Emergency department management of pediatric asthma

Emergency department management of pediatric asthma

For the physician providing acute care for children, knowledge of optimal management of pediatric asthma is essential. Asthma is one of the most commo...

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For the physician providing acute care for children, knowledge of optimal management of pediatric asthma is essential. Asthma is one of the most common diseases of childhood, with a prevalence rate of 5.4% in the pediatric population, accounting for 17% of pediatric encounters in US emergency departments. Asthma is characterized by bronchial hyperreactivity, airway inflammation, and reversible airway obstruction. New developments in the understanding of the underlying physiology and pharmacologic treatment of pediatric asthma have occurred in recent years. Although inhaled beta-adrenergic agonists remain the initial treatment of choice for acute bronchospasm in asthma, there is increased understanding of the importance of inflammation in the disease process. There is also recognition of the role of cholinergic-mediated airway obstruction. This review focuses on the clinical applications of these concepts in the emergency management of pediatric asthma, the role of newer treatment modalities, and the value of implementing an emergency department management protocol. Clin Ped Emerg Med 5:256-269. © 2004 Elsevier Inc. All rights reserved. INDEX WORDS: Acute pediatric asthma treatment, acute pediatric asthma management protocol.

Emergency Department Management of Pediatric Asthma By Robert G. Bolte SALT LAKE CITY, UTAH

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From the Division of Pediatric Emergency Medicine, Department of Pediatrics, University of Utah School of Medicine, Primary Children’s Medical Center, Salt Lake City, UT. Address reprint requests to Robert Bolte, MD, USA, Division of Pediatric Emergency Medicine, 127 South 500 East, Suite 600, Salt Lake City, UT 84102. E-mail: [email protected] 1522-8401/$—see front matter © 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.cpem.2004.09.002

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N THE ACUTE CARE OF PEDIATRIC ASTHMA, knowledge of the optimal management is essential. Asthma is one of the most common diseases of childhood, with a prevalence rate of 5.4%. The prevalence in boys is 50% greater than that among girls. The prevalence in African-American children is 44% higher than that among Caucasian children. Hispanic children have a prevalence rate generally comparable to Caucasians. Children living in a household earning less than the poverty level have a 12% higher prevalence of asthma. Asthma accounts for 17% of pediatric encounters in US emergency departments (EDs). These ED visits result in approximately a quarter of a million hospital admissions. AfricanAmerican children are hospitalized at a rate ⬎3 times that of Caucasian children. The financial cost of pediatric asthma in the United States is measured in the billions of dollars, and the social cost includes 10 million lost school days. Mortality rates in pediatric asthma (in those ⬍18 years of age) more than doubled between 1980 and 1996. A disproportionate number of deaths occur in inner city areas. In the United States in 1998, an African-American child was greater than 4 times more likely to die from asthma than a Caucasian child.1 The highest mortality rates occur in adolescents. Persons who have had prior asthmatic exacerbations requiring intubation are at significantly increased risk for subsequent fatal exacerbations. Inappropriate delay in seeking medical attention and limited access to care are probably the most significant factors in pediatric asthma deaths. Underuse of anti-inflammatory agents and overuse of beta agonists are also significant factors.

M A N A GEMENT O F P EDIA T R IC A S T HM A / R O B ERT G . B OLTE

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Asthma is characterized by bronchial hyperreactivity, airway inflammation, and reversible airway obstruction. New developments in the understanding of the underlying physiology and pharmacologic treatment of pediatric asthma have occurred in recent years. Although inhaled beta-adrenergic agonists remain the initial treatment of choice for acute bronchospasm in asthma, there is an increased understanding of the importance of inflammation in the disease process. There is also recognition of the role of cholinergic-mediated airway obstruction. This review will focus on clinical applications of these concepts in the emergency management of pediatric asthma, the role of some newer treatment modalities, and the value of implementing an ED management protocol.

Inhaled Beta-Adrenergic Agonists Inhaled beta-adrenergic agents are the mainstay of acute asthma therapy.2,3 The side effects of these agents are minor and their margin of safety is wide. Inhalation delivers the agonist directly to the target organ. Thus, only a relatively small amount of the drug is required to achieve the desired therapeutic effect. As a result, side effects are substantially minimized. Even the more beta2-selective agents, however, can produce cardiovascular effects at very high doses. Less than 10% of an inhaled drug is actually retained in the lungs.4,5 In addition, for a given volume of aerosolized agent, the amount of drug actually inhaled may be directly proportional to the size and therefore the tidal volume of the child. The duration of bronchodilation depends on the dose as well as on the initial physiologic state of the smooth muscle. If the baseline smooth-muscle tone is increased, the intensity and duration of bronchodilation is decreased. Albuterol is currently the beta agonist of choice for delivery by the inhaled route in the treatment of acute pediatric asthma.2 Albuterol is a beta agonist with relatively high beta2 selectivity and minimal toxicity. When delivered by inhalation, cardiac stimulation is generally clinically insignificant even with high-dose regimens. Mild tremor (a specific beta2 effect) is common, and vomiting is occasionally seen. Albuterol has a duration of activity of 4 to 6 hours when delivered by inhalation. Frequent, repetitive dosing maximizes improvement in pulmonary functions. The current National Institutes of Health (NIH) dosing recommendation for frequently administered albuterol (nebulization every

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20 minutes for three treatments) is 0.15 mg/kg/dose (⫽0.03 ml/kg/dose of the 0.5% [5 mg/ml] respirator solution) with a minimum dose of 0.5 ml and a maximum dose of 1.0 ml. Since the margin of safety with albuterol is wide and there is self-regulation of the delivered dose based on the tidal volume, a more simplistic dosage scheme seems reasonable. A simplified weight-based dosing scheme is 2.5 mg (0.5 ml) of albuterol per dose for ⬍50 kg; 5.0 mg (1 ml) for ⬎50 kg. Nebulization should be powered by a continuous flow of oxygen at 6 to 8 L per minute. This helps to correct the hypoxemia frequently associated with acute asthma. Clinical assessment often underestimates the degree of hypoxemia present6 and pulse oximetry can be a useful adjuvant. The hypoxemia is primarily related to ventilation-perfusion mismatch. Both inhaled and parenteral adrenergic agents can aggravate ventilation-perfusion mismatch. This effect is seen frequently with the inhaled beta2-selective agents. Paradoxically, this decrease in oxygen saturation occurs despite improvement in pulmonary functions. This effect can last up to 30 minutes. The suggested mechanism involves a relative increase in perfusion (beta2-mediated pulmonary vasodilation) to a relatively hypoventilated, atelectatic segment of lung. This complication can be avoided by increasing the fraction of inspired oxygen. During the nebulization treatment, most older children can use the hand-held mouthpiece. For infants and young or uncooperative children (generally younger than 5 years), a firmly fitting face mask is appropriate. Albuterol is known to decrease serum potassium levels through beta2 stimulation of the membrane-bound sodium-potassium pump. Although this issue is rarely of clinical relevance in the ED setting, in patients requiring continuous albuterol therapy over many hours, serum potassium should be monitored and supplemented as needed. If one reflects on current NIH guidelines, the “every 20 minutes times 3” treatment regimen essentially constitutes continuous therapy over the first hour. The logistical reality of most EDs, however, makes the delivery of this dosing regimen very problematic. Truly continuous administration of albuterol has been shown to be both safe and effective.7-13 Cardiotoxicity is minimal, with most studies documenting a decrease in heart rate with continuous-administration protocols. If continuous albuterol regimens are routinely used in the ED, the

