxide [pCO2] noted on venous, arterial, or capillary blood gas sample).

There are also several ordinal scales available for the assessment of the initial severity of the exacerbation and level of treatment needed. We use the Pulmonary Index Score (PIS) (table 2), with a PIS 1 to 6 = mild, PIS 7 to 11 = moderate, or PIS ≥12 = severe [2]. An alternative scale is the Pediatric Respiratory Assessment Measure (PRAM) (table 3). Assessment of the severity of an acute asthma exacerbation, including review of other available scores, is discussed in detail separately. (See "Acute asthma exacerbations in children younger than 12 years: Overview of home/office management and severity assessment", section on 'Assessment of exacerbation severity'.)

ELEMENTS OF TREATMENT — The treatment of an acute asthma exacerbation in the ED includes both bronchodilators to address acute bronchospasm (table 4) and, in most patients, systemic glucocorticoids to address underlying airway inflammation (table 5). Supportive care for children with acute asthma exacerbations includes administration of supplemental oxygen and fluids to make up for evaporative losses (oral preferred if patient is able) as necessary.

Management of hypoxemia and hypercapnia — Many 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, especially among this sickest subset of children. Hypoxemia is alleviated by administration of supplemental humidified oxygen 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. Hypercapnia usually improves with reversal of airflow obstruction. (See "Continuous oxygen delivery systems for the acute care of infants, children, and adults".)

Management of bronchospasm — Additional bronchodilators used in children with moderate or severe asthma may include intravenous magnesium sulfate and parenteral beta-agonists such as terbutaline or epinephrine.

Inhaled short-acting beta-2 agonists — Inhaled short-acting beta-2 agonists (beta-agonists or SABAs), particularly albuterol (salbutamol), are the standard emergent treatment for acute asthma exacerbations in all patients based upon adult data, a few early trials in children, and many ensuing years of clinical use [1,4]. Two such small trials in children in the early 1980s demonstrated that nebulized albuterol was similar in efficacy to subcutaneous epinephrine with regard to need for repeat treatment during the initial ED visit, admission on initial visit, return to the ED after discharge, admission on return visit, clinical score, vital signs, and pulmonary function measures but was less likely to cause adverse effects [5,6]. Subsequent studies have focused on the dosing and route of administration for SABAs. Albuterol has never been compared with placebo. (See "Acute exacerbations of asthma in adults: Emergency department and inpatient management", section on 'Inhaled beta-agonists' and "Beta agonists in asthma: Acute administration and prophylactic use", section on 'Use in acute exacerbations of asthma'.)

SABAs are administered by intermittent nebulization, continuous nebulization, or metered-dose inhaler with a valved holding chamber (MDI-VHC) or spacer (MDI-S) (table 4). Albuterol (salbutamol) is the SABA used for most patients. The choice of drug and delivery systems are discussed in detail separately and are reviewed briefly here (see "Beta agonists in asthma: Acute administration and prophylactic use" and "Delivery of inhaled medication in children" and "Use of medication nebulizers in children" and "The use of inhaler devices in children"):

Racemic albuterol versus levalbuterol – Racemic albuterol is an equal mixture of two mirror-imaged enantiomers: R-albuterol, the active bronchodilator, and S-albuterol, a possible weak bronchoconstrictor. Levalbuterol is pure R-albuterol. In theory, pure active R-albuterol would be more effective than racemic albuterol because there is no bronchoconstricting effect from the S-isomer. However, studies of levalbuterol for acute asthma in children have had conflicting results, and, overall, levalbuterol appears to have no clinically significant advantage over racemic albuterol [7-10]. Thus, we use racemic albuterol rather than levalbuterol for children with acute asthma exacerbations, unless the patient has a known history of adverse effects from albuterol. Use of levalbuterol is discussed in greater detail separately. (See "Beta agonists in asthma: Acute administration and prophylactic use", section on 'Levalbuterol'.)

Nebulizer versus inhaler – Clinical trials and meta-analyses indicate that the administration of SABAs via MDI-VHC/S (eg, 4 to 12 puffs of albuterol) is at least as effective and possibly superior to delivery of medication by small-volume nebulizer (SVN) in reversing bronchospasm in children of all ages and with a wide range of illness severity [1,11-13]. Thus, the choice of one over the other for intermittent administration of SABAs mainly depends upon the frequency of dosing required. 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. Additional advantages of SVN delivery compared with MDI-VHC/S include the ability to simultaneously deliver humidified oxygen and ipratropium bromide and to passively administer drug therapy to a child in respiratory distress. Thus, many ED clinicians choose to treat moderately to severely ill patients with albuterol delivered via SVN. However, when using SVNs, up to 90 percent of drug remains in the machine or is lost to the atmosphere [14]. (See "The use of inhaler devices in children", section on 'pMDI or nebulizer?' and "The use of inhaler devices in children", section on 'Spacers and holding chambers'.)

Intermittent versus continuous delivery – Studies comparing continuous versus intermittent nebulized delivery of beta-agonists have found similar outcomes and side effect profiles with both methods [15-20]. We prefer continuous therapy over intermittently nebulized or MDI-VHC/S therapy for children with moderate-to-severe exacerbations. 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 "Use of medication nebulizers in children", section on 'Continuous nebulization' and "Delivery of inhaled medication in children", section on 'Patient technique, acceptance, and preference'.)

Dosing of albuterol depends upon route of administration and the severity of the asthma exacerbation (table 4) (see 'Mild exacerbation' below and 'Moderate exacerbation' below and 'Severe exacerbation' below):

Albuterol via MDI-VHC/S – Optimal dosing for albuterol administered by MDI-VHC/S is not well established, and protocols used vary by institution. 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 SABA by MDI with a VHC or by 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 minimum of four puffs (360 micrograms) and 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 continuous albuterol nebulization:

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 up to every 20 minutes for three doses, then every one to four hours as needed.

