Asthma Management Handbook

Other comorbidities and asthma

Recommendations

Identify and manage co-occurring allergic rhinitis in adults and children with asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • de Groot et al. 20121
  • Kersten et al. 20122
  • Pawankar et al. 20093
  • Price et al. 20054
  • Thomas et al. 20055
  • Wallace et al. 20086

Consider the possibility of upper airway dysfunction as an alternative or coexisting diagnosis in adults and children with asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • Benninger et al. 20117
  • Deckert and Deckert, 20108
  • Weinberger and Abu-Hasan, 20079
  • Morris and Christopher, 201010

Consider the possibility of coexisting obstructive sleep apnoea in people with asthma, particularly in those who are also obese. Offer referral for investigation as appropriate.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • Alkhalil et al. 200811
  • Alkhalil et al. 200912
  • Boulet, 200913
  • Dixon et al. 201114
  • Ross et al. 201215
  • Teodorescu et al. 201016
  • Teodorescu et al. 201217

For adults with obstructive sleep apnoea or children with sleep-disordered breathing, offer specialist referral.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

For Aboriginal and Torres Strait Islander children, routinely ask about coughing (frequency and quality), even if parents or carers do not mention cough.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • Morey et al. 201318

Consider the possibility of other chronic lung disease (e.g. bronchiectasis, chronic suppurative lung disease, pneumonia) as an alternative or coexisting diagnosis in Aboriginal and Torres Strait Islander adults and children with respiratory symptoms, particularly in remote regions. 

How this recommendation was developed

Adapted from existing guidance

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

  • Chang et al. 200819

Consider the possibility of asthma–COPD overlap in patients with asthma who also have features of COPD (e.g. adult onset, history of smoking, history of emphysema or chronic bronchitis, limited relief from short-acting bronchodilators, recurrent cough, sputum production).

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

In older patients, consider whether the presence of other common comorbid conditions (e.g. obesity, gastro-oesophageal reflux disease, obstructive sleep apnoea syndrome, osteoporosis, hypertension, cardiovascular disease) or their treatments may affect asthma control, increase the potential for drug–interactions, or affect the person’s ability to self-manage their asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

  • Gibson et al. 201020

More information

Upper airway dysfunction

Upper airway dysfunction is intermittent, abnormal adduction of the vocal cords during respiration, resulting in variable upper airway obstruction. It often mimics asthma78 and is commonly misdiagnosed as asthma.910 It can cause severe acute episodes of dyspnoea that occur either unpredictably or due to exercise.9 Inspiratory stridor associated with vocal cord dysfunction is often described as ‘wheezing’,9 but symptoms do not respond to asthma treatment.821

Upper airway dysfunction can coexist with asthma.7 People with asthma who also have upper airway dysfunction experience more symptoms than those with asthma alone and this can result in over-treatment if vocal cord dysfunction is not identified and managed appropriately.7

Upper airway dysfunction probably has multiple causes.7 In some people it is probably due to hyperresponsiveness of the larynx in response to intrinsic and extrinsic triggers.722 Triggers can include exercise, psychological conditions, airborne irritants, rhinosinusitis, gastro-esophageal reflux disease, and medicines.810

Upper airway dysfunction should be considered when spirometry shows normal FEV1/FVC ratio in a patient with suspected asthma10 or symptoms do not respond to short-acting beta2 agonist reliever. The shape of the maximal respiratory flow loop obtained by spirometry may suggest the diagnosis.9 Direct observation of the vocal cords is the best method to confirm the diagnosis of upper airway dysfunction.7

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Links between allergic rhinitis and asthma

Prevalence, aetiology and symptoms

Asthma and allergic rhinitis frequently coexist. At least 75% of patients with asthma also have rhinitis, although estimates vary widely.23 Patients with asthma may have both allergic and non-allergic rhinitis.

Allergic rhinitis that starts early in life is usually due to a classical IgE hypersensitivity. Adult-onset asthma or inflammatory airway conditions typically have more complex causes. Chronic rhinosinusitis with nasal polyps is not a simple allergic condition and generally needs specialist care.24

Symptoms and signs of allergic rhinitis can be local (e.g. nasal discharge, congestion or itch), regional (e.g. effects on ears, eyes, throat or voice), and systemic (e.g. sleep disturbance and lethargy). Most people with allergic rhinitis experience nasal congestion or obstruction as the predominant symptom. Ocular symptoms (e.g. tearing and itch) in people with allergic rhinitis are usually due to coexisting allergic conjunctivitis.25

Patients may mistake symptoms of allergic rhinitis for asthma and vice versa. Allergic rhinitis is sometimes more easily recognised only after asthma has been stabilised.

