Managing asthma in the pediatric ED
By Blake Bulloch, MD; Richard M. Ruddy, MD
Peer Reviewer: Jeffrey Linzer, MD
Guest Editor: Larry B. Mellick, MD, MS, FAAP, FACEP
[Editor's note: This is the second of a three-part series on managing asthma in the pediatric emergency department (ED). Asthma is one of the most common causes for pediatric hospital admissions, with the ED often serving as the point of entry.
In last month's Asthma Management, we covered the clinical evaluation, physical examination, and diagnosing of the pediatric asthma patient. In this issue, we cover standard medications and management steps for the treatment of asthma exacerbations in the ED.
In next month's issue, we will cover procedures for those cases in which the pediatric patient is in respiratory failure, as well as some of the controversial issues in emergency management.]
Asthma medications are now divided into two groups. The first group is the quick-relief or "rescue" medications used to treat acute symptoms and exacerbations.1 Medications in this group consist of the short-acting beta2-agonists, anticholinergics, and systemic corticosteroids. (See Table 1, p. 37.) The second group is referred to as the long-term control medications and are used to achieve and maintain control of persistent asthma.
Beta-agonists act by increasing levels of cAMP in bronchial smooth muscle and in mast cells by activating the enzyme adenylate cyclase. Increased cAMP leads to increased binding of intracellular calcium to the endoplasmic reticulum, which decreases myoplasmic calcium and causes bronchial smooth muscle relaxation.2
High-dose, short-acting beta2-agonists, specifically albuterol, remain the treatment of choice for relief of acute symptoms.3 Bitolterol and pirbuterol also are inhaled short-acting beta2-agonists, but they have not been sufficiently studied.
Possible adverse effects from beta-agonist therapy can include a decrease in PaO2 due to a transient worsening of the ventilation/perfusion ratio, cardiac stimulation (i.e., tachycardia and ectopy), skeletal muscle tremor, and central nervous system stimulation.
Ipratropium bromide (Atrovent) is a quaternary ammonium derivative of atropine that limits its systemic absorption and decreases the side effects that were seen with the use of atropine. As such, it is the only anticholinergic currently used in the treatment of acute asthma exacerbations. It is delivered by aerosolization and inhibits smooth muscle contraction and mast cell mediator release. It has a slower onset of action than beta2-agonists, with a peak effect occurring over two hours but lasting up to six hours.4,5 When compared directly to albuterol, it is not as potent a bronchodilator.
Osmond and Klassen reported a meta-analysis of randomized controlled trials using ipratropium bromide with beta2-agonists and found a statistically significant improvement in percentage predicted FEV1 over beta2-agonists alone.4 The studies did not find a clinically significant difference, but patients were compared after only one dose of ipratropium bromide and with the use of low-dose beta-agonists.
Schuh and colleagues later performed a triple-armed, randomized, double-blind placebo controlled trial comparing ipratropium bromide 0.25 mg every 20 minutes for three doses, with a second group receiving one dose of ipratropium bromide during the first hour, and a third group receiving placebo.5 All patients received high-dose albuterol (0.15 mg/kg) every 20 minutes for the first hour. Patients showed a statistically significant improvement in FEV1 with the use of frequently administered ipratropium bromide, and the difference was more marked the more severe the exacerbation.
It is currently recommended that ipratropium bromide be used as a quick relief medication along with beta2-agonists. It may be repeated with the first three beta2-agonist treatments during an acute exacerbation, as it appears there may be a dose response curve. It is available as both a nebulizer solution (0.25 mg/mL) and as an MDI (18 mcg/puff). Only the nebulizer solution is recommended for use in acute asthma exacerbations since the MDI has not been studied under these conditions.
Corticosteroids appear to work by the inhibition of phospholipase A2 activity, which blocks the release of inflammatory mediators, thereby suppressing the migration of polymorphonuclear leukocytes. They also increase the number and affinity of beta-adrenergic receptors and reverse the increased capillary permeability seen in exacerbations. A number of studies have verified that systemic corticosteroids improve exacerbations and reduce length of symptoms. They should be routinely prescribed to all asthmatics experiencing an exacerbation.
A meta-analysis by Rowe and colleagues that examined the role of corticosteroids in acute asthma exacerbations came to the following conclusions:6 Corticosteroid treatment results in a decreased relapse rate in the first week to 10 days. Administration of steroids within 30 minutes in the acute care setting leads to a reduced admission rate.6,7
Based on their calculations, the number of children you would need to treat early in an ED visit in order to prevent one hospital admission would be six to 11 based on a baseline admission rate of 20%.6 There is no evidence to suggest that route of administration of the corticosteroid (oral vs. intravenous) improves the patient's outcome. Despite this conclusion, clinicians treating severe asthma exacerbations likely still would choose the IV route in specific patients with vomiting, ileus, or evidence of other factors that may delay steroid delivery.
Prednisone or its active form, prednisolone, is the oral corticosteroid of choice, while methyprednisolone is the IV steroid of choice. Side effects from the short-term use of corticosteroids are more limited than with chronic use. These include mood changes, hypertension, fluid retention, and an increase in appetite, all of which will resolve with discontinuation of the corticosteroids. Unusual complications of steroid therapy include peptic ulcer disease or aseptic necrosis of the hip.8 Most children have minimal effect from three to four courses of five-day corticosteroid therapy over a year. Children requiring more than four courses of corticosteroids in a year are at greater risk for adrenal suppression and adverse effects on bone calcium. Care needs to be taken to not extend courses to greater than 10 days, nor to fail to initiate corticosteroid therapy because of concern over side effects. Repeated use would be good reason for an allergy or pulmonology referral.