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use of a large-volume nebulizer improves convenience and efficiency, justifying the slightly increased equipment cost (see “Model ED Asthma Protocol”). If respiratory failure is impending, continuous albuterol nebulization should always be promptly initiated. A reasonable dosing regimen is 0.5 mg/kg/hour (maximum of 15 mg/hour).2

Albuterol Delivery by Metered-Dose Inhaler Several pediatric studies in ED settings have convincingly demonstrated that a metered-dose inhaler (MDI) combined with a spacer device can deliver inhaled beta agonists with effectiveness comparable to nebulization.14-17 Leversha et al,18 addressing a limitation of earlier studies, included younger and more severely ill patients in their study. Even in the young child with a more severe asthmatic exacerbation, they found MDI administration to be comparable to nebulization.18,19 Depending on the usage pattern of ED nursing or respiratory therapy personnel, the routine use of MDIs with spacers may result in significant overall cost reductions, although equipment/medication costs may actually increase.20 Similar to nebulization delivery, a mask rather than a mouthpiece is generally preferable in the child older than 5 years. Six puffs of albuterol per MDI (100 ␮g per puff or 600 ␮g total) is an estimated equivalent to a dose of 2.5 mg of nebulized albuterol. Therefore, 6 puffs represents a reasonable ED dosing regimen for a single treatment. To optimize delivery, the MDI should be shaken before each actuation and medication administered one actuation at a time about 1 minute apart, delivered just before inhalation and then cleared from the spacer with a minimum of 5 tidal breaths between actuations. This treatment regimen may be repeated every 20 minutes, similar to conventional nebulization therapy. Note that the electrostatic charge present in a new spacer chamber can reduce albuterol delivery by up to 66% for the initial few treatments. This effect can be overcome by priming the chamber with 10 actuations before the first use.18 Unquestionably, the use of an MDI with a spacer device (versus nebulizer) in the home setting represents a major cost saving and is also generally much more convenient. At a minimum, MDI with spacer should be the standard albuterol delivery system prescribed at ED discharge, even for younger asthmatics. Note that for routine home therapy, 2 puffs administered every 4 hours is a reasonable regimen (see “Model ED Asthma Protocol”).

Levalbuterol The standard formulation of albuterol is a 50/50 mixture of the R and S isomers. The R isomer is responsible for bronchodilation. Animal and in vitro studies have raised a concern that the S isomer may stimulate a bronchoconstrictive response. Levalbuterol is a formulation containing only the active R isomer. It is available only as a nebulizer solution and is more expensive than standard albuterol. Data regarding the effect of levalbuterol (versus albuterol) in children with acute asthmatic exacerbations is somewhat limited. In general, clinically significant differences in effect on pulmonary functions, heart rate, tremor, and serum potassium have not been found. Carl et al21 found a lower admission rate with levalbuterol versus albuterol (37% vs. 45%, p ⫽ 0.05). However, the admit rate in the albuterol cohort was quite high (45%). Furthermore, there were no objective differences at disposition (respiratory rate, oxygen saturation) to account for the difference in admission rate.22 At present, this author concurs with The Medical Letter23 and Asmus and Hendeles,24 who conclude that levalbuterol appears to have no clinically significant advantage over racemic albuterol and is more costly. However, further research to define an appropriate niche for the ED use of levalbuterol is certainly warranted.

Parenteral Beta Agonists When beta agonists are delivered by the intravenous (IV) route rather than by inhalation, selectivity is diminished and side effects are increased. However, if the asthmatic child in impending respiratory failure is recalcitrant to aggressive inhalation therapy (continuous albuterol/frequent ipratropium nebulizations) and IV magnesium sulfate, IV administration of a beta agonist is reasonable in an attempt to avoid mechanical ventilation. IV aminophylline has no additive benefit when inhalation therapy is maximized. Only side effects are increased.25-30 1997 NIH guidelines2 specifically advise against the use of IV isoproterenol “because of the danger of myocardial toxicity.” There is no role for the routine use of beta agonists (such as epinephrine or terbutaline) administered by subcutaneous injection in the treatment of pediatric asthma. Terbutaline is a relatively beta2-selective agonist. It has significantly less cardiotoxicity than isoproterenol.31 However, moderate increases in pulse and systolic blood pressure accompanied by

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decreases in diastolic blood pressure are common.32 Headache and tremor are also often-seen side effects. The IV loading dose is 10 ␮g/kg over 10 minutes followed by an IV infusion of 0.4 ␮g/kg/ min. If necessary, the infusion can be increased by 0.2 ␮g/kg/min every 30 minutes up to a maximum dosage of 6.0 ␮g/kg/min.33 Continuous monitoring of all cardiorespiratory parameters is necessary with administration of IV terbutaline. Concomitant epinephrine infusions may be required to treat systemic vasodilation associated with low diastolic blood pressures. IV salbutamol (albuterol) has a pharmacologic profile similar to IV terbutaline and has potentially significant side effects. It is not currently available in the United States. Browne et al34,35 have published two Australian pediatric studies suggesting more rapid improvement and shorter hospitalization in children with acute severe asthma who received a single bolus of IV salbutamol (15 ␮g/kg administered over 10 minutes) in addition to standard therapy. No significant adverse side effects were noted in these two small studies.

Inhaled Anticholinergic Agents Inhalation therapy with anticholinergic agents originated thousands of years ago in India. Various plants were prepared as combustible powders and their smoke was inhaled for relief of respiratory distress. These practices were incorporated into Western medicine in the early 19th century. However, as epinephrine and ephedrine became available in the first half of the 20th century, anticholinergic drugs for the treatment of asthma fell into disuse.36 Advances in understanding of the role of parasympathetic bronchomotor tone and the development of less toxic anticholinergic agents have renewed interest in inhaled anticholinergic drugs as therapeutic agents in the treatment of asthma.