To maximize drug delivery, a VHC (preferred) or a spacer should be employed by all patients, and infants and young children should use such a device with a facemask, low dead space, and a low-resistance valve. Mouthpieces are preferable to facemasks for older children to avoid nasal filtering of drug, which may reduce lung deposition. Children should take a slow and deep breath at the same time that the MDI canister is depressed. The breath should be held for a count of five. For young children who are unable to breath-hold, the facemask should be held in place for five to six breaths for inhalation of all of the medication. (See "The use of inhaler devices in children", section on 'Spacer devices'.)

Intermittent albuterol nebulization – The standard dose for nebulized albuterol is 0.15 mg/kg (minimum 2.5 mg; maximum 5 mg) [1,21]. Nebulized albuterol can be administered every 20 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. Blow-by techniques for aerosol delivery, rather than using a mask or mouthpiece, should be avoided because they significantly decrease the inspired dose, limiting treatment efficacy. (See "Delivery of inhaled medication in children", section on 'Special considerations in infants and young children'.)

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 [22-25], 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 nebulization – The optimal dose for continuous albuterol nebulization therapy has not been determined, and protocols used vary by institution. One dosing schedule, stratified by weight, is as follows:

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

For children who weigh 10 to 20 kg, the dose is 10 to 12.5 mg/hour

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

Ipratropium bromide — Ipratropium bromide is an inexpensive and safe anticholinergic agent that provides bronchodilation through smooth muscle relaxation [26]. We recommend treating children with a moderate-to-severe asthma exacerbation with ipratropium bromide in addition to a beta-agonist. In randomized trials, systematic reviews, and meta-analyses [27-31], treatment with two to three doses of inhaled ipratropium combined with an inhaled beta-agonist was shown to reduce hospital admissions and improve lung function in children, most with moderate-to-severe asthma exacerbations, compared with an inhaled beta-agonist alone. In a 2013 systematic review, combination therapy was found to reduce the risk of hospitalization (relative risk [RR] 0.73, 95% CI 0.63-0.85, 15 studies, 2497 children), with 23 out of 100 children who received only beta-agonists hospitalized compared with 17 out of 100 who were treated with combination therapy [31]. Thus, 16 children (95% CI 12-29) with an asthma exacerbation of any severity would need to be treated with combination therapy rather than inhaled beta-agonists alone to avoid one hospital admission. The incidence of nausea and tremor was lower in the combination therapy group, but no difference was seen in the rate of vomiting.

Ipratropium can be administered via SVN or MDI-VHC/S (table 5). We prefer the nebulized form (250 micrograms per dose for children who weigh <20 kg; 500 micrograms per dose for children who weigh ≥20 kg). We administer ipratropium bromide with each of the first three albuterol treatments [27]. Alternatively, ipratropium may be administered with the second and third treatments [28]. If administered by MDI-VHC/S, the NAEPP guidelines recommend a dose of four to eight puffs (each puff is 18 micrograms) [1]. The NAEPP guidelines also comment that the MDI dose is low and has not been studied in asthma exacerbations.

Magnesium sulfate — Magnesium is inexpensive, has minimal adverse effects at the doses indicated, and is widely available. We suggest using intravenous magnesium sulfate in children over four years of age with severe asthma exacerbations and in children over four years of age with moderate asthma exacerbations who have not responded to initial treatment with beta-agonists, ipratropium bromide, and systemic glucocorticoids. Magnesium sulfate administered intravenously causes relaxation of bronchial smooth muscle, and there is accumulating evidence of its benefits in adults and children with severe asthma [32,33]. A meta-analysis of five studies (182 children) found that magnesium sulfate was effective in preventing hospitalization in children with moderate-to-severe acute asthma when added to bronchodilators and glucocorticoids (absolute risk reduction 0.26, 95% CI 0.12-0.39) [34]. Four children would need to be treated to avoid one hospitalization (95% CI 3-8). Two other systematic reviews and meta-analyses assessed the same five studies and found that the use of magnesium was also associated with significant improvements in pulmonary function tests [35,36]. A subsequent meta-analysis that included six trials was consistent with previous findings [37]. However, a randomized trial of intravenous magnesium sulfate (40 mg/kg) or placebo in 61 children aged six months to four years with acute, severe virus-induced wheezing unresponsive to initial treatment with short-acting bronchodilators in the emergency department found no difference between the two groups in the change in respiratory distress scores from baseline to six hours after treatment [38].

The NAEPP guidelines suggest 25 to 75 mg/kg (maximum 2 grams) intravenously for severe exacerbations unresponsive to initial treatments after one hour and as add-on therapy for life-threatening exacerbations (table 5) [1]. Given its relative safety and the critical importance of early effective treatment, in our practice, we use a dose of 50 mg/kg (maximum 2 grams), given intravenously and administered over 20 minutes. A fluid bolus may be administered to prevent clinically significant hypotension, a rare side effect of magnesium infusion. Magnesium infusion is relatively contraindicated in kidney failure. We do not advocate the use of nebulized magnesium sulfate, due to lack of demonstrated clinically important benefits in randomized trials [39].

Parenteral beta-agonists — Subcutaneous and intramuscular beta-agonists (eg, epinephrine, terbutaline) are reserved for children with a severe asthma exacerbation who often have poor inspiratory flow (eg, markedly decreased breath sounds) and/or cannot cooperate with nebulized therapy due to agitation. Additionally, intravenous terbutaline may be used in children with a severe asthma exacerbation who have not responded to initial therapy.

