- 1.0 Aim
- 2.0 Introductory summary
- 3.0 Definition of severe asthma
Last updated: Febuary 2020
POCKET GUIDE TO SYSTEMATIC ASSESSMENT AND MANAGEMENT OF POSSIBLE SEVERE ASTHMA IN ADULTS –2020
Nordic consensus statement on the systematic assessment and management of possible severe asthma in adults
: Anna von Bülow1, Asger Sverrild1, Charlotte Ulrik2,3, Tina Skjold4, Vibeke Backer5, Ole Hilberg6, Birger Laerum7, Sverre Lehman8,9, Bernt Bøgvald9, Christer Janson10, Thomas Sandström11, Leif Bjermer12, Apostolos Bossios13, Barbro Dahlen13, Valentyna Yasinska13, Helena Backman14, Bo Lundbäck15, Dora Ludviksdottir16, Unnur Björnsdottir16,17, Alan Altraja18, Maritta Kilpeläinen19,20, Arja Viinanen19,20, Lauri Lehtimäki21,22, Paula Kauppi23, Jussi Karjalainen24, Hannu Kankaanranta21,24 and Celeste Porsbjerg1,2
1Respiratory research unit, Department of Respiratory Medicine, Bispebjerg Hospital, Copenhagen, Denmark; 2 Institute of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark; 3Department of Respiratory Medicine, Hvidovre Hospital, Denmark; 4Department of Respiratory Medicine, Aarhus University Hospital, Aarhus, Denmark; 5Centre of Physical Activity Research, Rigshospitalet, Copenhagen, Denmark; 6Department of Respiratory Medicine, Vejle Hospital, Vejle, Denmark; 7LHL-klinikkene Bergen, Nesttun, Norway; 8Department of Clinical Science, University of Bergen, Bergen, Norway; 9Department of Thoracic Medicine, Haukeland University Hospital, Bergen, Norway; 10Department of Medical Sciences: Respiratory, Allergy & Sleep Research, Uppsala University, Uppsala, Sweden; 11Department of Public Health and Clinical Medicine, Department of Public Health and Clinical Medicine, Medicine unit, Umeå University, Umeå, Sweden; 12Department of Respiratory Medicine and Allergology, Skåne University Hospital, Lund, Sweden; 13Department of Respiratory Medicine and Allergy, Karolinska University Hospital, and Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden; 14Section of Sustainable Health, The OLIN Unit, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden; 15Krefting Research Centre, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden; 16Department of Allergy, Respiratory Medicine and Sleep Landspitali University Hospital Reykjavik Iceland, University of Iceland, Reykjavik, Iceland; 17Faculty of Medicine, University of Iceland, Reykjavik, Iceland; 18Department of Pulmonary Medicine, University of Tartu and Lung Clinic, Tartu University Hospital, Tartu, Estonia; 19Division of Medicine, Department of Pulmonary Diseases, Turku University Hospital, Turku, Finland. 20Department of Pulmonary Diseases and Clinical Allergology, University of Turku, Turku, Finland; 21Faculty of Medicine and Health Technology, Tampere University, Tampere Finland; 22Allergy Centre, Tampere University Hospital, Tampere, Finland; 23Department of Allergy, Respiratory Diseases and Allergology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; 24Department of Respiratory Medicine, Seinäjoki Central Hospital, Seinäjoki, Finland
The purpose of this pocket guide is to provide a condensed, practical and pragmatic clinical overview on the assessment and management of possible severe asthma in adults.
The content of this pocket guide is based on the recommendations from the Nordic consensus statement on the systematic assessment and management of possible severe asthma in adults 20181, where a more detailed description is found.
This Pocket guide is developed by the Nordic Severe Asthma Network (NSAN) established under the Nordic Respiratory Academy (NORA) with severe asthma specialists from Norway, Sweden, Denmark, Iceland, Finland and Estonia as members.
Asthma is increasingly recognised as a complex, heterogeneous disease consisting of a variety of clinical, pathophysiological and inflammatory characteristics with an inconsistent and variable response to treatment 2–4. Most patients can achieve well-controlled asthma on low to medium dose of inhaled corticosteroids (ICS). However, a small group of patients remains a major challenge as they persistently require intensive asthma therapy, including high doses of inhaled steroids as well as “second controllers”5–7. Poor asthma control may, however, be due to several factors. Hence, patients, who are prescribed high-dose asthma treatment, should undergo a thorough systematic assessment in a specialist care setting to confirm the diagnosis of asthma and identify and address potential aggravating comorbidities and environmental triggers, poor adherence to controller medication before being classified as having severe asthma5–8.
The prevalence of severe asthma is estimated to be up to 8 percent of all asthma patients9–12. However, this relatively small proportion of patients with asthma presents the largest burden of disease due to frequent exacerbations, poor quality of life and increased health care costs13,14. Additionally, different targeted, biological therapies are becoming increasingly available for subsets of patients with severe asthma. However, these treatments target very specific pathways in the immune systems and are thus only effective in selected subgroups of severe asthma. Therefore, highlighting the need for a detailed phenotyping of patients with severe asthma.