Physiology and Pharmacology The baseline level of bronchomotor tone (airway caliber) is predominantly controlled by the parasympathetic nervous system.37 Increased vagal stimulation leads to increased intracellular concentrations of cyclic guanosine monophosphate within smooth bronchial muscle, resulting in bronchoconstriction. This cholinergic-mediated bronchoconstriction can be blocked by anticholinergic agents, which competitively antagonize acetylcholine at its receptor sites. Anticholinergic drugs may also in-

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hibit acute airway obstruction by interfering with the release of inflammatory mediators from the mast cell. Ipratropium is a synthetic derivative of atropine. It has been used clinically as a bronchodilator in Europe since the mid-1970s. When delivered by inhalation, it is a much more selective bronchodilator than atropine because it is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier. Therefore, the therapeutic margin for ipratropium administration is wide.37 The lack of gastrointestinal absorption is significant because at least 90% of the dose of an inhaled drug is deposited in the oropharynx and then swallowed.38 Ipratropium does not affect mucus secretion, viscosity, or transport rates. The bronchodilating effect of nebulized ipratropium begins 5 to 15 minutes after administration, plateaus at 45 to 60 minutes, and lasts for up to 6 hours.39 When compared directly with albuterol, the bronchodilating effect of ipratropium is less potent. Because of its poor gastrointestinal absorption and lack of central nervous system effects, nebulized ipratropium produces no significant systemic toxic effects, even at doses many times those required for maximal bronchodilation.40 Dry mouth is a complaint in about 10% of patients. Pupillary dilation with the use of nebulized ipratropium (a direct topical effect) has been infrequently reported.41,42 This effect produces nebulized ipratropium’s only significant toxicity, which is precipitation of acute angle-closure glaucoma in children with the rare condition of pre-existing glaucoma.41,43 Ipratropium is available as a nebulizer solution in a 2.5-ml, 500-␮g vial as well as a MDI. The MDI form of ipratropium is contraindicated in patients with egg or soy allergy; however, this is not an issue with the nebulizer solution.

Clinical Studies and Treatment Guidelines In an ED study of children with severe asthma, Schuh et al44 found that multiple-dose ipratropium nebulizations significantly improved pulmonary function (versus placebo). Hospitalization rate was reduced only in the most severely affected group (forced expiratory volume in 1 second [FEV 1] ⬍ 30%). However, the reduction in the hospitalization rate in this most severe group was dramatic (83% hospitalization rate in the no-ipratropium cohort vs. 27% in the cohort receiving three ipratropium nebulizations). Qureshi et al45 found that two doses of ipratropium improved pulmonary functions (versus placebo) in the moderate-to-severe pediatric

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asthmatic when used in the ED in conjunction with albuterol nebulizations. The decrease in the rate of hospitalization in the ipratropium-treated group did not reach statistical significance. Zorc et al,46 in an ED study of 427 children presenting with asthma, found that the addition of three doses of ipratropium reduced ED treatment time and resulted in fewer albuterol nebulizations. Hospital admission rate was not significantly reduced in the children receiving ipratropium. Ipratropium does not replace beta-adrenergic agents such as albuterol in the acute treatment of pediatric asthma. However, repetitive dosing as an adjuvant to beta-agonist therapy does appear to have a significant role in the treatment of severe acute pediatric asthma. Because of its very favorable safety profile, relatively low cost, and the potential for reduction of hospitalization, inclusion of ipratropium in acute care of moderate to severe pediatric asthma is reasonable (see “Model ED Asthma Protocol”). The continued use of ipratropium in the child hospitalized for asthma has not been shown to be of additional benefit.47

Corticosteroids Corticosteroids have been used in the treatment of asthma for more than 50 years.48 Although they were initially hailed as miracle drugs, significant side effects became evident with their chronic use. Multiple studies since the mid-1980’s have helped to clarify the important role of corticosteroids in the management of acute pediatric asthma in the ED.

Physiology and Pharmacology Although the exact mechanisms through which corticosteroids exert their anti-asthmatic effects are not entirely clear, several theories have been advanced (Table 1). 49 An underlying principle is that corticosteroids do not interact directly with receptors on the cell surface; rather, they exert their effects by modifying protein synthesis at the nuclear level. Implicit in this concept is an inherent delay before the onset of clinical effectiveness. Recent data suggest that this delay may in fact be relatively brief, with significant clinical effects seen as early as 2 to 4 hours after administration.50-54 This relatively rapid onset of action has important implications for the clinical treatment of asthma in the ED. Adverse effects associated with the administration of short courses of corticosteroid are infre-

TABLE 1. Postulated Mechanisms for Corticosteroids in the Treatment of Asthma 1. Interference with synthesis and release of inflammatory mediators 2. Enhanced response to catecholamines 3. Stimulation of cyclic adenosine monophosphate metabolism 4. Restoration or increased synthesis of beta-adrenergic receptors 5. Inhibition of catechol-O-methyltransferase 6. Inhibition of phosphodiesterase 7. Diminished effects of cholinergic stimulation through inhibition of cyclic guanosine monophosphate 8. Improved mucociliary clearance 9. Stabilization of lysosomes 10. Alteration in leukocyte number and activity. quent and generally clinically insignificant.55 Varicella infection is one of the few contraindications for corticosteroid administration. Pituitaryadrenal recovery after a single course of high-dose short-term corticosteroid therapy occurs within 2 weeks.56 Although a recent study by Ducharme et al57 provides reassuring data regarding the relative infrequency of adrenal suppression, most authors suggest that if high-dose corticosteroids are administered for longer than 10 days or if 4 or more short high-dose courses per year are given, the risk of pituitary-adrenal suppression must be considered for up to 1 year post-treatment. Therefore, if these conditions are present, stress doses of corticosteroid are recommended if the child requires emergency surgery or sustains multiple trauma.56,58

Clinical Studies and Treatment Guidelines Prevention of hospitalization and repeated ED visits is a significant priority in the management of a child with asthma. Corticosteroids have been widely used in an effort to achieve these ends. Several studies of high-dose corticosteroids administered early in the course of ED treatment have documented significantly decreased hospital admission rates. Littenberg and Gluck,50 in a double-blind, placebo-controlled, randomized trial, administered an IV bolus of methylprednisolone (approximately 2 mg/kg), in addition to conventional treatment, to adults with acute asthma exacerbations on presentation to the ED. Despite an

