- Email: [email protected]
Diagnosis and treatment of exercise-induced bronchospasm
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Oral Presentations / Paediatric Respiratory Reviews 13S1 (2012) S1–S50
[10] Henderson J, Granell R, Heron J, et al. Associations of wheezing phenotypes in the first 6 years of life with atopy, lung function and airway responsiveness in mid-childhood. Thorax. 2008; 63: 974–80. [11] Marinho S, Simpson A, Soderstr ¨ om ¨ L, et al. Quantification of atopy and the probability of rhinitis in preschool children: a population-based birth cohort study. Allergy. 2007; 62: 1379–86. [12] Castro-Rodriguez JA, Rodrigo GJ. Efficacy of inhaled corticosteroids in infants and pre-schoolers with recurrent wheezing and asthma: a systematic review with meta-analysis. Pediatrics 2009; 123: e519–25 [13] Schultz A, Devadason SG, Savenije OE, Sly PD, Le Souef ¨ PN, Brand PL. The transient value of classifying preschool wheeze into episodic viral wheeze and multiple trigger wheeze. Acta Paediatr. 2010; 99: 56–60 [14] Harris JM, Bush A, Wilson N, et al. Preschool wheezing phenotypes in a representative school cohort. Thorax 2010; 65 [Suppl IV]: A37 [15] Sonnappa S, Bastardo CM, Wade A, Saglani S, McKenzie SA, Bush A, Aurora P. Symptom-pattern and pulmonary function in preschool wheezers. J Allergy Clin Immunol 2010; 126: 519–26 [16] Sonnappa S, Bastardo CM, Saglani S, et al. Relationship between past airway pathology and current lung function in preschool wheezers. Eur Respir J 2011; 38: 1431–1436 [17] Marguet C, Jouen-Boedes F, Dean TP, Warner JO. Bronchoalveolar cell profiles in children with asthma, infantile wheeze, chronic cough, or cystic fibrosis. Am J Respir Crit Care Med. 1999; 159: 1533–40. [18] Oommen A, McNally T, Grigg J. Eosinophil activation and preschool viral wheeze. Thorax. 2003; 58: 876–9. [19] Oommen A, Patel R, Browning M, Grigg J. Systemic neutrophil activation in acute preschool viral wheeze. Arch Dis Child. 2003; 88: 529–31. [20] Guilbert TW, Morgan WJ, Zeiger RS, et al. Long-term inhaled corticosteroids in preschool children at high risk for asthma. N Engl J Med. 2006; 354: 1985–97. [21] Murray CS, Woodcock A, Langley SJ, Morris J, Custovic A; IFWIN study team. Secondary prevention of asthma by the use of Inhaled Fluticasone propionate in Wheezy INfants (IFWIN): double-blind, randomised, controlled study. Lancet. 2006; 368: 754–62. [22] Bisgaard H, Hermansen MN, Loland L, et al. Intermittent inhaled corticosteroids in infants with episodic wheezing. N Engl J Med. 2006; 354: 1998–2005. [23] Castro-Rodriguez JA, Holberg CJ, Wright AL, Martinez FD. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med 2000; 162: 1403–1406 [24] Devulapalli CS, Carlsen KC, Haland ˚ G, et al. Severity of obstructive airways disease by age 2 years predicts asthma at 10 years of age. Thorax. 2008; 63: 8–13. [25] Robertson CF, Price D, Henry R, et al. Short Course Montelukast for Intermittent Asthma in Children: a Randomised Controlled Trial. Am J Respir Crit Care Med. 2007; 175: 323–9 [26] Ducharme FM, Lemire C, Noya FJ, et al. Preemptive use of high-dose fluticasone for virus-induced wheezing in young children. N Engl J Med. 2009; 360: 339–53. [27] Zeiger RS, Mauger D, Bacharier LB, et al. Daily or intermittent budesonide in preschool children with recurrent wheezing. N Engl J Med. 2011; 365: 1990–2001. [28] Bacharier LB, Phillips BR, Zeiger RS, et al; CARE Network. Episodic use of an inhaled corticosteroid or leukotriene receptor antagonist in preschool children with moderate-to-severe intermittent wheezing. J Allergy Clin Immunol. 2008; 122: 1127–1135 [29] Oommen A, Lambert PC, Grigg J. Efficacy of a short course of parentinitiated oral prednisolone for viral wheeze in children aged 1–5 years: randomised controlled trial. Lancet. 2003; 362: 1433–8. [30] Panickar J, Lakhanpaul M, Lambert PC, et al. Oral prednisolone for preschool children with acute virus-induced wheezing. N Engl J Med. 2009; 360: 329–38. [31] Bush A. Practice Imperfect – Treatment for Wheezing in Preschoolers. N Engl J Med. 2009; 360: 409–410.