Subcutaneous or intramuscular epinephrine or terbutaline – Typically, subcutaneous or intramuscular therapy is given within minutes of arrival to a severely ill patient who is aerating poorly, concurrent with starting albuterol therapy and obtaining intravenous access. While terbutaline is more beta-2-selective at lower doses than epinephrine, terbutaline may lower blood pressure, whereas epinephrine can increase cardiac output and raise blood pressure. In addition, epinephrine is also suitable for anaphylaxis, which can have a similar presentation to a severe asthma attack. In a sick patient, the preferred medication is the one most readily available, which is epinephrine (in the form of autoinjectable epinephrine devices for intramuscular administration) in most cases.

Early studies showed that inhaled beta-agonists were as efficacious as subcutaneous or intramuscular epinephrine [5,6]. However, inhaled beta-agonists are poorly delivered in severely ill children with markedly diminished aeration. Theoretically then, in this setting, the rapid subcutaneous or intramuscular administration of beta-agonists (epinephrine or terbutaline) may be superior to inhaled beta-agonists. Another subgroup who may benefit from this mode of therapy is anxious, young children who are uncooperative with and have suboptimal response to initial aerosolized therapy. The intramuscular route may provide for more rapid drug absorption compared with the subcutaneous route, although direct comparisons are lacking.

The dose of intramuscular or subcutaneous epinephrine for bronchodilation is 0.01 mg/kg (0.01 mL/kg a 1 mg/mL solution), with a maximum dose of 0.4 mL (0.4 mg) (table 5). The dose of subcutaneous or intramuscular terbutaline for bronchodilation is 0.01 mg/kg/dose (0.01 mL/kg of a 1 mg/mL solution), with a maximum dose of 0.4 mg (0.4 mL). The dose may be repeated every 20 minutes for three doses unless significant side effects (eg, extreme hypertension, persistent emesis) develop, although most patients are switched to an intravenous medication (eg, magnesium sulfate, terbutaline) if they do not respond after the second dose of subcutaneous or intramuscular terbutaline or epinephrine. The dosing interval may be decreased to 5 to 10 minutes for children who continue with severe respiratory distress; autoinjectable epinephrine may be used for this purpose to avoid a delay in drawing up the medication.

Intravenous terbutaline – Severely ill patients who are poorly responsive to conventional therapy may be treated with a combination of intravenous beta-agonists and inhaled beta-agonists, although additional studies are needed to clarify the role of intravenous beta-agonists. A systematic review of studies published through September 2012 [40] found only two randomized trials that met inclusion criteria [41,42]. Limited evidence from these two trials suggests that there is shorter recovery time and improved pulmonary index scores (PIS) with the addition of intravenous beta-agonists in children poorly responsive to conventional interventions (including inhaled beta-agonists and ipratropium, systemic glucocorticoids, and magnesium sulfate). Although at least one pediatrics study found no significant adverse effects with continuous intravenous terbutaline, the possible benefit needs to be weighed against increased side effects associated with this therapy, including dysrhythmias, hypertension, and myocardial ischemia [43,44]. Thus, there is no role for using intravenous beta-agonists as initial therapy, even for severely ill children. Alternative treatment options include noninvasive positive pressure ventilation (NPPV) and high-flow nasal cannula. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Preintubation therapies'.)

Dosing for intravenous terbutaline in the ED setting is as follows: 10 micrograms/kg bolus over 10 minutes, followed by 0.3 to 0.5 micrograms/kg/minute; every 30 minutes the infusion may be increased by 0.5 micrograms/kg/minute to a maximum of 3 micrograms/kg/minute. Use of higher doses in the intensive care unit (ICU) setting have been described (up to 6 to 10 micrograms/kg/minute). However, in clinical practice, the maximum dose is often limited to 2 to 3 micrograms/kg/minute because of drug toxicities (eg, troponin leak, electrocardiogram changes). (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management", section on 'Pharmacotherapy'.)

Management of inflammation — The other primary treatment for acute asthma exacerbations in the ED is systemic glucocorticoids.

Systemic glucocorticoids — Systemic glucocorticoids are a well-established asthma therapy and are indicated for all children who present to the ED with a moderate-to-severe acute asthma exacerbation. Most children with mild exacerbations are also treated with systemic glucocorticoids, although it is reasonable to omit this treatment in children who have not received beta-agonist therapy within a few hours of presenting for medical care and who respond promptly to a single albuterol treatment in the ED. Systemic glucocorticoids have been used for the treatment of acute asthma exacerbations for over 60 years [45]. The anti-inflammatory action of glucocorticoids effectively reduces the airway edema and secretions associated with acute asthma exacerbations, and their effects may be noted within two to four hours of administration [2,46]. Treatment of moderate-to-severe exacerbations with systemic glucocorticoids in the ED is associated with a decreased rate of hospitalization in placebo-controlled trials (RR 0.58 [95% CI 0.37-0.92] in an analysis of two trials in preschool children, for example) [2,47], and admission rates are similar in children whether they are given oral or intravenous glucocorticoids [48].

When indicated, we recommend administering systemic glucocorticoids as soon as possible after arrival in the ED. Oral administration is suitable and preferred for most patients. Dexamethasone has become the oral glucocorticoid of choice to treat children with acute asthma because of its prolonged half-life and similar efficacy compared with prednisone [49,50]. The dosing of systemic glucocorticoids is reviewed in the table (table 5). 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 [51-53].

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 [54]. The following results were reported:

Early administration of systemic glucocorticoids reduced admission rates (pooled odds ratio [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.

Another 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 [55]. Nursing initiation of glucocorticoids was associated with a reduced likelihood of admission (OR 0.56, 95% CI 0.36-0.87), as well as significantly decreased times to clinical improvement and discharge.