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average ED stay of only 4 hours, there was a 60% lower admission rate in the corticosteroid group (19%, vs. 47% for placebo) with no increased incidence of repeated ED visits or subsequent readmission to the hospital. Tal et al51 conducted a similar double-blind, placebo-controlled, randomized trial with a group of pediatric asthmatics presenting to the ED with an acute exacerbation. Methylprednisolone (4 mg/kg intramuscularly [IM]) or placebo was given on arrival to the ED in addition to albuterol nebulizations. Disposition was made 3 hours after initiation of treatment. Again, hospitalization rate was significantly decreased in the steroid-treated group. Scarfone et al52 published a double-blind, placebocontrolled, randomized trial studying early ED use of oral steroids in a group of pediatric asthmatics with acute exacerbations. Oral prednisone (2 mg/kg, maximum dose of 60 mg) or placebo was given within 5 minutes of completing the first albuterol nebulization. Frequent albuterol nebulizations were continued in both groups. The decision regarding hospitalization was made 4 hours into the ED stay. This study demonstrated a significantly lower hospitalization rate in the cohort receiving oral steroids. Analysis of Scarfone’s data suggests that the steroid effect becomes apparent 2 to 4 hours after oral administration. Among patients who had a suboptimal response to initial beta-agonist therapy (and therefore would have been hospitalized if ED care had been restricted to 2 hours), 45% of the prednisone group ultimately required hospitalization at 4 hours versus 83% in the placebo group. Implicit in Scarfone’s data is the value of a period of observation in the ED for 3 to 4 hours after steroid administration. This allows time for the potential steroid-related clinical improvement to become apparent and thus possibly eliminate the need for hospitalization. These data, as well as the studies by Littenberg and Gluck,50 Tal et al,51 and Barnett et al,54 emphasize the importance of early administration of steroids in the ED treatment of the child with moderate to severe disease. This argues for the development of an ED management protocol (see “Model ED Asthma Protocol”). Based on these data, it is clear that if a child with a significant asthma exacerbation is referred to an ED from another facility, administration of corticosteroid before transfer is recommended. Qureshi et al,59 in a large clinical study involving 533 asthmatic children, found that two oral doses of dexamethasone (0.6 mg/kg/dose, maximum dose 16 mg, given once a day for 2 days) provided efficacy similar to 5 days of prednisone. Not surprisingly, compliance was better in the two-dose dexametha-

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sone group, even in the research setting. In the typical nonstudy environment, improved compliance would likely be very significant as half of the entire steroid regimen is administered under direct medical supervision in the ED60 (See “Model ED Asthma Protocol”.) If the child is unable to tolerate the oral corticosteroid, a single IM dose of dexamethasone phosphate (0.6 mg/kg, maximum dose 16 mg) is a reasonable alternative.61 The IM route should not be routine, since the oral corticosteroid offers the advantages of cost savings as well as minimizing pain. Minimizing pain is a particularly important principle when treating a child whose chronic disease can lead to multiple ED visits. Obviously, if the child presents in impending respiratory failure, the IV route is preferable. Inhaled corticosteroids are the mainstay of chronic asthma management in children. However, data regarding their potential utility in acute asthma management have been conflicting. Despite some encouraging preliminary data,62,63 a recent well-designed pediatric study64 convincingly demonstrated that a potent inhaled high-dose steroid (fluticasone) was not as effective as oral prednisone in children presenting to the ED with severe acute asthma. The hospitalization rate in the inhaled fluticasone cohort (31%) was significantly higher than that in the oral prednisone group (10%). Moreover, 25% of the inhaled fluticasone group (versus 0% in the oral prednisone group) showed deterioration in pulmonary functions 4 hours into therapy. For the child with an acute asthma exacerbation who responds to ED treatment and is able to be discharged to home, a short course of high-dose oral steroid should be strongly considered to help prevent clinical relapse with the potential for additional ED visits or hospitalization. Extensive clinical experience has shown that short courses of high-dose oral steroid are both safe and effective.55,65,66 They are clearly indicated in the child with a moderate to severe exacerbation requiring significant ED treatment or if the exacerbation was incompletely responsive to reasonable bronchodilator therapy at home before ED intervention. A history of frequent hospital admissions or repeated ED visits may also influence the decision to prescribe a short course of steroids at discharge. Tapering the doses is not necessary for the standard steroid short course.2 Explicit discharge instructions regarding guidelines for ED reevaluation and the arrangement of follow-up with a primary care physician are also important aspects of the disposition plan. In the child with a history of moderate asthma who is not on chronic control medications,

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the additional initiation of a maintenance inhaledsteroid regimen is a reasonable consideration. At a minimum, discussing this issue and arranging outpatient primary care follow-up should be routine. If the child is hospitalized, steroids are indicated to facilitate more rapid improvement of airway obstruction.2 An oral regimen, which is both less expensive and less painful, is preferable to the IV route. Becker et al67 demonstrated that a 2-mg/kg dose of oral prednisone (max. 120 mg) given twice daily was comparable to 1 mg/kg of methylprednisolone given IV every 6 hours. If the IV route is required, methylprednisolone (2 mg/kg IV bolus followed by a 1 mg/kg dose every 8 hours) is a reasonable choice.

Magnesium Sulfate The pediatric literature on magnesium sulfate is somewhat limited but suggests efficacy, particularly in the severe pediatric asthmatic.

Pharmacology Theoretically, magnesium sulfate acts as a physiologic calcium antagonist affecting calcium uptake in smooth muscle, resulting in smooth muscle relaxation. As beta-agonist therapy can decrease serum magnesium, it is possible that normalization of serum levels are in part responsible for the bronchodilating effect of magnesium.68 Only the IV route seems to be effective. Bronchodilating effects appear about 20 minutes postinfusion and may persist for up to 3 hours. Contraindications include renal disease, heart block or a history of myocardial damage, myasthenia gravis, or pregnancy. Side effects with currently recommended dosing regimens appear clinically insignificant and include mild blood pressure depression, flushing, and burning at the IV site. Significant adverse effects have not been reported to date. It is important to stress that the recommended magnesium sulfate dosages must be delivered as a continuous infusion over 20 minutes (not a rapid IV push) to avoid significant cardiotoxic effects.

Clinical Studies and Treatment Guidelines Pediatric data are limited, but three placebocontrolled studies, Ciarallo et al69,70 and Myers et al71 suggest efficacy in the severe asthmatic. Monem et al72 and Scarfone73 have also published limited series supporting the efficacy and safety of IV magnesium sulfate.

Scarfone et al74 also published a larger study demonstrating that early, routine use of high-dose IV magnesium did not provide significant added benefit (improved pulmonary function or decreased hospitalization rate) for children with moderate to severe acute asthma. When interpreting this study, it is important to note that the study design administered the IV magnesium to all children presenting to the ED with moderate to severe acute asthma and not to a group of children initially refractory to multiple albuterol nebulizations. This selection bias may have lead to an erroneous conclusion regarding the effectiveness of magnesium in the most severe group, those refractory to aggressive conventional therapies. Rowe et al,75 in a meta-analysis of seven controlled trials (five adult and two pediatric studies, 668 total patients) concluded that only in the subgroup of severe asthmatics did pulmonary function and hospitalization rates improve. This suggests that the Ciarallo et al69,70 and Scarfone’s et al74 data may, in fact, not be inconsistent and that magnesium should be selectively used in the severe asthmatic unresponsive to conventional treatment. Therefore, in the child with a very severe asthma exacerbation (eg, potential intensive-care unit admission, impending respiratory failure) not promptly responding to aggressive conventional treatment regimens (continuous albuterol inhalation, multiple ipratropium nebulizations), IV magnesium at 75 mg/kg (maximum 2.5 g) administered as a continuous infusion over 20 minutes in 100 to 200 mL of normal saline seems a prudent modality to expeditiously implement. Toxicity appears to be minimal (certainly less than IV beta adrenergics) and clinical response is relatively rapid.