Obstructive Lung Diseases Asthma update OLD-02 Diagnosis and treatment of exercise-induced bronchospasm L.C. Lands. Professor of Pediatrics, McGill University, Director, Pediatric Respiratory Medicine, Montreal Children’s Hospital-McGill University Health Centre, Montreal, Canada Exercise-Induced Bronchospasm is any airway narrowing associated with exercise. If it is associated with asthma, it is termed ExerciseInduced Asthma. It was first recognized in ancient Greece by Aretaeus the Cappaocian: ‘If from running or gymnastics breath grows short this is called asthma’. Exercise-induced asthma is “a syndrome of cough and/or wheezing, or chest symptoms of tightness or pain associated with 6–8 minutes of continuous or strenuous exercise” (C Randolph, Clin Rev Allerg Immunol 2008; 34: 205–216). The most accepted theory for why bronchospasm develops during exercise is that breathing in dry air results in evaporative losses from the airway surface. This leads to an increase in airway surface osmolarity, cell contraction, and release of mediators such as histamine and leukotrienes, which lead to airway smooth muscle contraction and airway wall edema (C Randolph, Clin Rev Allerg Immunol;34: 205–216, 2008). In other words, it is an indirect process. A variety of symptoms are associated with Exercise-Induced Bronchospasm, the most common being post-exercise cough, wheezing chest tightness or pain, and shortness of breath. However, a variety of other clinical entities can produce similar symptoms. These include poor physical conditioning, vocal cord dysfunction, habit cough, and exercise-induced hyperventilation (Weinberger and Abu-Hasan, 2007; Seear et al, 2005). This makes it important to accurately diagnose exercise-induced bronchospasm. Furthermore, a variety of factors may influence the severity of Exercise-Induced Bronchospasm (Dryden et al, AHRQ publication 10-E001, 2010). These include environmental factors external to the individual, such as air temperature and humidity, airborne pollutants and allergens, and factors that relate to the individual, such as the type, duration and intensity of the exercise, the time since the last exercise, the physical condition of the individual, the presence of respiratory infections, current asthma control if the individual has asthma, medications, and foods ingested just prior to exercise. Randolph has proposed a schemata for investigation and treatment (Randolph C, Curr Allergy Asthma Rep 2011; 11: 482–490). Following a thorough history and physical exam, if pulmonary function testing reveals a bronchodilator response, then the individual should be treated for asthma. If there is no bronchodilator response but lung function is reduced, then a trial of asthma therapy may be warranted. If lung function is within normal limits, then the individual should be tested for Exercise-Induced Bronchospasm. Testing for exercise-induced bronchospasm/exercise-induced asthma: The gold standard for diagnosing Exercise-Induced Bronchospasm is an exercise challenge. According to ATS/ERS standards, Exercise-Induced Bronchospasm is defined as at least a 10% decline in FEV1 following exercise. The challenge test should last for 6–8 minutes at 80–90% of predicted maximal heart rate (treadmill); testing done using a cycle ergometer employs work rate targets (80–90% of predicted maximal work capacity). Pulmonary function testing should be performed at 2, 5, 10, 15, 20, 25, and 30 min post-exercise. Some use dry and cool (15–20°C) air to increase the sensitivity. A recent systematic review has been conducted comparing alternative tests to the gold standard (Dryden et al, AHRQ publication
Oral Presentations / Paediatric Respiratory Reviews 13S1 (2012) S1–S50