Effects on asthma

Allergic rhinitis is an independent risk factor for developing asthma in children and adults.26, 27, 28, 29, 30 However, the use of antihistamines in children has not been shown to prevent them developing asthma.23

The presence of allergic rhinitis is associated with worse asthma control in children and adults.5, 4, 31, 1 The use of intranasal corticosteroids in patients with concommitant allergic rhinitis and asthma may improve asthma control in patients who are not already taking regular inhaled corticosteroids.32

Both rhinitis and asthma can be triggered by the same factors, whether allergic (e.g. house dust mite, pet allergens, pollen, cockroach) or non-specific (e.g. cold air, strong odours, environmental tobacco smoke).

Food allergies do not cause allergic rhinitis. Most people with allergic rhinitis are sensitised to multiple allergens (e.g. both pollens and house dust mite), so symptoms may be present throughout the year.

Pollens (e.g. grasses, weeds, trees) and moulds are typically seasonal allergens in southern regions, but can be perennial in tropical northern regions.24 However, ryegrass is not found in tropical regions (see Thunderstorm-triggered asthma).

Pollen calendars provide information on when airborne pollen levels are likely to be highest for particular plants.

Thunderstorm-triggered asthma

Seasonal allergic rhinitis, which in Australia is typically associated with sensitisation to perennial ryegrass (Lolium perenne), is an important risk factor for thunderstorm-triggered asthma.33

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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: http://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.32, 23, 34 Intranasal corticosteroid are most effective when taken continuously.32

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in adults and adolescents with allergic rhinitis.32, 23 They are also effective for ocular symptoms.35

All available intranasal corticosteroids appear to be equally effective.32

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

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.34

Intranasal corticosteroids are well tolerated. Common (>1%) adverse effects include nasal stinging, itching, nosebleed, sneezing, sore throat, dry mouth, cough.37 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.38

Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects when given in recommended doses.32, 6 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.32

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.37

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.32, 34, 33

The onset of therapeutic action is approximately 30 minutes after dosing.33

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.39

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms.34, 40 They can provide adequate relief for some individuals when taken continuously or intermittently.32 Available agents appear to be equally effective.6

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.32, 41 In adults with allergic rhinitis, oral antihistamines usually produce no further improvement when added to intranasal corticosteroid treatment.32

Common (>1%) adverse effects include drowsiness, fatigue, headache, nausea and dry mouth.37 Oral antihistamines can also cause ocular dryness.42

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.23

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.32 They have a rapid onset of action (15–30 minutes).32

The most common (>1%) adverse effect is local irritation.37 Bitter taste is more common intranasal antihistamines than with intranasal corticosteroids.32

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.23, 34 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.32, 23 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.34

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.43, 44, 45, 46, 47 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares, depression, and aggression.47 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.47

Other nasal sprays

Ipratropium bromide spray is effective in managing persistent rhinorrhoea in patients with allergic rhinitis, but not blockage or itch.23 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.6

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: http://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.32, 23 However, there is weaker evidence to support their efficacy in children than in adults.23 There is limited evidence to guide the treatment of allergic rhinitis in preschool children.34

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.34

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.48 Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects in children when given in recommended doses.326 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.32 One knemometry study showed reduced lower leg growth rate in children using intranasal budesonide.32 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.32

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.39

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms,34, 40 including in preschool children. 34 They can provide adequate relief for some individuals when taken continuously or intermittently.32 Available agents appear to be equally effective.6

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.32, 41 The addition of oral antihistamines to intranasal corticosteroids has not been demonstrated to be an effective strategy in children.49

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.23

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.32 They have a rapid onset of action (15–30 minutes).32

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.23, 34 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.32, 23 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.34

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.43, 44, 45, 46 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).47 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.47

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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Non-recommended medications for allergic rhinitis

Intranasal decongestants have a limited role in the management of allergic rhinitis because they should only be used for very short courses (up to 5 days maximum). Repeated or long-term use can cause rebound swelling of nasal mucosa (rhinitis medicamentosa), which can lead to dose escalation by patients, with a risk of atrophic rhinitis. Intranasal decongestants can be considered for a patient with severe nasal congestion to gain rapid relief of symptoms until the full effect of intranasal corticosteroids is achieved.