Heliox Heliox is a mixture of helium and oxygen that decreases the turbulence of flow in the airway. The use of heliox for severe upper airway obstruction is well established; however, its efficacy in lower-respiratory tract disease remains controversial. By decreasing the work of breathing, substitution of heliox for oxygen-enriched air could theoretically improve the outcome for a child with impending respiratory failure, possibly obviating the need for intubation and mechanical ventilation. However, the relatively low inhaled oxygen concentration (20%-30%) utilized in heliox administration may inherently limit its use in the hypoxic patient. Adult studies provide conflicting results regarding the utility of heliox in the ED treatment of asthma.

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Pediatric data are very limited; two published studies found differing results. Carter et al,76 in a small pediatric study (N ⫽ 11) found no significant improvement in pulmonary functions in those randomized to receive a 70:30 helium-oxygen mixture. Kudukis et al,77 in another small pediatric study (N ⫽ 18), found significant improvement in peak flow and work of breathing (possibly averting the need for intubation in 3 patients) in those randomized to receive an 80:20 helium-oxygen mixture. At present, this author concurs with the conclusion of Rodrigo et al in their review78 that the current literature does not support the use of heliox in the ED management of the moderate to severe asthmatic. Further studies are warranted.

Inhaled Nitric Oxide Nitric oxide delivered by inhalation is a potent, selective pulmonary vasodilator that may also have significant bronchodilating effects. Published pediatric experience in the non-neonatal population is very limited. Pfeffer et al79 found that inhaled nitric oxide had no effect in nonacute children with chronic stable asthma. However, Nakagawa et al80 demonstrated significant rapid improvement in 4 of 5 intubated children with life-threatening status asthmaticus who received inhaled nitric oxide. Further studies are warranted.

Ancillary Studies: Peak Flow Measurements and Chest Radiographs Ideally, peak flow measurements should be incorporated into the routine ED management of any child 5 years old or older with a known diagnosis of asthma.2 However, interpretation of isolated results are problematic. A comparison with previously established personal-best values provides the most meaningful information. Certainly, peak flow data are an important tool in outpatient management of the chronic asthmatic. Chest radiographs are not recommended in the routine ED evaluation of the child with known asthma presenting with an acute exacerbation.2 Since viral respiratory infections are the most common trigger of an asthma exacerbation in a child, the mere presence of fever is not an indication to obtain a chest radiograph. Chest radiographs should be reserved for cases with clinically suspected complicating cardiopulmonary processes (such as pneumothorax, pneumomediatstinum, or, rarely, bacterial pneumonia) and for the severe,

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unresponsive exacerbation requiring admission to an intensive care unit.

Summary: Utility of an ED Protocol for Pediatric Asthma The ED management of pediatric asthma is an example of a common and relatively well-defined disease process with a reasonable consensus regarding current best-practice standards. Despite the general intellectual acceptance of national guidelines for acute pediatric asthma care,2 the actual delivery of care in the ED often falls short of the ideal.81 This dissonance suggests the need for the implementation of a protocol-based management plan. An effective protocol should improve timeliness and overall efficiency in the delivery of care. The data demonstrating a significant decrease in hospitalization rate with early ED administration of corticosteroid also provides a compelling reason to implement a well-organized approach. An example of such a protocol, currently used in the ED at Primary Children’s Medical Center in Salt Lake City, Utah, is included as an advance with this article.

References 1. Akinbami LJ, Schoendorf KC: Trends in childhood asthma: Prevalence, health care utilization, and mortality. Pediatrics 110:315-322, 2002. 2. Guidelines for the diagnosis and management of asthma. National Asthma Education Program, Expert Panel Report. US Department of Health and Human Services, National Institutes of Health. Publication No. 974051, pp. 59-70, April 1997. 3. Global initiative for asthma: Global strategy for asthma management and prevention. NHLBI/WHO Workshop Report. National Institutes of Health. Publication No. 95-3659. January 1995. 4. Brain JD, Valberg PA: Deposition of aerosol in the respiratory tract. Am Rev Respir Dis 120:1325-1373, 1979. 5. Newman SP, Pavia D, Moren F, et al: Deposition of pressurized aerosols in the human respiratory tract. Thorax 36:52-55, 1981. 6. Hurwitz ME, Burney RE, Howatt WF, et al: Clinical scoring does not accurately assess hypoxemia in pediatric asthma patients. Ann Emerg Med 13:1040-1043, 1984. 7. Olshaker J, Jerrard D, Barish RA, et al: The efficacy and safety of a continuous albuterol protocol for the treatment of acute adult asthma attacks. Am J Emerg Med 11:131-133, 1993. 8. Katz RW, Kelly W, Crowley MR, et al: Safety of continuous nebulized albuterol for bronchospasm in infants and children. Pediatrics 92:666-669, 1993.

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9. Rudnitsky GS, Eberlein RS, Schoffstall JM, et al: Comparison of intermittent and continuously nebulized albuterol for treatment of asthma in an urban emergency department. Ann Emerg Med 22:1842-1846, 1993. 10. Lin RY, Sauter D, Newman T, et al: Continuous versus intermittent albuterol in the treatment of acute asthma. Ann Emerg Med 22:1847-1853, 1993. 11. Levitt MA, Gambrioli EF, Fink JB: Comparative trial of continuous nebulization versus metered-dose inhaler in the treatment of acute bronchospasm. Ann Emerg Med 26:273-277, 1995. 12. Craig VL, Bigos D, Brilli RJ: Efficacy and safety of continuous albuterol nebulization in children with severe status asthmaticus. Pediatr Emerg Care 12:1-5, 1996. 13. Papo MC, Frank J, Thompson SE: A prospective, randomized study of continuous versus intermittent nebulized albuterol for severe status asthmaticus in children. Crit Care Med 21:1479-1486, 1993. 14. Benton G, Thomas RC, Nickerson BG, et al: Experience with a metered-dose inhaler with a spacer in the pediatric emergency department. Am J Dis Child 143: 678-681, 1989. 15. Kerem E, Levison H, Schuh S, et al: Efficacy of albuterol administered by nebulizer versus spacer in children with acute asthma. J Pediatr 123:313-317, 1993. 16. Chou KJ, Cunningham SJ, Crain EF: Metered-dose inhalers with spacers vs nebulizers for pediatric asthma. Arch Pediatr Adolesc Med 149:201-205, 1995. 17. Williams JR, Bothner JP, Swanton RD: Delivery of albuterol in a pediatric emergency department. Pediatr Emerg Care 12:263-267, 1996. 18. Leversha AM, Campanella SG, Aickin RP, et al: Costs and effectiveness of spacer versus nebulizer in young children with moderate and severe acute asthma. J Pediatr 16:497-502, 2000. 19. Kercsmar CM: Aerosol treatment of acute asthma: And the winner is . . . . J Pediatr 16:428-430, 2000. 20. Bowton DL, Goldsmith RRT, Haponik EF: Substitution of metered-dose inhalers for hand-held nebulizers: Success and cost savings in a large acute-care hospital. Chest 101:305-308, 1992. 21. Carl JC, Myers TR, Kirchner HL, et al: Comparison of racemic albuterol and levalbuterol for the treatment of acute asthma. J Pediatr 143:731-736, 2003. 22. Kattan M: Mirror images: Is levalbuterol the fairest of them all? J Pediatr 143:702-704, 2003. 23. Levalbuterol for asthma. The Medical Letter Vol. 41 (issue 1054), June 4 1999. 24. Asmus MJ, Hendeles L: Levalbuterol nebulizer solution: Is it worth five times the cost of albuterol? Pharmacotherapy 20:123-129, 2000. 25. Fanta CH, Rossing TH, McFadden ER, Jr: Emergency room treatment of asthma: Relationships among therapeutic combinations, severity of obstruction and time course of response. Am J Med 72:416-422, 1982. 26. Siegel D, Sheppard D, Gelb A, et al: Aminophylline increases the toxicity but not the efficacy of an inhaled beta-adrenergic agonist in the treatment of acute exacerbations of asthma. Am Rev Respir Dis 132:283-286, 1985.

