Asthma Management Handbook

Preventing thunderstorm-triggered asthma in individuals

Recommendations

Warn people with allergic rhinitis and allergy to ryegrass pollen (i.e. most people with springtime allergic rhinitis symptoms) that they may be at risk of thunderstorm-triggered asthma if they live in, or are travelling to, a region with seasonal high grass pollen levels – even if they have never had asthma symptoms before.

How this recommendation was developed

Based on selected evidence

Based on a limited structured literature review or published systematic review, which identified the following relevant evidence:

  • Davies, 20171
  • Girgis et al, 20002
  • Marks et al, 20013

For people with seasonal allergic rhinitis who do not use intranasal corticosteroid treatment all year, advise intranasal corticosteroid starting 6 weeks before the pollen season (or exposure) and continuing until pollen levels abate (e.g. in Victoria, ideally 1 September–31 December).

Note: Refer to ASCIA's Pollen calendar

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • NACA, 20174

For people with asthma who are at risk of thunderstorm-triggered asthma:

  • prescribe regular inhaled corticosteroids for continuous use if indicated (most adults and older adolescents with asthma)
  • for patients for whom preventer therapy is not otherwise indicated, prescribe regular inhaled corticosteroids for at least 2 weeks before and throughout the pollen season (e.g. in Victoria, ideally 1 September–31 December)
  • provide training in correct inhaler technique, and check technique and adherence regularly
  • advise patients to carry a reliever inhaler and replace it before the expiry date
  • provide an up-to-date written asthma action plan that includes thunderstorm advice and instructs the person to increase doses of both inhaled preventer and reliever (as well as starting oral corticosteroids, if indicated) in response to flare-ups.

Notes:

Most adults and older adolescents with asthma should be using a regular inhaled corticosteroid long term.

People with asthma are particularly at risk of thunderstorm-triggered asthma if they have seasonal (springtime) allergic rhinitis (i.e. allergic to ryegrass pollen), and live in or are travelling to an area with high grass pollen levels. People with allergy to ryegrass pollen without known asthma are also at risk of thunderstorm-triggered asthma.

Refer to ASCIA’s Pollen calendar for information on local high-risk periods.

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • NACA, 20174

More information

Thunderstorm-triggered asthma

Certain types of thunderstorms in spring or early summer in regions with high grass pollen concentrations in the air can cause life-threatening allergic asthma flare-ups in sensitised individuals, even if they have not had asthma before.5, 1, 6, 3, 2 People at risk of acute asthma flare-ups triggered by a thunderstorm include those with seasonal allergic rhinitis (with or without asthma), those with asthma (or a history of asthma), and those with undiagnosed asthma.1

Epidemics of thunderstorm-triggered asthma can occur when such a storm travels across a region and triggers asthma in many susceptible individuals, causing a high demand on ambulance and health services.6 However, epidemic thunderstorm asthma events are uncommon.

Data from thunderstorm asthma epidemics suggest that the risk of asthma flare-ups being triggered by a thunderstorm is highest in adults who are sensitised to grass pollen and have seasonal allergic rhinitis (with or without known asthma).1 The worst outcomes are seen in people with poorly controlled asthma. Regular treatment with an inhaled corticosteroid asthma preventer was significantly protective in a well-conducted Australian case-control study.2

Prevention and management are based on:4

  • year-round asthma control, including inhaled corticosteroid-containing preventers where indicated
  • preventive inhaled corticosteroid treatment for adults and adolescents with asthma who have known or suspected allergy to grass pollens (e.g. concomitant allergic rhinitis, a history of spring flare-ups in asthma symptoms) but are not already taking regular medication. Treatment should at least 2 weeks (ideally 6 weeks) before exposure to springtime high pollen concentrations and thunderstorms and continue throughout the local grass pollen season. For children, asthma should be managed according to age group.
  • preventive intranasal corticosteroid treatment for adults and adolescents with seasonal allergic rhinitis, because it can be reasonably assumed that they are allergic to ryegrass pollen. Treatment should start at least 2 weeks (ideally 6 weeks) before exposure to springtime high pollen concentrations and thunderstorms and continue throughout the local grass pollen season. For children, allergic rhinitis should be managed according to age group.
  • advice for at-risk patients to avoid being outdoors just before and during thunderstorms in spring and early summer, especially during wind gusts that precede the rain front
  • advice to ensure appropriate access to relievers during grass pollen season.
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Treatment of allergic rhinitis in adults and adolescents