Oral decongestants (e.g. pseudoephedrine or phenylephrine) should not generally be used in the management of allergic rhinitis. They are indicated for short-term use only (e.g. acute infectious rhinitis, or during air travel by a patient with symptomatic rhinitis, as a single tablet taken one hour before landing). They are associated with adverse effects including palpitations, tachycardia and insomnia.

Oral corticosteroids should be avoided as a treatment for allergic rhinitis. In exceptional circumstances, their use might be considered in consultation with an allergy specialist.

Topical ocular alpha agonist vasoconstrictors (including in combination with antihistamines) should not be used for allergic conjunctivitis because they can cause conjunctivitis medicamentosa.

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Nasal saline irrigation for allergic rhinitis

Nasal irrigation (via a syringe, rinse bottle, spray or other device) can improve nasal symptoms, mucociliary clearance, and quality of life.50 Saline administered by spray or other devices was used at least twice daily in most studies that showed a benefit.50

Isotonic solution is preferable to hypertonic solution because it supports optimal mucociliary clearance.50 Isotonic saline is solution is inexpensive and has no known adverse effects.50 Patients can use either commercially manufactured saline solutions or home-made normal saline: 1 teaspoon (5 g) rock or sea salt in 500 mL of water (preferably bottled or boiled).

There is not enough evidence to determine:

  • whether solutions should be buffered or non-buffered, sterile or non-sterile
  • whether various additives provide any advantage
  • whether inhaling steam or an irritant decongestant (e.g. eucalyptus, menthol) before saline irrigation provides any extra benefit. However, patients are more likely to adhere to simple and convenient regimens, regardless of theoretical advantages. Caution is required with steam inhalation to avoid burns.

If patients are using both saline irrigation and an intranasal corticosteroid or intranasal H1‑antihistamine, they should perform saline irrigation first. Saline can be used again after waiting at least an hour after using an intranasal corticosteroid.

Young children are unlikely to tolerate nasal irrigation.

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Surgical turbinate reduction

Turbinate reduction surgery can be considered when nasal obstruction is due to turbinate hypertrophy and symptoms do not respond to medical treatment. It should not be performed in young children except after thorough investigation and review.

Inferior turbinate hypertrophy secondary to inflammation is a common cause of nasal obstruction in patients with allergic rhinitis.51 Several surgical procedures are available to correct this problem.52 The ideal surgical reduction should preserve the mucosa and physiological function.51

Short-term adverse outcomes of inferior turbinate reduction include nasal bleeding, scarring and crusting. Rarely, it may worsen symptoms when patients have non-specific rhinitic conditions or sino-nasal somatisation disorders (‘empty nose syndrome’).52 There is no evidence that turbinate surgery creates these conditions, but sino-nasal surgery may exacerbate the symptoms.

 

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Comorbidity in older adults

Many older people with asthma also have multiple comorbidities and complex healthcare needs.2053 Common conditions in older people that may affect asthma control include:20

  • obesity
  • gastro-oesophageal reflux disease
  • obstructive sleep apnoea syndrome and other sleep disorders
  • osteoporosis (vertebral fractures can impair respiratory capacity)
  • cardiovascular disease (some medicines may worsen asthma).

The presence of diabetes can affect decisions about the use of systemic corticosteroids, while heart disease or anaemia can mimic symptoms.

There is limited clinical trial evidence to guide asthma management in older people with common comorbid conditions, because most asthma treatment trials have excluded people with these conditions.5420 Guidelines for one disease condition may have to be modified for older people with multiple chronic diseases to avoid potential adverse effects including drug–drug interactions.20

Common age-related problems such as cognitive impairment, poor eyesight, hearing loss, poor coordination or osteoarthritis can affect a person’s ability to use inhaler devices correctly.

Medicare items for chronic disease management (e.g. GP Management Plans, Team Care Arrangements, Multidisciplinary Care Plans) apply to patients with asthma.