27. Self TH, Abou-Shala N, Burns R, et al: Inhaled albuterol and oral prednisone therapy in hospitalized adult asthmatics: Does aminophylline add any benefit? Chest 98:1317-1321, 1990. 28. DiGiulio GA, Kercsmar CM, Krug SE, et al: Hospitalized treatment of asthma: Lack of benefit from theophylline given in addition to nebulized albuterol and intravenously administered corticosteroid. J Pediatr 122: 464-469, 1993. 29. Carter E, Cruz M, Chesrown S, et al: Efficacy of intravenously administered theophylline in children hospitalized with severe asthma. J Pediatr 122:470-476, 1993. 30. Strauss RE, Wertheim DL, Bonagura VR, et al: Aminophylline therapy does not improve outcome and increases adverse effects in children hospitalized with acute asthmatic exacerbation. Pediatrics 93:205-210, 1994. 31. Mikhail MS, Hunsinger SY, Goodwin SR, et al: Myocardial ischemia complicating therapy of status asthmaticus. Clin Pediatr 26:419-421, 1987. 32. Fuglsang G, Pedersen S, Borgstrom L: Dose-response relationships of intravenously administered terbutaline in children with asthma. J Pediatr 114:315-320, 1989. 33. DeNicola LK, Monem GF, Gayle MO, et al: Treatment of critical status asthmaticus in children. Pediatr Clin North Am 41:1293-1324, 1994. 34. Browne GJ, Penna AS, Phung X, et al: Randomised trial of intravenous salbutamol in early management of acute severe asthma in children. Lancet 349:301-305, 1997. 35. Browne GJ, Trieu L, Van Asperen P: Randomized, double-blind, placebo-controlled trial of intravenous salbutamol and nebulized ipratropium bromide in early management of severe acute asthma in children presenting to an emergency department. Crit Care Med 30:448453, 2002. 36. Gandevia B: Historical review of the use of parasympatholytic agents in the treatment of respiratory disorders. Postgrad Med J 51:13-20, 1975. 37. Gross NJ, Skorodin MS: Anticholinergic, antimuscarinic bronchodilators. Am Rev Respir Dis 129:856-870, 1984. 38. Davies DS: Pharmacokinetics of inhaled substances. Scand J Respir Dis 103:44-49, 1979. 39. Gross NJ: A new anticholinergic bronchodilator. Am Rev Respir Dis 112:823-828, 1975. 40. Rebuck AS, Chapman KR, Abboud R, et al: Nebulized anticholinergic and sympathomimetic treatment of asthma and chronic obstructive airways disease in the emergency room. Am J Med 82:59-64, 1987. 41. Malani JT, Robinson GM, Seneviratne EL: Ipratropium bromide induced angle closure glaucoma (letter). N Z Med J 95:749, 1982. 42. Jannun DR, Mickel SF: Anisocoria and aerosolized anticholinerigics. Chest 90:148-149, 1986. 43. Shah P, Dhurjon L, Metcalfe T, et al: Acute angle closure glaucoma associated with nebulized ipratropium bromide and salbutamol. BMJ 304:40-41, 1992.

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44. Schuh S, Johnson DW, Callahan S, et al: Efficacy of frequent nebulized ipratropium bromide added to frequent high-dose albuterol therapy in severe childhood asthma. J Pediatr 126:639-645, 1995. 45. Qureshi F, Zaritsky A, Lakkis H: Efficacy of nebulized ipratropium in severely asthmatic children. Ann Emerg Med 29:205-211, 1997. 46. Zorc JJ, Pusic MV, Ogborn CJ, et al: Ipratropium bromide added to asthma treatment in the pediatric emergency department. Pediatrics 103:748-752, 1999. 47. Goggin N, Macarthur C, Parkin PC: Randomized trial of the addition of ipratropium bromide to albuterol and corticosteroid therapy in children hospitalized because of an acute asthma exacerbation. Arch Pediatr Adolesc Med 155:1329-1334, 2001. 48. Carryer HM, Koelsche GA, Prickman LE, et al: Effects of cortisone on bronchial asthma and hay fever occurring in subjects sensitive to ragweed pollen. Mayo Clin Proc 25:482-486, 1950. 49. Fiel SB: Should corticosteroids be used in the treatment of acute, severe asthma? I: A case for the use of corticosteroids in acute, severe asthma. Pharmacotherapy 5:327-331, 1985. 50. Littenberg B, Gluck EH: A controlled trial of methylprednisolone in the emergency treatment of acute asthma. N Engl J Med 314:150-152, 1986. 51. Tal A, Levy N, Bearman JE: Methylprednisolone therapy for acute asthma in infants and toddlers: A controlled clinical trial. Pediatrics 86:350-356, 1990. 52. Scarfone RJ, Fuchs SM, Nager AL, et al: Controlled trial of oral prednisone in the emergency department treatment of children with acute asthma. Pediatrics 92:513-518, 1993. 53. Scarfone RJ, Loiselle JM, Wiley JF, et al: Nebulized dexamethasone versus oral prednisone in the emergency treatment of asthmatic children. Ann Emerg Med 26:480-486, 1995. 54. Barnett PLJ, Caputo GL, Baskin M, et al: Intravenous versus oral corticosteroids in the management of acute asthma in children. Ann Emerg Med 29:212-217, 1997. 55. Harris JB, Weinberger MM, Nassif E, et al: Early intervention with short courses of prednisone to prevent progression of asthma in ambulatory patients incompletely responsive to bronchodilators. J Pediatr 110:627633, 1987. 56. Streck WF, Lockwood DH: Pituitary adrenal recovery following short-term suppression with corticosteroids. Am J Med 66:910-914, 1979. 57. Ducharme FM, Chabot G, Polychronakos C, et al: Safety profile of frequent short course of oral glucocorticoids in acute pediatric asthma: Impact on bone mineralization, bone density, and adrenal function. Pediatrics 111:376-383, 2003. 58. Chamberlin P, Meyer WJ: Management of pituitary-adrenal suppression secondary to corticosteroid therapy. Pediatrics 67:245-251, 1981. 59. Qureshi F, Zaritsky A, Poirier MP: Comparative efficacy of oral dexamethasone versus oral prednisone in acute pediatric asthma. J Pediatr 139:20-26, 2001.