10-E001, 2010). Of note, except for inhaled mannitol, the other tests (self-reporting, methacholine challenge testing, sport-specific challenge, eucapneic voluntary hyperventilation, free-running) have low evidence for their recommendation. Self-reporting may have some utility in detecting post-exercise cough. Methacholine challenge, which is a direct test provoking airway reactivity, rather than the indirect challenge of exercise, has highly variable sensitivity and specificity. In fact, when analyzed from a receiver-operand perspective, it is little better than chance at predicting a positive exercise challenge. Sport-specific challenges may be best to rule out Exercise-Induced Asthma or Bronchospasm, ie, they have relatively good negative predictive value. Eucapneic Voluntary Hyperventilation is the test recommended by the International Olympic Committee. It has a high false positivity in those with no known history of ExerciseInduced Bronchospasm. The intensity should be at least 95% of max heart rate, and dry air should be used for at least in last 4 minutes. The exercise device utilized needs to be tailored to the athlete: cycle ergometer for cyclists, skaters, downhill skiers; treadmill for runners and cross-country skiers. Free Running has limited sensitivity and specificity, possibly due to lack of control of intensity. The dry powdered mannitol challenge induces hyperosmolarity like exercise. It has minimal equipment requirements (inhaled powder device and spirometer). It uses fixed doses of mannitol. A positive test is a 15% decrease in FEV1 at a cumulative dose of less than 635 mg or a 10% drop between consecutive doses. It is more sensitive in those with known asthma. In summary, for the diagnosis of Exercise-Induced Bronchospasm or exercise-induced asthma, the signs and symptoms are not specific and there is often underlying asthma. History and questionnaires are useful but not adequate. A methacholine challenge does not reflect exercise-induced pathogenesis, and so the gold standard is Exercise Challenge Testing. An office-based alternative may be inhaled dried mannitol. Treatment of exercise-induced bronchospasm/exercise-induced asthma: Treatment can be divided into non-pharmacological and pharmacological treatments, and they are not mutually exclusive. Warm-up exercises should begin one hour prior to competition and include short recurrent exercises with 10–15 minutes of calisthenics with extension exercises raising the heart rate to 50–60% max; there should be inclusion of a warm-down period following exercise. Physical fitness is important, with those being more fit exhibiting less Exercise-Induced Bronchospasm. There are devices to warm and humidify inhaled air, but these may interfere with the ability to compete. Inhaling through the nose and exhaling through the mouth is useful. Of note, Exercise-Induced Bronchospasm alone (ie, without the presence of asthma) in the elite athlete is often due to overtraining and responds to a reduction in the number of training hours to <20 hours/week. One additional note is that if nasal allergies are present, they should be treated with nasal corticosteroids. Overall, when looking at preventative therapies, warm up exercise provide a certain degree of protection, but may require additional pharmacological therapies. Short-acting beta-agonists, such as salbutamol are effective (Inman and O’Byrne, AJCCM 1996; 153: 65–69). However, regular use does result in tachyphyllaxis. Long-acting beta-agonists can have a longer effect, up to 12 hours if inhaled at a high flow rate for dry powders (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). Further, formoterol has a more rapid onset of action than salmeterol. However, long-acting beta-agonists also demonstrate tachyphyllaxis (Dryden et al, AHRQ publication 10-E001, 2010). Inhaled corticosteroids are effective in children with exerciseinduced asthma (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). The combination of a short-acting beta-agonist with inhaled corticosteroids does appear to be superior to inhaled corticosteroids alone in protecting against exercise-induced asthma (Spooner C, Spooner GR, Rowe BH. Cochrane Review 2009).