A meta-analysis comparing a three- to five-day course of oral prednisolone or prednisone (2 mg/kg/day for the first day and then 1 to 2 mg/kg/day for the subsequent two to four days) with dexamethasone given as a single intramuscular dose (0.3 to 1.7 mg/kg) or one to two daily oral doses (0.6 mg/kg) 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 [56]. Similar results were seen in two subsequent randomized, open-label trials. The first of these compared a single oral dose of dexamethasone (0.3 mg/kg) to a three-day course of prednisolone (1 mg/kg/day), with equivalent Pediatric Respiratory Assessment Measure (PRAM) scores at day 4 after the ED visit [57]. The second compared two daily oral doses of dexamethasone (0.6 mg/kg/dose, maximum dose 12 mg) to a five-day course of prednisone/prednisolone (1.5 mg/kg/day, maximum 60 mg, on day 1 and 1 mg/kg/day, maximum 60 mg, on days 2 through 5), with no difference seen in asthma symptoms and quality of life at day 7, admission rate, or unscheduled return visits to the ED [58]. In the first trial and in the meta-analysis, 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 [56,57]. 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.

Most patients do not require delivery glucocorticoids via the intravenous route, even among those being hospitalized. However, for severely ill patients, intravenous access should be established, and intravenous methylprednisolone may be administered (table 5).

Inhaled glucocorticoids — The 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, although one systematic review found no differences between inhaled and systemic glucocorticoids [59]. 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 the management 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) [60,61].

Other studies have found oral glucocorticoids and inhaled glucocorticoids to have similar outcomes [62-64].

One study found improved pulmonary function and a lower relapse rate with oral prednisone compared with inhaled fluticasone [65].

Two randomized trials found no additional benefit to adding nebulized budesonide to standard therapy (systemic glucocorticoids and inhaled albuterol and ipratropium) early in the course of treatment [66,67].

Nonstandard therapies — There are insufficient data to support the routine administration of heliox, ketamine, or leukotriene receptor antagonists (LTRAs) in the treatment of bronchospasm in children with acute asthma exacerbations.

Heliox — In theory, a mixture of helium and oxygen may enhance beta-agonist delivery because the lower gas density should result in decreased flow resistance. The 2007 NAEPP guidelines suggest administration of beta-agonists with heliox in patients with life-threatening exacerbations or who are not responding to conventional therapy [1]. However, the use of heliox should not delay intubation once it is considered necessary. Heliox is not used if the patient requires greater than 40 percent oxygen, because the beneficial effect of using a low-density gas is diminished as the oxygen fraction increases. (See "Physiology and clinical use of heliox", section on 'Use in children' and 'Endotracheal intubation' below.)

The benefits of continuous beta-agonist administration delivery by heliox compared with oxygen were evaluated in a controlled trial in 30 children (2 to 18 years) with moderate-to-severe asthma (PIS ≥8) (table 2) [68]. After initial treatment with albuterol inhalation and prednisone or prednisolone, the patients were randomly assigned to receive continuous albuterol nebulization delivered by heliox or oxygen. At 240 minutes, patients in the heliox group had greater decrease in PIS from baseline (decrease of 7 versus 3 points). In addition, more patients in the heliox group were discharged from the hospital in less than 12 hours (73 versus 33 percent).

Ketamine — Due to its bronchodilating properties, the dissociative agent ketamine is the drug of choice to provide sedation and analgesia before intubating a child with asthma (see 'Endotracheal intubation' below). Although several small case series of nonintubated children treated with ketamine suggest that ketamine improves acute asthma [69,70], the one randomized trial found that ketamine was no better than standard therapy in nonintubated children with severe acute asthma [71,72]. (See "Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation", section on 'Sedation and paralysis'.)

Leukotriene receptor antagonists — The data do not support the routine use of LTRA therapy to treat children with acute asthma exacerbations requiring urgent or emergent care [73]. LTRA add-on therapy in acute asthma has shown promise in adults [74,75]. However, it does not appear to provide additional benefit in children when added to standard therapy for acute asthma [76]. (See "Acute exacerbations of asthma in adults: Emergency department and inpatient management", section on 'Ineffective therapies'.)

A randomized trial of 117 children aged 5 to 15 years treated in the ED found no difference in the Modified Pulmonary Index Score (MPIS) between those treated with a single age-appropriate dose of montelukast versus placebo [76]. Intravenous montelukast was not effective in improving forced expiratory volume in one second (FEV1) in a randomized trial of children with acute asthma [77].

ADVICE RELATED TO COVID-19 PANDEMIC — The United States Centers for Disease Control and Prevention (CDC) have identified asthma as a risk factor for severe coronavirus disease 2019 (COVID-19; severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) [78]. Expert groups have advised continuing usual ED management in patients with asthma [79-82]. This includes following the usual guidelines for prompt initiation of systemic glucocorticoids for asthma exacerbations since delaying therapy is known to increase the risk of a life-threatening exacerbation. One exception to routine care is that use of nebulized medications should be minimized, if possible, because of the risk of aerosolizing SARS-CoV-2 resulting in nosocomial infection. For most children, clinicians should initiate metered-dose inhaler with spacer (MDI-S) therapy and only switch to nebulized beta-agonist therapy if the child is moderately or severely ill and has poor response to MDI-S therapy. If nebulized therapy or noninvasive ventilation is employed, all health care workers should wear full personal protective equipment, including an N-95 mask or respirator, eye protection, gloves, and a gown. In addition, clinicians should have a low threshold for testing for COVID-19 in all children with an acute asthma exacerbation; any such child with fever should be tested. (See "COVID-19: Clinical manifestations and diagnosis in children".)

INITIAL TREATMENT — Treatment is based upon the initial assessment of severity (table 2) followed by ongoing monitoring of response to therapy (algorithm 1). All drug doses and routes are shown in the tables (table 4 and table 5). (See 'Assessment of severity' above and 'Monitoring' below.)