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60. Jones MA, Wagener JS: Managing acute pediatric asthma: Keeping it short. J Pediatr 139:3-5, 2001. 61. Klig JE, Hodge D: Symptomatic improvement following emergency department management of asthma: A pilot study of intramuscular dexamethasone versus oral prednisone. J Asthma 34:419-425, 1997. 62. Scarfone RJ, Loiselle JM, Wiley JF, et al: Nebulized dexamethasone versus oral prednisone in the emergency treatment of asthmatic children. Ann Emerg Med 26:480-486, 1995. 63. Devidayal, Singhi S, Kumar L, et al: Efficacy of nebulized budesonide compared to oral prednisolone in acute bronchial asthma. Acta Paediatr 88:835-840, 1999. 64. Schuh S, Reisman J, Alshehri M, et al: A comparison of inhaled fluticasone and oral prednisone for children with severe acute asthma. N Engl J Med 343:689694, 2000. 65. Fiel SB, Swartz MA, Glanz K, et al: Efficacy of short-term corticosteroid therapy in outpatient treatment of acute bronchial asthma. Am J Med 75:259-262, 1983. 66. Brunette MG, Lands C, Thibodeau LP: Childhood asthma: Prevention of attacks with short-term corticosteroid treatment of upper respiratory tract infection. Pediatrics 81:624-629, 1988. 67. Becker JM, Arora A, Scarfone RJ, et al: Oral versus intravenous corticosteroids in children hospitalized with asthma. J Allergy Clin Immunol 103:586590, 1999. 68. Bodenhamer J, Bergstrom R, Brown D, et al: Frequently nebulized beta-agonists for asthma: Effects on serum electrolytes. Ann Emerg Med 21:1337-1342, 1992. 69. Ciarallo L, Sauer A, Shannon M: Intravenous magnesium therapy for moderate to severe pediatric asthma: Results of a randomized, placebo-controlled trial. J Pediatr 129:809-814, 1996. 70. Ciarallo L, Brousseau D, Reinert S: Higher-dose intravenous magnesium therapy for children with moderate to severe acute asthma. Arch Pediatr Adolesc Med 154:979-983, 2000. 71. Myers JH, Shook JE, Ward MA: Intravenous magnesium for moderate to severe childhood asthma. Pediatr Emerg Care 11:325, 1995 (Abst). 72. Monem GF, Kissoon N, DeNicola L: Use of magnesium sulfate in asthma in childhood. Pediatr Ann 25:136144, 1996. 73. Scarfone RJ: Use of magnesium sulfate in the treatment of children with acute asthma. Clin Pediatr Emerg Med 1:6-12, 1999. 74. Scarfone RJ, Loiselle JM, Joffe MD, et al: A randomized trial of magnesium sulfate in the emergency department treatment of children with asthma. Ann Emerg Med 36:572-578, 2000. 75. Rowe BH, Bretzlaff JA, Bourdon C, et al: Intravenous magnesium sulfate treatment for acute asthma in the emergency department: A systematic review of the literature. Ann Emerg Med 36:181-189, 2000.

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76. Carter ER, Webb CR, Moffitt DR: Evaluation of heliox in children hospitalized with acute severe asthma: A randomized cross-over trial. Chest 109:1256-1261, 1996. 77. Kudukis TM, Manthous CA, Schmidt GA, et al: Inhaled helium-oxygen revisited: Effect of inhaled helium-oxygen during the treatment of status asthmaticus in children. J Pediatr 130:217-224, 1997. 78. Rodrigo G, Pollack C, Rodrigo C, et al: Heliox for nonintubated acute asthma patients. Cochrane Database Syst Rev (4):CD002884, 2003. 79. Pfeffer KD, Ellison G, Robertson D, et al: The effect of inhaled nitric oxide in pediatric asthma. Am J Respir Crit Care Med 153:747-751, 1996. 80. Nakagawa TA, Johnston SJ, Falkos SA, et al: Lifethreatening status asthmaticus treated with inhaled nitric oxide. J Pediatr 137:119-122, 2000. 81. Crain ER, Weiss KB, Fagan MJ: Pediatric asthma care in US emergency departments: Current practice in the context of the NIH guidelines. Arch Pediatr Adolesc Med 149:893-901, 1995.

Addendum: Model ED Asthma Protocol I. PURPOSE: A. To more efficiently and effectively deliver care for the pediatric asthmatic patient in the ED, thereby improving patient and parent satisfaction and possibly decreasing the hospital admission rate. II. NURSING ASSESSMENT/INTERVENTIONS/ EVALUATION/DOCUMENTATION: A. Triage Nurse 1. Identifies potential asthma protocol patient at triage 2. Exclusions from protocol entry: a. Impending respiratory failure requiring emergent ICU admission b. Age ⬍ 2 years c. No prior history of wheezing 3. If ⬍ 2 years and h/o recurrent wheezing/ RAD, possible protocol candidate. Check with ED attending 4. Notifies Charge Nurse B. Charge Nurse 1. Notifies ED attending regarding status of protocol patient 2. Places distressed patient in room 3. Assigns patient care nurse 4. Places patient on supplemental oxygen if: a. Distressed or, b. Oxygen saturation ⱕ90% or c. Peak flow ⬍ 80% of predicted or personal best (ⱖ5 years of age) C. ED Nurse 1. Ensures

a. Patient is on supplemental oxygen 1. If distressed, or 2. Oxygen saturation ⱕ90%, or b. Peak flow ⬍ 80% of predicted or personal best (ⱖ5 years of age) c. Medical baseline assessment has been done d. Nursing assessment to determine i. Current medications ii. Prior ICU or intubated admissions iii. Retractions iv. Wheezing v. Vital signs with oxygen saturation (a). On room air unless significantly distressed (b). Places on oxygen if distressed and records initial saturation vi. Severity of asthma exacerbation (see Severity of Asthma Exacerbation chart at end of the protocol) (a). Method of administering nebulized treatments (small vs large volume nebulizer) (b). Use of steroids (c). Medications to use in nebulizer e. If patient is age ⱖ5 years of age i. Height in inches ii. Peak flows are performed and documented ● Before the 1st, 2nd, and 3rd treatment ● 10 minutes after the 3rd treatment and at discharge 2. Documentation a. History of Congenital Glaucoma b. History of exposure to varicella (chicken pox) in the past three weeks c. Response to therapy after each treatment (if using small volume nebulizer) or q20 minutes (if using continuous large volume nebulizer) i. PEFR and percentage of predicted or personal best ii. Retractions iii. Wheezes iv. Adequacy of air movement v. Condition at time of discharge 3. Initiates nebulization treatments, options include a. If severity of exacerbation is determined to be mild, use “back to back” nebulization treatments, as needed. If patient is ⱖ 5 years of age, peak flow measurements should be performed