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While monteleukast does diminish the fall in FEV1 , the pooled evidence does not support a claim for providing complete protection (Dryden et al, AHRQ publication 10-E001, 2010). However, tolerance to the effect of monteleukast does not seem to develop over the short-term (four weeks), and the effect appears to be independent of the use of inhaled corticosteroids in asthmatic children (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). When directly compared to salmeterol, montelukast’s effect may last up to 24 hours, and again, there does not appear to be a waning of effect over eight weeks (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53;Kemp JP, Therapeutics and Clinical Risk management, 2009; 5: 923–934). Further, the combination of monteleukast with inhaled corticosteroids may be superior to combining inhaled corticosteroids with a long-acting beta-agonist. Ipratroprium, an inhaled anticholinergic agent, can offer complete protection, but the number of subjects studied is small (Dryden et al, AHRQ publication 10-E001, 2010). Looked through an optic of providing a greater than 50% improvement over placebo in the proportion of individuals being protected, mast cell stabilizers are not as potent as short-acting beta-agonists (Spooner C, Spooner GR, Rowe BH. Cochrane Review 2009). In summary, treatment should be iindividualized, environmental triggers limited, and warm-ups and cool-downs implemented. If Exercise-Induced Bronchospasm is really a trigger for poorly controlled asthma, then asthma should be treated as per standard guidelines. Short-acting beta-agonists (eg, salbutamol) 15 minutes prior to exercise are effective, but there is a risk of tachyphyllaxis. Long-acting beta-agonists may also work, but there is a slower onset of action using salmeterol compared to formoterol, and again tachyphyllaxis can occur. If needed, inhaled corticosteroids or leukotriene modifiers such as montelukast can be added in. Montelukast may be added to inhaled corticosteroids, and may provide additional benefits, compared to adding a long-acting betaagonist. Anticholinergics may help in some patients, as may mast cell stabilizers. OLD-03 Effective delivery of medications to your asthmatic patients S. Devadason. School of Paediatrics and Child Health, University of Western Australia, Perth, Australia Aerosol therapy is currently the primary delivery method for asthma medications to children, apart from leukotriene antagonists which are administered in oral tablet form. The selection of the most appropriate inhalation device can be difficult, particularly when treating infants and very young children. Device selection can be dependent on the drug formulation to be administered and the area of the airways to be targeted for optimal therapeutic effect. In infants and preschool children, the transition from mask to mouthpiece and the ability to learn how to perform specific inhalation manoeuvres, rather than simple tidal breathing, will also play a role in the choice of device. Finally lack of adherence of both parents and children to prescribed therapeutic regimens is an important issue, and the most difficult to address. The two choices of delivery device for asthmatic children under 6 years of age are (a) pressurised metered dose inhalers (pMDIs) with valved holding chambers (spacers) or (b) nebulisers [1]. During acute, severe asthma exacerbations, equivalent clinical outcomes have been shown when comparing bronchodilator administration using pMDI-spacers and nebulisers in both adults and children [2–4]. Dry powder inhalers (DPIs) may be considered as alternatives to pMDIs and nebulisers for children and adolescents who can consistently generate inspiratory flows of more than 30 to 60 L per minute [5]. Face masks are required when delivering aerosols to infants and preschool, however drug delivery varies considerably and factors such as leakage around face-mask, lack of co-operation and crying
Oral Presentations / Paediatric Respiratory Reviews 13S1 (2012) S1–S50
[10] Henderson J, Granell R, Heron J, et al. Associations of wheezing phenotypes in the first 6 years of life with atopy, lung function and airway responsiveness in mid-childhood. Thorax. 2008; 63: 974–80. [11] Marinho S, Simpson A, Soderstr ¨ om ¨ L, et al. Quantification of atopy and the probability of rhinitis in preschool children: a population-based birth cohort study. Allergy. 2007; 62: 1379–86. [12] Castro-Rodriguez JA, Rodrigo GJ. Efficacy of inhaled corticosteroids in infants and pre-schoolers with recurrent wheezing and asthma: a systematic review with meta-analysis. Pediatrics 2009; 123: e519–25 [13] Schultz A, Devadason SG, Savenije OE, Sly PD, Le Souef ¨ PN, Brand PL. The transient value of classifying preschool wheeze into episodic viral wheeze and multiple trigger wheeze. Acta Paediatr. 2010; 99: 56–60 [14] Harris JM, Bush A, Wilson N, et al. Preschool wheezing phenotypes in a representative school cohort. Thorax 2010; 65 [Suppl IV]: A37 [15] Sonnappa S, Bastardo CM, Wade A, Saglani S, McKenzie SA, Bush A, Aurora P. Symptom-pattern and pulmonary function in preschool wheezers. J Allergy Clin Immunol 2010; 126: 519–26 [16] Sonnappa S, Bastardo CM, Saglani S, et al. Relationship between past airway pathology and current lung function in preschool wheezers. Eur Respir J 2011; 38: 1431–1436 [17] Marguet C, Jouen-Boedes F, Dean TP, Warner JO. Bronchoalveolar cell profiles in children with asthma, infantile wheeze, chronic cough, or cystic fibrosis. Am J Respir Crit Care Med. 1999; 159: 1533–40. [18] Oommen A, McNally T, Grigg J. Eosinophil activation and preschool viral wheeze. Thorax. 