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Obstructive sleep apnoea and asthma

Links with asthma

The risk of obstructive sleep apnoea is higher among people with asthma than in the general population.12

Obstructive sleep apnoea is associated with upper and lower airway inflammation.13 Pharyngeal inflammation in obstructive sleep apnoea may promote upper airway collapse.13

Obstructive sleep apnoea syndrome is an independent risk factor for asthma flare-ups.12

In adults, unrecognised obstructive sleep apnoea may contribute to persistent asthma daytime or night-time asthma symptoms, based on cohort study evidence.1716

In obese adults, obstructive sleep apnoea may contribute to poor asthma control.14

Obstructive sleep apnoea may also interact with gastro-oesophageal reflux disease to affect asthma control in adults.14

In children, sleep-disordered breathing in children appears to be a risk factor for severe asthma, independent of obesity.15

Effects of obstructive sleep apnoea treatment on asthma

Continuous positive airway pressure (CPAP) may improve asthma in adults with concomitant obstructive sleep apnoea syndrome.11

Among children with obstructive sleep apnoea, asthma control (measured by frequency of acute asthma flare-ups, reliever use, and asthma symptoms) may improve after adenotonsillectomy.55 Tonsillectomy or adenotonsillectomy is indicated in the management of upper airway obstruction in children with obstructive sleep apnoea.56

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Respiratory disease in Aboriginal and Torres Strait Islander peoples

Morbidity and mortality from respiratory diseases among Aboriginal and Torres Strait Islander people is higher than among non-Indigenous Australians across all age groups and regions.57 Among Aboriginal and Torres Strait Islander people living in remote areas, the rate of hospitalisation for respiratory disease is approximately three times the rate among Aboriginal and Torres Strait Islander people living in major cities.58 However, from 1997 to 2010 there was a 39% reduction in deaths due to respiratory disease among Aboriginal and Torres Strait Islander people.59

Detection, diagnosis and management of asthma may be complicated by increased rate of respiratory infections and chronic lung disease in rural remote Aboriginal and Torres Strait Islander communities.

  • Approximately 30% of Aboriginal and Torres Strait Islander people report respiratory problems.19
  • Chronic cough in Aboriginal and Torres Strait Islander children may be under-reported because it is so common that is considered normal by parents and caregivers.18
  • Pneumonia and COPD are the most common causes of hospitalisation for respiratory disease among Aboriginal and Torres Strait Islander people.58 The prevalence of COPD among Aboriginal and Torres Strait Islander people cannot be accurately estimated.60 The rate of death due to COPD among Aboriginal and Torres Strait Islander people is five times the rate among non-Indigenous Australians.61
  • The prevalence of bronchiectasis is disproportionately high in remote Aboriginal communities, particularly in Central Australia, but is underdiagnosed.1962 High-resolution computed tomography of the chest is necessary to diagnose bronchiectasis in adults.19 In Aboriginal and Torres Strait Islander adults, it may be difficult to distinguish between asthma, COPD and bronchiectasis.60 Bronchiectasis is associated with relatively rapid decline in lung function.19 
  • Chronic suppurative lung disease is highly prevalent among Aboriginal and Torres Strait Islander children in remote communities.19 The diagnosis of chronic suppurative lung disease is made in children who have symptoms and signs of bronchiectasis without radiographic features of bronchiectasis.19 In Aboriginal and Torres Strait Islander children, it may be difficult to distinguish between asthma and bronchiectasis or chronic suppurative lung disease.60 
  • Protracted bacterial bronchitis is often misdiagnosed as asthma,63, 64 but can also co-occur with asthma.64 Protracted bacterial bronchitis might precede chronic suppurative lung disease, but this is not yet well understood.64 Inadequate treatment of protracted bacterial bronchitis might put Aboriginal and Torres Strait Islander children at risk for chronic suppurative lung disease.64 Recurrent episodes of protracted bacterial bronchitis that does not resolve after treatment (e.g. a 14-day course of antibiotics) require investigation for chronic suppurative lung disease, bronchiectasis and aspiration.64

Notes

† Chronic suppurative lung disease is defined as a clinical syndrome of respiratory symptoms and signs due to chronic endobronchial suppuration, including continuous, wet or productive cough > 8 weeks, with or without other features (e.g. exertional dyspnoea, symptoms of reactive airway disease, recurrent chest infections, growth failure, clubbing, hyperinflation or chest wall deformity).65

‡ Bronchiectasis is diagnosed in patients with both chronic suppurative lung disease and the presence of radiological features on a chest high-resolution computed tomography scan.65

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Non-respiratory comorbidity among Aboriginal and Torres Strait Islander peoples

Aboriginal and Torres Strait Islander peoples have a high burden of chronic diseases that may affect asthma control and management, including:59