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b.

c.

d.

e.

f.

and documented before the 1st, 2nd, and 3rd treatment and 10 minutes after the 3rd treatment. Medication dosing for 1st “back to back” nebulization treatment: i. ⬍50 kg: Albuterol (one plastic bullet ⫽2.5mg⫽3 ml) ii. ⱖ50 kg: Albuterol (two plastic bullets⫽5mg⫽ 6 ml) Medication dosing for 2nd and/or 3rd “back to back” nebulization treatments: i. Albuterol dosing as listed above ii. Ipratropium (one-half plastic bullet ⫽250 micrograms ⫽ 0.25 mg ⫽ 1.25 ml) Treatment to be given at 20 to 30 minute intervals, timed from the initiation of one treatment to the initiation of the next, for the first three treatments as needed. Note: Not every patient will require three nebulizations. If the nurse feels that all three nebulizations are not necessary (based on a significant response to therapy), this should be discussed with the ED physician. If ED discharge is anticipated and the family does not currently use home nebulizations, the “last” albuterol aerosol should be administered by MDI with a spacer device (2 puffs). A MDI with spacer device regimen should be incorporated into their out-patient management plan. If severity of asthma exacerbation is determined to be moderate to severe use the “continuous” aerosol therapy with the large volume nebulizer.(MiniHEART ® Hi-Flo Continuous Nebulizer). Suggested dosages for large volume nebulizer: i. Albuterol: ● ⬍50 kg: (Three plastic bullets ⴝ7.5 mgⴝ 9 ml) ● ⱖ50 kg: (Six plastic bullets ⴝ15mgⴝ 18 ml) ii. Ipratropium (Atrovent ®): ● Regardless of patient weight: (Two plastic bulletsⴝ 1.0 mgⴝ 5 ml) iii. For ⬍ 50 kg, add extra diluent of 6 cc NS (20 ml total)

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iv. For ⱖ50 kg, no extra NS diluent needed (23 ml total) v. Total solution is delivered over a one hour period with 8 liters of oxygen/minute. g. If “continuous” nebulization is used, the patient must be reassessed every 20 minutes during the nebulization. 4. Administers steroids concurrently with the nebulized treatment in the moderate to severe exacerbation patients. a. Contraindications for steroid administration i. Active varicella or herpes infection, or history of exposure to varicella in past 3 weeks. ii. Appropriate dose of oral steroids already given in last 6 hours. iii. If parents decline steroids, document. b. Dosage of oral dexamethasone i. Initial dose 0.6 mg/kg rounded up to the nearest 4 mg increment (maximum dose of 16 mg). ii. May be repeated at full dose in cases of emesis within 30 minutes of administration. (a). Parenteral equivalents may be used at the discretion of the ED attending (based on the patient⬘s severity or inability to tolerate the oral route). (b). The patient should be sent home with a filled prescription for a second dose of decadron to take 12-24 hours after first dose. 5. Ensures appropriate patient teaching is delivered prior to discharge a. MDI and spacer use b. Home nebulizers c. Home peak flow meters d. Determines need of involvement of respiratory therapy who will be available for discharge teaching within a reasonable time frame. 6. Ensures discharge instructions include: a. Medication regimen b. Expected/routine follow-up plan i. Generally with primary care MD c. Emergent follow-up plan i. Return to PCMC ED

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III. PHYSICIAN ASSESSMENT/INTERVENTION/ DOCUMENTATION: D. ED Attending 1. Concurs with the initiation of protocol 2. Assigns ED resident to patient and/or performs baseline assessment 3. CXR ordered only if: a. No baseline films have been obtained during prior evaluations b. Suggestion of air leak (clinical signs of pneumothorax or pneumomediastium) c. Clinical indication of bacterial pneumonia d. Clinical indication of foreign body aspiration

4. Ensures timely disposition of patient a. Most patients can be discharged 30 to 60 minutes after last nebulizer treatment. b. Potential admissions to hospital (persistantly symptomatic patients) generally should be treated in the ED for approximately 3 hours after the administration of steroids before making a final disposition decision (unless clinical status deteriorates), allowing steroids time to take effect. 5. Notifies primary care physician of the current ED visit and discharge plan.

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SEVERITY OF ASTHMA EXACERBATIONS Mild Breathlessness

Moderate

Severe

Respiratory Arrest Imminent

While walking

While talking

While at rest

Some difficulty feeding

Difficulty feeding

Infant stops feeding

Activity Level

Can lie down

Prefers sitting

Hunched forward

Talks In

Sentences

Phrases

Words

Alertness

May be agitated

Usually agitated

Usually agitated, maybe drowsy

Respiratory Rate

Normal to increased

Increased

Often ⬎30/min

Accessory Muscle Use

Usually none or subcostal

Usually subcostal and/or intercostal

Usually intercostal and suprasternal

Paradoxical thoracoabdominal movement

Wheeze

Moderate, often only endexpiratory

Loud, expiratory

Usually loud, often inspiratory and expiratory

Absence of wheeze

Pulse

⬍100

100-120

⬎120

Bradycardia

Peak Flow

Over 80%

Aprox. 60-80%

⬍60%

SaO2% (on RA)

⬎92%

88-92%

⬍88%

Treatment

Use small volume nebulizer Albuterol only No initial steroids

Use small or large volume nebulizer Albuterol and Atrovent Steroids with start of neb.

Use large volume nebulizer Alluterol and Atrovent Steroids with start of neb.

Drowsy or confused

% predicted of personal best

*Table adapted from Global Iniative for Asthma. National Institute of Health. Publication number 95-3659. January 1995. Pg.100. Abbreviations: SaO2 ⫽ arterial oxygen saturation; RA ⫽ room air; ICU ⫽ intensive care unit; RAD ⫽ reactive airway disease; ED ⫽ emergency department; q ⫽ every; PEFR ⫽ peak expiratory flow rate; kg ⫽ kilogram; mg ⫽ milligram; ml ⫽ milliliter; MDI ⫽ metered dose inhaler; NS ⫽ normal saline; PCMC ⫽ Primary Children’s Medical Center; CXR ⫽ chest x-ray. Guide to rates of breathing associated with respiratory distress in awake children: Age

Normal Rate

⬍2 mon

⬍60/min

2-12 mon

⬍50/min

1-5 years

⬍40/min

6-8 years

⬍30/min

Guide to limits of normal pulse rate in children: Infants

2-12 months

⬍160/min

Preschool

1-2 years

⬍120/min

School Age

2-8 yars

⬍110/min