 

Table. Overview of efficacy of allergic rhinitis medicines for specific symptoms Opens in a new window Please view and print this figure separately: https://www.asthmahandbook.org.au/table/show/102

Intranasal corticosteroids

If continuous treatment is required, an intranasal corticosteroid is the first-choice treatment unless contraindicated. Intranasal corticosteroids are more effective in the treatment of allergic rhinitis than other drug classes including oral H1-antihistamines, intranasal H1-antihistamines and montelukast.7, 8, 2 Intranasal corticosteroid are most effective when taken continuously.7

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in adults and adolescents with allergic rhinitis.7, 8 They are also effective for ocular symptoms.9

All available intranasal corticosteroids appear to be equally effective.7

The onset of action is between 3 and 36 hours after first dose and, in practice, the full therapeutic effect takes a few days.10

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.2

Intranasal corticosteroids are well tolerated. Common (>1%) adverse effects include nasal stinging, itching, nosebleed, sneezing, sore throat, dry mouth, cough.11 Nose bleeds are usually due to poor spray technique or crusting. Evidence from studies mainly in adults suggests that intranasal corticosteroids do not cause atrophy of nasal epithelium.12

Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects when given in recommended doses.7, 13 Studies in adults evaluating effects on the hypothalamic-pituitary axis using morning cortisol concentrations, cosyntropin stimulation, and 24-hour urinary free cortisol excretion show no adverse effects with beclomethasone dipropionate, budesonide, ciclesonide, fluticasone propionate, fluticasone furoate, or triamcinolone acetonide.7

In patients with asthma already taking inhaled corticosteroids, both the intranasal corticosteroid dose and the inhaled corticosteroid dose should be taken into account when calculating the total daily corticosteroid dose. Drug–drug interactions (e.g. with CYP3A4 inhibitors such as such as erythromycin, clarithromycin, ritonavir and itraconazole) may change the metabolism or increase absorption of corticosteroids administered by any route, increasing the risk of adrenal suppression.11

Combination intranasal corticosteroid plus intranasal antihistamines

Combined intranasal fluticasone propionate and azelastine hydrochloride in a single device is more effective than fluticasone propionate alone for a range of nasal and ocular symptoms.7, 2, 1

The onset of therapeutic action is approximately 30 minutes after dosing.1

Oral antihistamines

Second-generation (less sedating) antihistamines (e.g. cetirizine, desloratadine, fexofenadine or loratadine) should be used in preference to older, more sedating antihistamines. Cetirizine is the most likely of the less sedating antihistamines to cause sedation, while fexofenadine and loratadine appear to be the least sedating.14

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms.2, 15 They can provide adequate relief for some individuals when taken continuously or intermittently.7 Available agents appear to be equally effective.13

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.7, 16 In adults with allergic rhinitis, oral antihistamines usually produce no further improvement when added to intranasal corticosteroid treatment.7

Common (>1%) adverse effects include drowsiness, fatigue, headache, nausea and dry mouth.11 Oral antihistamines can also cause ocular dryness.17

Intranasal antihistamines

Intranasal antihistamines are at least equally effective as second-generation, less sedating oral H1-antihistamines for the treatment of allergic rhinitis, but are generally less effective than intranasal corticosteroids.8

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.7 They have a rapid onset of action (15–30 minutes).7

The most common (>1%) adverse effect is local irritation.11 Bitter taste is more common intranasal antihistamines than with intranasal corticosteroids.7

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.8, 2 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.7, 8 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.2

Montelukast is approved by TGA for treatment of in adults with asthma or seasonal allergic rhinitis.

It is generally very well tolerated, but has been infrequently associated with neuropsychiatric adverse effects, including suicidal ideation, in children and young people.18, 19, 20, 21, 22 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares, depression, and aggression.22 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.22

Other nasal sprays

Ipratropium bromide spray is effective in managing persistent rhinorrhoea in patients with allergic rhinitis, but not blockage or itch.8 It is indicated for use in adults and adolescents over 12 years old.

Intranasal sodium cromoglycate is less effective than intranasal corticosteroids, but is effective in some patients for prevention and treatment of allergic rhinitis and is associated with minimal adverse effects.13

Specific allergen immunotherapy

Specific allergen immunotherapy (desensitisation) is effective in reducing allergic rhinitis symptoms (see separate topic).