Mild exacerbation — For children with a mild asthma exacerbation (see 'Assessment of severity' above), the approach is as follows (algorithm 1):

Administer albuterol inhalation therapy via small-volume nebulizer (SVN) or metered-dose inhaler with spacer (MDI-S). If repeated doses are needed, they should be given up to every 20 minutes for three doses [1]. (See 'Inhaled short-acting beta-2 agonists' above.)

Give systemic glucocorticoids (eg, oral prednisolone/prednisone or dexamethasone) to those who fail to show sustained improvement or worsen after one inhalation therapy or who have a history of severe or recurrent exacerbations in the past. (See 'Systemic glucocorticoids' above.)

Moderate exacerbation — For children with a moderate asthma exacerbation (see 'Assessment of severity' above), the following therapies are administered (algorithm 1):

Nebulized albuterol combined with ipratropium bromide up to every 20 minutes for three doses or continuously for one hour. (See 'Inhaled short-acting beta-2 agonists' above and 'Ipratropium bromide' above.)

Systemic glucocorticoids (oral administration of prednisolone/prednisone or dexamethasone is suitable for most patients) within 30 to 60 minutes after arrival in the ED in a manner that does not delay the initiation of beta-agonist therapy. (See 'Systemic glucocorticoids' above.)

Severe exacerbation — For children with a severe asthma exacerbation (see 'Assessment of severity' above), the approach is as follows (algorithm 1):

Continuous nebulized albuterol combined with ipratropium, as noted above for moderate exacerbation, for the first hour. Most children with a severe exacerbation will need ongoing administration of continuous rather than intermittent nebulized albuterol, unless they experience dramatic improvement after their first hour of albuterol therapy. (See 'Moderate exacerbation' above.)

Children with very poor inspiratory flow or severely ill children who cannot cooperate with nebulized therapy can be treated with terbutaline or epinephrine administered intramuscularly or subcutaneously instead of inhaled albuterol and ipratropium. The intramuscular route has the theoretical advantage of more rapid distribution, and, unlike epinephrine, terbutaline is a beta-selective agent. (See 'Inhaled short-acting beta-2 agonists' above and 'Ipratropium bromide' above and 'Parenteral beta-agonists' above.)

Intravenous methylprednisolone, which can be started as soon as intravenous access is obtained. (See 'Systemic glucocorticoids' above.)

Intravenous magnesium sulfate. (See 'Magnesium sulfate' above.)

Impending respiratory failure — The pediatric intensive care unit (PICU) and/or anesthesia should be consulted when a patient has signs of impending respiratory failure (algorithm 1), including cyanosis, inability to maintain respiratory effort (respiratory rate may be inappropriately normal to low), depressed mental status (lethargy or agitation), pulse oxygen saturation (SpO2) <90 percent, and/or respiratory acidosis (elevated partial pressure of carbon dioxide [pCO2] noted on venous, arterial, or capillary blood gas sample). Intravenous terbutaline in addition to inhaled short-acting beta-2 agonists (SABAs) and noninvasive positive pressure ventilation (NPPV) or endotracheal intubation may be indicated for these children. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management" and 'Noninvasive positive pressure ventilation' below and 'Endotracheal intubation' below.)

Intravenous terbutaline — For the child with impending respiratory failure, the risk-benefit ratio favors the use of intravenous terbutaline in addition to continuously nebulized albuterol (table 5). (See 'Parenteral beta-agonists' above.)

Noninvasive positive pressure ventilation — NPPV (continuous positive airway pressure [CPAP] or bilevel positive airway support [BPAP]) is sometimes used to treat severely ill children with asthma who are responding poorly to other interventions, although there are little data proving the efficacy of this approach [83]. This strategy of employing positive pressure has the theoretical benefit of decreasing the workload of fatigued muscles by decreasing the pressure needed to initiate a breath and helping to prevent airway collapse on exhalation. Subsets of patients, as yet hard to define, do have demonstrable benefit from the use of NPPV. As such, it is reasonable for clinicians to employ this option in children with severe exacerbations refractory to other interventions, with the caveat that NPPV should be discontinued if there is clinical deterioration. NPPV is discussed in greater detail separately. (See "Noninvasive ventilation for acute and impending respiratory failure in children" and "Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation".)

Endotracheal intubation — Intubation should be approached cautiously in patients with status asthmaticus because manipulation of the airway can cause increased airflow obstruction due to exaggerated bronchial responsiveness. Clinicians must be prepared to manage acute deterioration after intubation. Adequate venous access, noninvasive monitoring, and sedation should be optimized before intubation. The clinician most experienced with airway management should perform the intubation. The indications for endotracheal intubation in children with asthma and the performance of the procedure are reviewed in detail separately. (See "Technique of emergency endotracheal intubation in children" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach" and "Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation", section on 'Endotracheal intubation and mechanical ventilation'.)

FURTHER EVALUATION

Indications for chest radiograph — Most children with asthma exacerbations do not require chest radiographs (CXRs), since they rarely provide information that alters the management of children with acute asthma exacerbation [84,85]. Indications for CXR to rule out pneumonia, atelectasis, and air leak include fever (>39ºC); presence of focal examination findings (eg, persistent crackles or decreased breath sounds, crepitus); persistent tachypnea, hypoxemia, or chest pain; severe disease; or uncertainty about the diagnosis [84]. (See "Evaluation of wheezing in infants and children", section on 'Radiography'.)