2003; 58: 876–9. [19] Oommen A, Patel R, Browning M, Grigg J. Systemic neutrophil activation in acute preschool viral wheeze. Arch Dis Child. 2003; 88: 529–31. [20] Guilbert TW, Morgan WJ, Zeiger RS, et al. Long-term inhaled corticosteroids in preschool children at high risk for asthma. N Engl J Med. 2006; 354: 1985–97. [21] Murray CS, Woodcock A, Langley SJ, Morris J, Custovic A; IFWIN study team. Secondary prevention of asthma by the use of Inhaled Fluticasone propionate in Wheezy INfants (IFWIN): double-blind, randomised, controlled study. Lancet. 2006; 368: 754–62. [22] Bisgaard H, Hermansen MN, Loland L, et al. Intermittent inhaled corticosteroids in infants with episodic wheezing. N Engl J Med. 2006; 354: 1998–2005. [23] Castro-Rodriguez JA, Holberg CJ, Wright AL, Martinez FD. A clinical index to define risk of asthma in young children with recurrent wheezing. Am J Respir Crit Care Med 2000; 162: 1403–1406 [24] Devulapalli CS, Carlsen KC, Haland ˚ G, et al. Severity of obstructive airways disease by age 2 years predicts asthma at 10 years of age. Thorax. 2008; 63: 8–13. [25] Robertson CF, Price D, Henry R, et al. Short Course Montelukast for Intermittent Asthma in Children: a Randomised Controlled Trial. Am J Respir Crit Care Med. 2007; 175: 323–9 [26] Ducharme FM, Lemire C, Noya FJ, et al. Preemptive use of high-dose fluticasone for virus-induced wheezing in young children. N Engl J Med. 2009; 360: 339–53. [27] Zeiger RS, Mauger D, Bacharier LB, et al. Daily or intermittent budesonide in preschool children with recurrent wheezing. N Engl J Med. 2011; 365: 1990–2001. [28] Bacharier LB, Phillips BR, Zeiger RS, et al; CARE Network. Episodic use of an inhaled corticosteroid or leukotriene receptor antagonist in preschool children with moderate-to-severe intermittent wheezing. J Allergy Clin Immunol. 2008; 122: 1127–1135 [29] Oommen A, Lambert PC, Grigg J. Efficacy of a short course of parentinitiated oral prednisolone for viral wheeze in children aged 1–5 years: randomised controlled trial. Lancet. 2003; 362: 1433–8. [30] Panickar J, Lakhanpaul M, Lambert PC, et al. Oral prednisolone for preschool children with acute virus-induced wheezing. N Engl J Med. 2009; 360: 329–38. [31] Bush A. Practice Imperfect – Treatment for Wheezing in Preschoolers. N Engl J Med. 2009; 360: 409–410.
Obstructive Lung Diseases Asthma update OLD-02 Diagnosis and treatment of exercise-induced bronchospasm L.C. Lands. Professor of Pediatrics, McGill University, Director, Pediatric Respiratory Medicine, Montreal Children’s Hospital-McGill University Health Centre, Montreal, Canada Exercise-Induced Bronchospasm is any airway narrowing associated with exercise. If it is associated with asthma, it is termed ExerciseInduced Asthma. It was first recognized in ancient Greece by Aretaeus the Cappaocian: ‘If from running or gymnastics breath grows short this is called asthma’. Exercise-induced asthma is “a syndrome of cough and/or wheezing, or chest symptoms of tightness or pain associated with 6–8 minutes of continuous or strenuous exercise” (C Randolph, Clin Rev Allerg Immunol 2008; 34: 205–216). The most accepted theory for why bronchospasm develops during exercise is that breathing in dry air results in evaporative losses from the airway surface. This leads to an increase in airway surface osmolarity, cell contraction, and release of mediators such as histamine and leukotrienes, which lead to airway smooth muscle contraction and airway wall edema (C Randolph, Clin Rev Allerg Immunol;34: 205–216, 2008). In other words, it is an indirect process. A variety of symptoms are associated with Exercise-Induced Bronchospasm, the most common being post-exercise cough, wheezing chest tightness or pain, and shortness of breath. However, a variety of other clinical entities can produce similar symptoms. These include poor physical conditioning, vocal cord dysfunction, habit cough, and exercise-induced hyperventilation (Weinberger and Abu-Hasan, 2007; Seear et al, 2005). This makes it important to accurately diagnose exercise-induced bronchospasm. Furthermore, a variety of factors may influence the severity of Exercise-Induced Bronchospasm (Dryden et al, AHRQ publication 10-E001, 2010). These include environmental factors external to the individual, such as air temperature and humidity, airborne pollutants and allergens, and factors that relate to the individual, such as the type, duration and intensity of the exercise, the time since the last exercise, the physical condition of the individual, the presence of respiratory infections, current asthma control if the individual has asthma, medications, and foods ingested just prior to exercise. Randolph has proposed a schemata for investigation and treatment (Randolph C, Curr Allergy Asthma Rep 2011; 11: 482–490). Following a thorough history and physical exam, if pulmonary function testing reveals a bronchodilator response, then the individual should