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Treatment of allergic rhinitis in children

 

Table. Overview of efficacy of allergic rhinitis medicines for specific symptoms Opens in a new window Please view and print this figure separately: https://www.asthmahandbook.org.au/table/show/102

Intranasal corticosteroids

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in school-aged children with allergic rhinitis.7, 8 However, there is weaker evidence to support their efficacy in children than in adults.8 There is limited evidence to guide the treatment of allergic rhinitis in preschool children.2

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.2

TGA-approved indications vary between age groups. Intranasal corticosteroids indicated for children aged under 12 years include fluticasone furoate (age 2 years and over), mometasone furoate (age 3 years and over), and budesonide (age 6 years and over).

Intranasal corticosteroids are well tolerated. Evidence from studies mainly in adults suggests that they do not cause atrophy of nasal epithelium.23 Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects in children when given in recommended doses.713 Studies in children evaluating effects on the hypothalamic-pituitary axis using morning cortisol concentrations, cosyntropin stimulation, and 24-hour urinary free cortisol excretion showed no adverse effects with ciclesonide, fluticasone propionate, fluticasone furoate, mometasone furoate, or triamcinolone acetonide.7 One knemometry study showed reduced lower leg growth rate in children using intranasal budesonide.7 In studies using stadiometry over 12 months, higher-than-recommended doses of intranasal beclomethasone dipropionate were associated with growth suppression, but fluticasone propionate and mometasone furoate showed no effects on growth compared with placebo.7

In children already taking inhaled corticosteroids, both the intranasal corticosteroid dose and the inhaled corticosteroid dose should be taken into account when calculating the total daily corticosteroid dose.

Oral antihistamines

Second-generation (less sedating) antihistamines (e.g. cetirizine, desloratadine, fexofenadine or loratadine) should be used in preference to older, more sedating antihistamines. Cetirizine is the most likely of the less sedating antihistamines to cause sedation, while fexofenadine and loratadine appear to be the least sedating.14

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms,2, 15 including in preschool children. 2 They can provide adequate relief for some individuals when taken continuously or intermittently.7 Available agents appear to be equally effective.13

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.7, 16 The addition of oral antihistamines to intranasal corticosteroids has not been demonstrated to be an effective strategy in children.24

TGA-approved indications vary between age groups. Less sedating oral antihistamines indicated for children under 12 years include cetirizine (1 year and over), loratatidine (1 year and over), desloratadine (6 months and over), and fexofenadine (6 months and over).

Intranasal antihistamines

Intranasal antihistamines are at least equally effective as second-generation, less sedating oral H1-antihistamines for the treatment of allergic rhinitis, but are generally less effective than intranasal corticosteroids.8

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.7 They have a rapid onset of action (15–30 minutes).7

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.8, 2 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.7, 8 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.2

Montelukast is approved by TGA for the treatment of asthma in children over 2 years, and for the treatment of seasonal allergic rhinitis.

It is generally very well tolerated, but has been infrequently associated with neuropsychiatric adverse effects, including suicidal ideation, in children and young people.18, 19, 20, 21 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares (especially in children), depression, and aggression (especially in children).22 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.22

The potential association of montelukast with behaviour-related adverse events should be mentioned to parents when commencing treatment, and treatment should be stopped if such adverse events are suspected.

Specific allergen immunotherapy

Specific allergen immunotherapy (desensitisation) is effective in reducing allergic rhinitis symptoms (see separate topic).

 