Alternative diagnoses and comorbidities — Patients who present with acute onset of wheezing and do not respond to the usual asthma therapies should be evaluated for alternative diagnoses and comorbidities (table 6 and table 7). In addition to asthma, acute onset of wheezing in a child is most often caused by an infectious process (particularly viral bronchiolitis in infants less than two years of age and atypical pneumonia in older children) or foreign body aspiration (FBA). Environmental allergies and obesity are among the more common comorbidities. Common triggers and comorbidities are reviewed in greater detail separately. (See "Evaluation of wheezing in infants and children", section on 'Acute wheezing (hours to days)' and "An overview of asthma management", section on 'Controlling asthma triggers'.)

MONITORING — 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 [86]. 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) in select patients (eg, a person with obesity, in whom assessment of aeration is more difficult). 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 it is most useful when it can be compared with the child's known personal best score. (See "Overview of pulmonary function testing in children", section on 'Peak expiratory flow rate'.)

Management decisions can be based upon the physical exam findings, along with oxyhemoglobin saturation assessed with pulse oximetry. In addition, an elevated end tidal CO2 measurement assessed noninvasively via capnometry may indicate impending respiratory failure. It is rarely necessary to obtain arterial blood gas (ABG) samples in children with acute asthma. ABGs obtained before aggressive intervention are often abnormal (hypercapnia) in moderately or severely ill children but rarely affect management and usually improve after therapy. In children who require admission to the intensive care unit (ICU), measurement of partial pressure of carbon dioxide (pCO2) via ABG after a clinical plateau has been reached provides an objective measure of disease severity. Data suggest that capillary blood is an acceptable sample alternative to arterial blood if only acid-base parameters (pH and pCO2) are of clinical interest [87]. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management".)

SUBSEQUENT MANAGEMENT — Subsequent management depends upon response to initial therapy (algorithm 1). All drug doses and routes are shown in the tables (table 4 and table 5). Discharge criteria for patients who do respond to therapy are reviewed below. (See 'Assessment of severity' above and 'Discharge to home' below.)

Poor response and severely ill — For patients with a poor response to initial treatment and severe signs and/or symptoms (see 'Assessment of severity' above), the following additional steps are taken while awaiting admission to the hospital (see 'Hospitalization' below):

Consult the pediatric intensive care unit (PICU) and/or anesthesia. (See "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management".)

Give continuously nebulized albuterol (or give intermittently every 30 to 45 minutes) without ipratropium (table 4). (See 'Inhaled short-acting beta-2 agonists' above.)

Administer intravenous magnesium sulfate if not already given and there is lack of clinical improvement or clinical deterioration despite treatment with albuterol, ipratropium bromide, and systemic glucocorticoids. (See 'Magnesium sulfate' above.)

For patients who do not respond to these interventions and have signs and/or symptoms of impending respiratory failure, administer intravenous terbutaline after completion of the magnesium sulfate infusion. Dosing for intravenous terbutaline in the ED setting is as follows: 10 microgram/kg bolus over 10 minutes, followed by 0.3 to 0.5 microgram/kg/minute; every 30 minutes the infusion may be increased by 0.5 microgram/kg/minute to a maximum of 3 microgram/kg/minute. (Higher doses are sometimes used in the ICU setting.) (See 'Parenteral beta-agonists' above and 'Impending respiratory failure' above.)

Assess for alternative diagnoses or comorbidities. (See 'Alternative diagnoses and comorbidities' above.)

Additional management may include noninvasive positive pressure ventilation (NPPV) or endotracheal intubation. (See 'Noninvasive positive pressure ventilation' above and 'Endotracheal intubation' above.)

Incomplete response and moderately ill — For patients with an incomplete response to initial treatment and continued moderate signs and/or symptoms (see 'Assessment of severity' above), the approach is as follows (algorithm 1):

Give nebulized albuterol continuously (or every 30 to 45 minutes).

Administer intravenous magnesium sulfate if it was not already given and symptoms are moderate.

Reassess response to therapy in one to three hours to determine whether to admit or discharge to home. (See 'Disposition' below.)

Incomplete response and mildly ill — For patients with an incomplete response to initial treatment and continued mild signs and/or symptoms (see 'Assessment of severity' above), the approach is as follows (algorithm 1):

Give nebulized albuterol every 30 to 45 minutes.

Reassess response to therapy in one to three hours to determine whether to admit or discharge to home. (See 'Disposition' below.)

Good response and minimal to no symptoms — Patients who have resolution of symptoms or marked improvement and the patient and parents/caregivers have a good understanding of asthma management and are able to adhere to therapy can be discharged to home (algorithm 1). (See 'Discharge to home' below.)

DISPOSITION — The decision regarding disposition (eg, discharge to home, continued observation, or hospitalization) is based upon both clinical and social factors.

Hospitalization — Patients who were moderately to severely ill on arrival and who have little improvement or worsen after initial therapy with beta-agonists and systemic glucocorticoids require hospitalization. This includes patients who continue to have significant wheezing and retracting and poor aeration.

Additional factors that suggest a need for hospitalization include [1]:

Beta-agonist therapy more often than four hours; patients who require treatment more often than every two hours may need to be admitted to an intensive care unit (ICU; this varies from institution to institution and is dependent upon the level of care that can be administered in the regular inpatient unit)

Requirement for supplemental oxygen/low oxygen saturation on pulse oximetry an hour or more after commencement of initial therapy

Inability to self-hydrate

A history of rapid progression of severity in past exacerbations

Poor adherence with outpatient medication regimen

Recent treatment with systemic glucocorticoids (includes current treatment with oral glucocorticoids at the time of presentation) or beta-agonist overuse

Inadequate access to medical care, including lack of transportation back to the hospital if deterioration occurs

Poor social support system at home, with inability of the caregiver(s) to provide medical care and supervision at home

Severely ill children with a poor response to ED interventions will require admission to a pediatric intensive care unit (PICU). Clinicians should have a low threshold to admit a child with altered mental status (may present as drowsiness or agitation) to an ICU. Other factors that may influence this decision include a history of severe exacerbations and/or a prior need for ICU management [88].