be treated for asthma. If there is no bronchodilator response but lung function is reduced, then a trial of asthma therapy may be warranted. If lung function is within normal limits, then the individual should be tested for Exercise-Induced Bronchospasm. Testing for exercise-induced bronchospasm/exercise-induced asthma: The gold standard for diagnosing Exercise-Induced Bronchospasm is an exercise challenge. According to ATS/ERS standards, Exercise-Induced Bronchospasm is defined as at least a 10% decline in FEV1 following exercise. The challenge test should last for 6–8 minutes at 80–90% of predicted maximal heart rate (treadmill); testing done using a cycle ergometer employs work rate targets (80–90% of predicted maximal work capacity). Pulmonary function testing should be performed at 2, 5, 10, 15, 20, 25, and 30 min post-exercise. Some use dry and cool (15–20°C) air to increase the sensitivity. A recent systematic review has been conducted comparing alternative tests to the gold standard (Dryden et al, AHRQ publication
Oral Presentations / Paediatric Respiratory Reviews 13S1 (2012) S1–S50
10-E001, 2010). Of note, except for inhaled mannitol, the other tests (self-reporting, methacholine challenge testing, sport-specific challenge, eucapneic voluntary hyperventilation, free-running) have low evidence for their recommendation. Self-reporting may have some utility in detecting post-exercise cough. Methacholine challenge, which is a direct test provoking airway reactivity, rather than the indirect challenge of exercise, has highly variable sensitivity and specificity. In fact, when analyzed from a receiver-operand perspective, it is little better than chance at predicting a positive exercise challenge. Sport-specific challenges may be best to rule out Exercise-Induced Asthma or Bronchospasm, ie, they have relatively good negative predictive value. Eucapneic Voluntary Hyperventilation is the test recommended by the International Olympic Committee. It has a high false positivity in those with no known history of ExerciseInduced Bronchospasm. The intensity should be at least 95% of max heart rate, and dry air should be used for at least in last 4 minutes. The exercise device utilized needs to be tailored to the athlete: cycle ergometer for cyclists, skaters, downhill skiers; treadmill for runners and cross-country skiers. Free Running has limited sensitivity and specificity, possibly due to lack of control of intensity. The dry powdered mannitol challenge induces hyperosmolarity like exercise. It has minimal equipment requirements (inhaled powder device and spirometer). It uses fixed doses of mannitol. A positive test is a 15% decrease in FEV1 at a cumulative dose of less than 635 mg or a 10% drop between consecutive doses. It is more sensitive in those with known asthma. In summary, for the diagnosis of Exercise-Induced Bronchospasm or exercise-induced asthma, the signs and symptoms are not specific and there is often underlying asthma. History and questionnaires are useful but not adequate. A methacholine challenge does not reflect exercise-induced pathogenesis, and so the gold standard is Exercise Challenge Testing. An office-based alternative may be inhaled dried mannitol. Treatment of exercise-induced bronchospasm/exercise-induced asthma: Treatment can be divided into non-pharmacological and pharmacological treatments, and they are not mutually exclusive. Warm-up exercises should begin one hour prior to competition and include short recurrent exercises with 10–15 minutes of calisthenics with extension exercises raising the heart rate to 50–60% max; there should be inclusion of a warm-down period following exercise. Physical fitness is important, with those being more fit exhibiting less Exercise-Induced Bronchospasm. There are devices to warm and humidify inhaled air, but these may interfere with the ability to compete. Inhaling through the nose and exhaling through the mouth is useful. Of note, Exercise-Induced Bronchospasm alone (ie, without the presence of asthma) in the elite athlete is often due to overtraining and responds to a reduction in the number of training hours to <20 hours/week. One additional note is that if nasal allergies are present, they should be treated with nasal corticosteroids. Overall, when looking at preventative therapies, warm up exercise provide a certain degree of protection, but may require additional pharmacological therapies. Short-acting beta-agonists, such as salbutamol are effective (Inman and O’Byrne, AJCCM 1996; 153: 65–69). However, regular use does result in tachyphyllaxis. Long-acting beta-agonists can have a longer effect, up to 12 hours if inhaled at a high flow rate for dry powders (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). Further, formoterol has a more rapid onset of action than salmeterol. However, long-acting beta-agonists also demonstrate tachyphyllaxis (Dryden et al, AHRQ publication 10-E001, 2010). Inhaled corticosteroids are effective in children with exerciseinduced asthma (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). The combination of a short-acting beta-agonist with inhaled corticosteroids does appear to be superior to inhaled corticosteroids alone in protecting against exercise-induced asthma (Spooner C, Spooner GR, Rowe BH. Cochrane Review 2009).