  • diabetes
  • cardiovascular disease
  • kidney disease
  • ear disease
  • mental health problems.
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References

  1. de Groot EP, Nijkamp A, Duiverman EJ, Brand PL. Allergic rhinitis is associated with poor asthma control in children with asthma. Thorax. 2012; 67: 582-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22213738
  2. Kersten ET, van Leeuwen JC, Brand PL, et al. Effect of an intranasal corticosteroid on exercise induced bronchoconstriction in asthmatic children. Pediatr Pulmonol. 2012; 47: 27-35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22170807
  3. Pawankar R, Bunnag C, Chen Y, et al. Allergic rhinitis and its impact on asthma update (ARIA 2008)–western and Asian-Pacific perspective. Asian Pac J Allergy Immunol. 2009; 27: 237-243. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20232579
  4. Price D, Zhang Q, Kocevar VS, et al. Effect of a concomitant diagnosis of allergic rhinitis on asthma-related health care use by adults. Clin Exp Allergy. 2005; 35: 282-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15784104
  5. Thomas M, Kocevar VS, Zhang Q, et al. Asthma-related health care resource use among asthmatic children with and without concomitant allergic rhinitis. Pediatrics. 2005; 115: 129-34. Available from: http://pediatrics.aappublications.org/content/115/1/129.long
  6. 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
  7. Benninger C, Parsons JP, Mastronarde JG. Vocal cord dysfunction and asthma. Curr Opin Pulm Med. 2011; 17: 45-49. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21330824
  8. Deckert J, Deckert L. Vocal cord dysfunction. Am Fam Physician. 2010; 81: 156-159. Available from: http://www.aafp.org/afp/2010/0115/p156.html
  9. Weinberger M, Abu-Hasan M. Pseudo-asthma: when cough, wheezing, and dyspnea are not asthma. Pediatrics. 2007; 120: 855-864. Available from: http://pediatrics.aappublications.org/content/120/4/855.full
  10. Morris MJ, Christopher KL. Diagnostic criteria for the classification of vocal cord dysfunction. Chest. 2010; 138: 1213-23. Available from: http://journal.publications.chestnet.org/article.aspx?articleid=1045155
  11. Alkhalil M, Schulman ES, Getsy J. Obstructive sleep apnea syndrome and asthma: the role of continuous positive airway pressure treatment. Ann Allergy Asthma Immunol. 2008; 101: 350-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18939721
  12. Alkhalil M, Schulman E, Getsy J. Obstructive aleep apnea syndrome and asthma: what are the links?. J Clin Sleep Med. 2009; 5: 71-78. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637171/
  13. Boulet LP. Influence of comorbid conditions on asthma. Eur Respir J. 2009; 33: 897-906. Available from: http://erj.ersjournals.com/content/33/4/897.long
  14. Dixon AE, Clerisme-Beaty EM, Sugar EA, et al. Effects of obstructive sleep apnea and gastroesophageal reflux disease on asthma control in obesity. J Asthma. 2011; 48: 707-13. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171804/
  15. Ross KR, Storfer-Isser A, Hart MA, et al. Sleep-disordered breathing is associated with asthma severity in children. J Pediatr. 2012; 160: 736-42. Available from: http://www.jpeds.com/article/S0022-3476(11)01047-X/fulltext
  16. Teodorescu M, Polomis DA, Hall SV, et al. Association of obstructive sleep apnea risk with asthma control in adults. Chest. 2010; 138: 543-50. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940069/
  17. Teodorescu M, Polomis DA, Teodorescu MC, et al. Association of obstructive sleep apnea risk or diagnosis with daytime asthma in adults. J Asthma. 2012; 49: 620-8. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3626099/
  18. Morey MJ, Cheng AC, McCallum GB, Chang AB. Accuracy of cough reporting by carers of Indigenous children. J Paediatr Child Health. 2013; 49: E199-203. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23438209
  19. Chang AB, Grimwood K, Maguire G, et al. Management of bronchiectasis and chronic suppurative lung disease in indigenous children and adults from rural and remote Australian communities. Med J Aust. 2008; 189: 386-93. Available from: https://www.mja.com.au/journal/2008/189/7/management-bronchiectasis-and-chronic-suppurative-lung-disease-indigenous
  20. Gibson PG, McDonald VM, Marks GB. Asthma in older adults. Lancet. 2010; 376: 803-813. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20816547
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