Inpatient and ICU therapy for acute asthma exacerbations in children are discussed separately. (See "Acute asthma exacerbations in children younger than 12 years: Inpatient management" and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management".)

Discharge to home — Children who have marked improvement in clinical parameters within the first one to two hours of therapy may be discharged home [1]. Marked improvement is manifested by diminished or absent wheezing and retracting and increased aeration that is sustained at least 60 minutes after the most recent albuterol dose.

Discharge medications — All patients seen for an acute asthma exacerbation should have an inhaled short-acting beta-2 agonist (SABA; eg, albuterol) available for treatment of symptoms [1]. We suggest treatment with a SABA (eg, albuterol) every four hours during waking hours and up to every four hours as needed during sleep for the first three days after an ED visit for an asthma exacerbation. After that, albuterol dosing should be weaned as tolerated, with the goal of discontinuing by day 5 to 7. (See "Asthma in children younger than 12 years: Quick-relief (rescue) treatment for acute symptoms", section on 'Short-acting beta agonists (SABAs)'.)

We treat children with a short course of oral glucocorticoids if they received a dose of systemic glucocorticoids in the ED. A meta-analysis of combined adult and pediatric data found that this treatment was associated with fewer relapses to additional care, a decreased number of subsequent hospitalizations, and less albuterol use [89]. As few as 10 patients need to be treated with systemic glucocorticoids to prevent relapse. A one- to two day course of dexamethasone given once per day has become the glucocorticoid of choice for post-ED asthma management [56]. It is well-tolerated and has the same efficacy as a five-day course of prednisone given twice each day. More prolonged glucocorticoid regimens may be indicated for those with persistent symptoms or those whose control regimen includes oral glucocorticoids. Glucocorticoids that are administered for less than 10 days do not require a taper at discontinuation [90].

Whether inhaled glucocorticoids offer any short-term benefits in addition to inhaled albuterol and oral glucocorticoids when started in the ED or at the time of discharge from the ED in patients who were not already receiving inhaled glucocorticoids as controller therapy is a question that remains unanswered [91,92]. However, patients may be started on an inhaled glucocorticoid in the ED, if controller therapy is indicated, to ensure that institution of this therapy is not delayed or forgotten [93]. Alternatively, the treating clinician in the ED can advise the parents/caregivers to address this issue during the follow-up visit with the child's primary care provider. (See "Asthma in children younger than 12 years: Management of persistent asthma with controller therapies".)

Benefits were not seen with leukotriene receptor antagonists (LTRAs) as monotherapy in children discharged from the ED after treatment for acute asthma was successful. A five-day course of montelukast was not as effective as a similar course of prednisolone in a randomized trial of 130 children with mild-to-moderate acute asthma exacerbations who were stabilized with prednisolone in the ED [94]. Treatment failure occurred in 8 percent of children treated with prednisolone compared with 22 percent treated with montelukast.

Discharge education — Prior to discharge from the ED, it is recommended that the following are reviewed with patients and their parents/caregivers [1]:

Signs and symptoms necessitating a return visit to the ED including worsening shortness of breath, difficulty speaking a complete sentence, or increased work of breathing

The need to follow-up with their primary care provider or asthma specialist within one week of the ED visit

Discharge medications, with respect to purpose, side effects, and proper technique for administration (see "Asthma in children younger than 12 years: Management of persistent asthma with controller therapies" and "Asthma in children younger than 12 years: Quick-relief (rescue) treatment for acute symptoms" and "The use of inhaler devices in children", section on 'Spacer devices' and "The use of inhaler devices in children", section on 'Valved-holding chambers')

A written asthma action plan (form 1A-B) (see "Asthma education and self-management")

Risk factors for asthma (see "Risk factors for asthma")

Prevention of acute exacerbations (see "Trigger control to enhance asthma management" and "Allergen avoidance in the treatment of asthma and allergic rhinitis")

Follow-up — Patients discharged from the ED should follow up with their primary care provider or asthma specialist within one week of the ED visit [1]. At the follow-up visit, the primary care provider can review the child's asthma control, asthma care plan, and initiate or alter controller therapy as indicated. (See "Asthma in children younger than 12 years: Management of persistent asthma with controller therapies".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Asthma in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: How to use your child's dry powder inhaler (The Basics)" and "Patient education: Asthma in children (The Basics)" and "Patient education: How to use your child's metered dose inhaler (The Basics)")

Beyond the Basics topics (see "Patient education: Asthma inhaler techniques in children (Beyond the Basics)" and "Patient education: Asthma treatment in children (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Determining exacerbation severity – The severity of an asthma exacerbation is primarily determined by assessment of clinical findings, occasionally supplemented by objective tests (table 1). The initial severity of the exacerbation and level of treatment needed can also be determined using an asthma exacerbation severity score such as the pulmonary index score (PIS) (table 2) or the Pediatric Respiratory Assessment Measure (PRAM) (table 3). (See 'Assessment of severity' above and "Acute asthma exacerbations in children younger than 12 years: Overview of home/office management and severity assessment", section on 'Assessment of exacerbation severity'.)

Mild – A mild exacerbation is characterized by normal alertness, slight tachypnea, expiratory wheezing only, a mildly prolonged expiratory phase, minimal accessory muscle use, and an oxygen saturation of >95 percent.

Moderate – A moderate exacerbation is defined as normal alertness, tachypnea, wheezing throughout expiration with or without inspiratory wheezing, an inspiratory-expiratory ratio of approximately 1:2, significant use of accessory muscles, and an oxygen saturation that is typically 92 to 95 percent.