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References

  1. Davies J, Queensland University of Technology. Literature review on thunderstorm asthma and its implications for public health advice. Final report. Victorian State Government Department of Health and Human Services, Melbourne, 2017.
  2. Girgis ST, Marks GB, Downs SH, et al. Thunderstorm-associated asthma in an inland town in south-eastern Australia. Who is at risk?. Eur Respir J. 2000; 16: 3-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10933077
  3. Marks GB, Colquhoun JR, Girgis ST, et al. Thunderstorm outflows preceding epidemics of asthma during spring and summer. Thorax. 2001; 56: 468-71. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746065/
  4. National Asthma Council Australia. Thunderstorm asthma. An information paper for health professionals. NACA, Melbourne, 2017.
  5. D'Amato G, Vitale C, D'Amato M, et al. Thunderstorm-related asthma: what happens and why. Clin Exp Allergy. 2016; 46: 390-6.
  6. Victoria State Government Department of Health and Human Services,. The November 2016 Victorian epidemic thunderstorm asthma event: an assessment of the health impacts. The Chief Health Officer’s Report, 27 April 2017. Victorian Government, Melbourne, 2017.
  7. Seidman MD, Gurgel RK, Lin SY, et al. Clinical practice guideline: Allergic rhinitis. Otolaryngol Head Neck Surg. 2015; 152: S1-43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25644617
  8. Brożek JL, Bousquet J, Baena-Cagnani CE, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines: 2010 Revision. J Allergy Clin Immunol. 2010; 126: 466-476. Available from: http://www.jacionline.org/article/S0091-6749(10)01057-2/fulltext
  9. Hong J, Bielory B, Rosenberg JL, Bielory L. Efficacy of intranasal corticosteroids for the ocular symptoms of allergic rhinitis: A systematic review. Allergy Asthma Proc. 2011; 32: 22-35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21262095
  10. Bousquet J, Schunemann HJ, Hellings PW, et al. MACVIA clinical decision algorithm in adolescents and adults with allergic rhinitis. J Allergy Clin Immunol Pract. 2016; 138: 367-374.e2. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27260321
  11. . Australian Medicines Handbook. Last modified July 2017. Australian Medicines Handbook Pty Ltd, 2017.
  12. Verkerk, M. M., Bhatia, D., Rimmer, J., et al. Intranasal steroids and the myth of mucosal atrophy: a systematic review of original histological assessments. Am J Rhinol Allergy. 2015; 29: 3-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25590306
  13. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: An updated practice parameter. J Allergy Clin Immunol. 2008; 122: S1-S84. Available from: http://www.jacionline.org/article/S0091-6749(08)01123-8/fulltext
  14. Mann RD, Pearce GL, Dunn N, Shakir S. Sedation with "non-sedating" antihistamines: four prescription-event monitoring studies in general practice. BMJ (Clinical research ed). 2000; 320: 1184-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10784544
  15. Bachert C, Maspero J. Efficacy of second-generation antihistamines in patients with allergic rhinitis and comorbid asthma. J Asthma. 2011; 48: 965-73. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21970671
  16. Bousquet J, Khaltaev N, Cruz AA, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008. Allergy. 2008; 63: 8-160. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2007.01620.x/full
  17. Ousler GW, Wilcox KA, Gupta G, Abelson MB. An evaluation of the ocular drying effects of 2 systemic antihistamines: loratadine and cetirizine hydrochloride. Ann Allergy Asthma Immunol. 2004; 93: 460-4.
  18. Schumock GT, Stayner LT, Valuck RJ, et al. Risk of suicide attempt in asthmatic children and young adults prescribed leukotriene-modifying agents: a nested case-control study. J Allergy Clin Immunol. 2012; 130: 368-75. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22698520
  19. Wallerstedt SM, Brunlöf G, Sundström A, Eriksson AL. Montelukast and psychiatric disorders in children. Pharmacoepidemiol Drug Saf. 2009; 18: 858-864. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19551697
  20. Philip G, Hustad C, Noonan G, et al. Reports of suicidality in clinical trials of montelukast. J Allergy Clin Immunol. 2009; 124: 691-6.e6. Available from: http://www.jacionline.org/article/S0091-6749(09)01247-0/fulltext
  21. Philip G, Hustad CM, Malice MP, et al. Analysis of behavior-related adverse experiences in clinical trials of montelukast. J Allergy Clin Immunol. 2009; 124: 699-706.e8. Available from: http://www.jacionline.org/article/S0091-6749(09)01248-2/fulltext
  22. Haarman MG, van Hunsel F, de Vries TW. Adverse drug reactions of montelukast in children and adults. Pharmacol Res Perspect. 2017; 5: e00341. Available from: http://onlinelibrary.wiley.com/doi/10.1002/prp2.341/full
  23. Verkerk MM, Bhatia D, Rimmer J, et al. Intranasal steroids and the myth of mucosal atrophy: a systematic review of original histological assessments. Am J Rhinol Allergy. 2015; 29: 3-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25590306
  24. Nasser M, Federowicz Z, Aljufairi H, McKerrow W. Antihistamines used in addition to topical nasal steroids for intermittent and persistent allergic rhinitis in children. Cochrane Database Syst Rev. 2010; Issue 7: . Available from: https://www.ncbi.nlm.nih.gov/pubmed/20614452