S9
While monteleukast does diminish the fall in FEV1 , the pooled evidence does not support a claim for providing complete protection (Dryden et al, AHRQ publication 10-E001, 2010). However, tolerance to the effect of monteleukast does not seem to develop over the short-term (four weeks), and the effect appears to be independent of the use of inhaled corticosteroids in asthmatic children (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53). When directly compared to salmeterol, montelukast’s effect may last up to 24 hours, and again, there does not appear to be a waning of effect over eight weeks (Grezlewsi T and Stelmach I, Drugs 2009; 69: 1533–53;Kemp JP, Therapeutics and Clinical Risk management, 2009; 5: 923–934). Further, the combination of monteleukast with inhaled corticosteroids may be superior to combining inhaled corticosteroids with a long-acting beta-agonist. Ipratroprium, an inhaled anticholinergic agent, can offer complete protection, but the number of subjects studied is small (Dryden et al, AHRQ publication 10-E001, 2010). Looked through an optic of providing a greater than 50% improvement over placebo in the proportion of individuals being protected, mast cell stabilizers are not as potent as short-acting beta-agonists (Spooner C, Spooner GR, Rowe BH. Cochrane Review 2009). In summary, treatment should be iindividualized, environmental triggers limited, and warm-ups and cool-downs implemented. If Exercise-Induced Bronchospasm is really a trigger for poorly controlled asthma, then asthma should be treated as per standard guidelines. Short-acting beta-agonists (eg, salbutamol) 15 minutes prior to exercise are effective, but there is a risk of tachyphyllaxis. Long-acting beta-agonists may also work, but there is a slower onset of action using salmeterol compared to formoterol, and again tachyphyllaxis can occur. If needed, inhaled corticosteroids or leukotriene modifiers such as montelukast can be added in. Montelukast may be added to inhaled corticosteroids, and may provide additional benefits, compared to adding a long-acting betaagonist. Anticholinergics may help in some patients, as may mast cell stabilizers. OLD-03 Effective delivery of medications to your asthmatic patients S. Devadason. School of Paediatrics and Child Health, University of Western Australia, Perth, Australia Aerosol therapy is currently the primary delivery method for asthma medications to children, apart from leukotriene antagonists which are administered in oral tablet form. The selection of the most appropriate inhalation device can be difficult, particularly when treating infants and very young children. Device selection can be dependent on the drug formulation to be administered and the area of the airways to be targeted for optimal therapeutic effect. In infants and preschool children, the transition from mask to mouthpiece and the ability to learn how to perform specific inhalation manoeuvres, rather than simple tidal breathing, will also play a role in the choice of device. Finally lack of adherence of both parents and children to prescribed therapeutic regimens is an important issue, and the most difficult to address. The two choices of delivery device for asthmatic children under 6 years of age are (a) pressurised metered dose inhalers (pMDIs) with valved holding chambers (spacers) or (b) nebulisers [1]. During acute, severe asthma exacerbations, equivalent clinical outcomes have been shown when comparing bronchodilator administration using pMDI-spacers and nebulisers in both adults and children [2–4]. Dry powder inhalers (DPIs) may be considered as alternatives to pMDIs and nebulisers for children and adolescents who can consistently generate inspiratory flows of more than 30 to 60 L per minute [5]. Face masks are required when delivering aerosols to infants and preschool, however drug delivery varies considerably and factors such as leakage around face-mask, lack of co-operation and crying