Severe – A severe exacerbation is defined as lethargy or agitation, inability to repeat a short phrase, extreme tachypnea, inspiratory and expiratory wheezing, an inspiratory-expiratory ratio exceeding 1:2, very poor aeration, significant use of accessory muscles, and an oxygen saturation that is typically <92 percent.

Initial management – The approach to the initial management of the child who presents to the emergency department (ED) with an asthma exacerbation is summarized in the algorithm (algorithm 1) and as follows, with dosing and route of administration summarized in the tables (table 4 and table 5) (see 'Initial treatment' above):

Patients with hypoxemia – Administration of supplemental oxygen is indicated if oxygen saturation is ≤92 percent in room air. (See 'Management of hypoxemia and hypercapnia' above.)

All patients – All patients seen in the ED for an acute asthma exacerbation require treatment with an inhaled short-acting beta-2 agonist (SABA or beta-agonist), such as albuterol (salbutamol) or an equivalent. Albuterol is administered by nebulizer or metered-dose inhaler with a valved holding chamber (preferred) or spacer (MDI-VHC/S) up to every 20 minutes for one to three doses or continuously via nebulizer. The delivery method and dose vary with the severity of the attack, and studies show similar outcomes with each mode of delivery. Subcutaneous or intramuscular administration of a beta-agonist (eg, terbutaline, epinephrine) is an alternative for children with poor inspiratory flow and/or who have moderate-to-severe symptoms and are uncooperative with inhalation therapy. (See 'Inhaled short-acting beta-2 agonists' above and 'Parenteral beta-agonists' above.)

Patients with mild exacerbations – We suggest oral glucocorticoids for children who present to the ED with a mild asthma exacerbation (Grade 2B), although it is reasonable to omit this therapy in children who have not received beta-agonist therapy within a few hours of presenting for medical care and who respond promptly to a single albuterol treatment in the ED. (See 'Systemic glucocorticoids' above.)

Patients with moderate-to-severe exacerbations For patients who present to the ED with a moderate-to-severe asthma exacerbation:

-We recommend systemic glucocorticoids (Grade 1B). Systemic glucocorticoids should be administered within 30 to 60 minutes after arrival in the ED. Oral agents (eg, dexamethasone, prednisolone, or prednisone) are preferred in those with moderate exacerbations. Dexamethasone is preferred because of its prolonged half-life, which allows for shorter dosing, and similar efficacy compared with prednisone and prednisolone. We administer systemic glucocorticoids intravenously in most patients with severe exacerbations since they are likely to require additional intravenous medications. (See 'Systemic glucocorticoids' above.)

-We recommend inhaled ipratropium bromide (Grade 1A). We administer ipratropium bromide combined with initial beta-agonist therapy (given as nebulizer treatments up to every 20 minutes for three doses or continuously); alternatively, it may be administered with the second and third treatments. (See 'Ipratropium bromide' above.)

-We suggest intravenous magnesium sulfate as part of the initial therapy only in patients with a severe exacerbation (Grade 2A).

Patients with impending respiratory failure – The pediatric intensive care unit (PICU) and/or anesthesia should be consulted when a patient has signs and/or symptoms of impending respiratory failure. (See 'Impending respiratory failure' above.)

Further evaluation in patients who are not responding to usual therapy – Most children with asthma exacerbations do not require chest radiographs (CXRs) as part of their evaluation. Patients who present with acute onset of wheezing and do not respond to the usual asthma therapies should be evaluated for alternative diagnoses and comorbidities (table 6 and table 7). (See 'Further evaluation' above.)

Subsequent management and disposition – The disposition of children with acute asthma exacerbation depends upon the response during the first one to two hours of therapy and subsequent severity of symptoms (algorithm 1) (see 'Subsequent management' above and 'Disposition' above):

Marked improvement – Children who have marked improvement in clinical parameters may be discharged home. All patients seen for an acute asthma exacerbation should have an inhaled SABA (eg, albuterol) available for treatment of symptoms. We typically advise treating with albuterol every four hours for the first three days after discharge from the ED; albuterol frequency may be weaned for the next two to three days following that, as tolerated. We treat children with a short course of oral glucocorticoids if they received a dose of systemic glucocorticoids in the ED. Patients discharged from the ED should follow-up with their primary care provider or asthma specialist within one week after the ED visit. (See 'Good response and minimal to no symptoms' above and 'Discharge to home' above.)

Poor or incomplete response – Children with no or incomplete improvement within the first two hours of therapy require continued observation and treatment (algorithm 1). (See 'Incomplete response and mildly ill' above and 'Incomplete response and moderately ill' above and 'Poor response and severely ill' above.)

-Inhaled SABA is continued in all patients.

-We suggest the administration of intravenous magnesium sulfate for patients who have a poor response to initial treatment with beta-agonist, ipratropium, and systemic glucocorticoids and have moderate-to-severe symptoms (Grade 2A). (See 'Magnesium sulfate' above.)

-We suggest administration of intravenous terbutaline if there is no response to intravenous magnesium sulfate and the patient has signs and/or symptoms of impending respiratory failure (Grade 2B). (See 'Parenteral beta-agonists' above.)

-Patients who continue to have symptoms and/or continued need for supplemental oxygen after treatment with bronchodilators and systemic glucocorticoids require hospitalization. Severely ill children with a poor response to ED interventions require admission to a PICU. (See 'Hospitalization' above and "Acute asthma exacerbations in children younger than 12 years: Inpatient management" and "Acute severe asthma exacerbations in children younger than 12 years: Intensive care unit management" and "Acute severe asthma exacerbations in children younger than 12 years: Endotracheal intubation and mechanical ventilation".)

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Topic 5740 Version 56.0

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