Management
The approach to the child who presents to the ED with an acute asthma exacerbation is outlined by the expert panel report shown in Table 5 (see p. 38).1 As mentioned previously, the initial evaluation begins with a rapid cardiopulmonary assessment with institution of therapy as indicated. A thorough history and physical exam with emphasis on color, auscultatory findings, use of accessory muscles, respiratory rate, and heart rate is performed. Oxygen saturation should be measured, and PEF and FEV1 should be considered except in children with severe obstruction or in children younger than 5.
If the patient is in mild to moderate distress or has a PEF or FEV1 50% or greater predicted, then inhaled beta2-agonist by MDI with spacer device or nebulizer is given. Patients should receive up to three treatments in the first hour. Oxygen should be administered as necessary to maintain a saturation of 90% or greater. If the patient does not clear completely with the first dose of beta-agonist, then oral corticosteroid should be given. If there are continued moderate symptoms, then inhaled short-acting beta2-agonists should be continued hourly.
A good response is indicated by an FEV1 or PEF 70% or higher that is maintained for at least one hour from the time of the last treatment, no respiratory distress, and a normal physical exam. If the patient demonstrates a good response he or she may be discharged home.
Patients who present with a severe exacerbation or an FEV1 or PEF lower than 50% predicted should be treated aggressively. Administer supplemental oxygen to maintain their saturation above 90% to 95% and initiate high-dose beta2- agonist therapy and anticholinergic continuously for one hour. Corticosteroids should be given parenterally in moderate to severe exacerbations and orally in children with mild to moderate exacerbation or showing improvement and not vomiting. These patients need to be monitored closely, and, at the end of the first hour of treatment, their response will dictate the extent of continued beta-agonist and anticholinergic frequency.
An incomplete response is indicated by an FEV1 or PEF 50% or higher but less than 70% after therapy. These patients may benefit from hos pitalization or a short-stay admission, depend ing on the facilities available. Hospital admission also is indicated if there is persistent respiratory distress (clinical asthma score greater than 2 or tachypnea) after initial aggressive therapy.
Other guidelines include: oxygen saturation less than 93% in room air, previous emergency treatment in the last 24 hours, or an inability to tolerate medications by mouth (i.e., vomiting). Children in high-risk categories also should be considered for admission to the hospital and include those with congenital heart disease, bronchopulmonary dysplasia, cystic fibrosis, or neuromuscular disorders.1,9,10,11
A poor response is defined as a physical exam that reveals the patient to remain in severe respiratory distress with a high clinical asthma score, a PCO2 42 mmHg or higher, or an FEV1 or PEF lower than 50%. These patients should be admitted to an intensive care setting for constant monitoring. Consider intensive care admission if there is 1) impending respiratory failure as evidenced by exhaustion or pulsus paradoxus higher than 25 mmHg, 2) worsening distress despite therapy, 3) requirement for continuous nebulization (beta-agonists less than one hour in frequency after the initial three treatments), 4) evidence of complications from an air leak.9
References
1. Highlights of the expert panel report 2: Guidelines for the diagnosis and management of asthma. National Institutes of Health, National Heart, Lung and Blood Institute; May 1997. NIH Publication No. 97-4051A.
2. McFadden ER. Evolving concepts in the pathogenesis and management of asthma. Adv Intern Med 1994; 39:357-394.
3. Schuh S, Parker P, Rajan A, et al. High versus low dose frequently administered nebulized albuterol in children with severe acute asthma. Pediatr 1989; 83:513-518.
4. Osmond M H, Klassen TP. Efficacy of Ipratropium Bromide in acute childhood asthma: A meta-analysis. Acad Emer Med 1995; 2:651-656.
5. Schuh S, Johnson DW, Callahan S, et al. Efficiency of frequent nebulized ipratropium bromide added to frequent high-dose albutrol therapy in severe childhood asthma. J Pediatr 1995; 126:639-645.
6. Rowe BH, Keller JL, Oxman AD. Effectiveness of steroid therapy in acute exacerbations of asthma: A meta-analysis. Am J Emerg Med 1992; 10:301-310.
7. Chapman KR, Verbeek PR, White JG, et al. Effect of a short course of prednisone in the prevention of early relapse after the emergency room treatment of acute asthma. N Engl J Med 1991; 324:788-794.
8. Darr CD. Asthma and bronchiolitis. In: Rosen P, Barkin R, eds. Emergency Medicine, Concepts and Clinical Practice. Mosby-Year book, Inc.; 1998, pp. 1,137-1,149.
9. Kulick RM, Ruddy RM. Allergic emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine, 3rd ed. Baltimore, MD: Williams and Wilkens; 1993, pp. 858-867.
10. Murphy SJ, Kelly MW. Advances in the management of acute asthma in children. Pediatr Rev 1996; 17:227-235.
11. Rubin BK Marcushamer S, Priel I, App EM. Emer gency management of the child with asthma. Pediatr Pulmonol 1990; 8:45-57.
(Editor's note: Next month's column will cover care and treatment of asthmatic children in respiratory failure. Richard M. Ruddy, MD, is the director of the division of emergency medicine at the Children's Hospital Medical Center in Cincinnati. Blake Bulloch, MD, is a fellow with the division. Jeffrey Linzer, MD, is assistant professor of pediatrics at Emory University School of Medicine in Atlanta. Larry B. Mellick, MD, MS, FAAP, FACEP, is director of pediatric emergency medicine at the Medical College of Georgia in Augusta.)
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