The ERS/ATS guidelines5,7 define severe asthma as asthma that remains uncontrolled or where acceptable control is only achieved when receiving high-dose ICS (Table 1) and a second controller (≥ 12 months) or systemic corticosteroids (≥6 months/previous year). The second controllers include long-acting beta-agonists (LABA), leukotriene antagonists (LTRA), long-acting muscarinic antagonists (LAMA) or methylxanthines. The definition excludes patients in whom the poor asthma control is related to external factors, such as poor adherence or unmanaged comorbidities (difficult-to-treat asthma) (Figure 1). To differentiate these two patient populations, other causes including comorbidities affecting asthma control should be addressed and managed, including reassessment in specialist care after 3-6 months, before a diagnosis of severe asthma is assigned.
Table 1. Definitions of high-dose inhaled steroids1,5
Daily dose (μg)
≥1000 (HFA MDI) ; ≥2000 (DPI)
HFA: hydroflouroalkane; MDI: metered dose inhaler; DPI: dry powder inhalers
Several factors including comorbidities and diseases of the upper and lower airways may influence asthma control and mimic severe asthma 5,8. Consequently, a careful stepwise systematic assessment is important to support the diagnosis of severe asthma5,8,15. There is evidence that after a careful systematic evaluation and management of patients with difficult asthma in a severe asthma centre, less than half can be classified as having severe asthma after 12 months of follow-up16. The main objective of systematic assessment is to differentiate between severe asthma and difficult-to-treat asthma, the latter being cases in which poor asthma control is mainly caused by external factors (such as poor adherence, untreated comorbidities and unaddressed triggers).
Overall, systematic evaluation is recommended to include three steps (Figure 2):
- Confirm the asthma diagnosis, assess asthma control, assess the phenotype
- Identify and address potential treatment barriers (adherence, poor inhaler technique)
- Evaluate and manage comorbidities and environmental exposures
A diagnosis of asthma requires a detailed history including the presence of asthma symptoms combined with objective confirmation of variable airflow limitation (Box 1). Be aware that an inconsistent response to treatment can be due to an alternative/overlapping diagnosis, especially if non-typical asthma symptoms are dominating or variable airflow limitation is lacking (Table 3).
1: History of typical asthma symptoms:
2: Objective confirmation of variable airflow limitation (current or historical):
PEF is a cost-effective complementary measurement that may add additional information, with regard to both confirming and rejecting variable airflow limitation.
Reversibility to SABA/ICS/OCS
Increase in FEV1 of >12% and >200 mL*6
Peak flow monitoring
Daily PEF for 2-3 weeks: diurnal PEF variability** >10%6
Bronchial challenge test
Methacholine (only if pre-bronchodilator FEV1 ≥60 %)
FEV1 ≥20% decrease with a cumulative dose of methacholine ≤8 μmol***17
Mannitol (only if pre-bronchodilator FEV1 ≥70 %)
FEV1 ≥15 % decrease from baseline with a provocation dose of mannitol ≤ 635 mg
*Measured 10-15 minutes after administration of SABA (200-400 mcg salbutamol or equivalent or after 4 weeks with anti-inflammatory treatment.
**Diurnal variability of PEF: ([Day’s highest – day’s lowest]/mean of day’s highest and lowest) x 100, then the average of each day’s value is calculated over 1–2 weeks.
***The cumulative dose may vary according to different dosimetric methods.
Exclusion of alternative diagnoses:
- Several conditions may mimic severe asthma.
- An alternative or overlapping diagnosis to asthma should always be kept in mind in patients with:
- Inconsistent response to treatment
- Atypical asthma symptoms
- Inability to verify the asthma diagnosis objectively
- Diagnostic work-up according to the clinical suspicion, see Table 3.
Some conditions co-exist in patients with difficult/severe asthma and are important contributors to asthma symptoms, these are listed in Table 6
Table 3: Alternative/overlapping diagnoses to severe asthma
Diffusing capacity, HRCT
Sweat test, genetic testing
Hyper-eosinophilic lung diseases
Blood eosinophils, HRCT, biopsy of affected organs,
anti-neutrophilic cytoplasmic antibodies
Recurrent pulmonary embolism
D-dimer, CT thorax angiography, ventilation/perfusion scintigraphy
Congestive heart failure
Transthoracic echocardiography, BNP
Endobronchial tumour/foreign body
Laryngeal video recording under attack or provocation
Dynamic CT thorax, bronchoscopy
Nijmegen questionnaire, BPAT, physiotherapist assessment
*May be an alternative diagnosis to severe asthma but is commonly a co-existing diagnosis
COPD: chronic obstructive pulmonary disease; HRCT: high resolution computer tomography;
Uncontrolled severe asthma according to the ERS/ATS guidelines5:
- Inadequate symptom control?
- ACQ ≥1.5
- ACT <20
- Uncontrolled according to GINA guidelines6: frequent symptoms or reliever use, activity limited by wheeze, chest tightness and cough interfere with daily activities, awakenings due to asthma
- ≥ 2 OCS requiring exacerbations in the last 12 months
- ≥1 serious exacerbation: hospitalisation, ICU stay or mechanical ventilation
- Airflow limitation (pre-bronchodilator FEV1 <80 % and FEV1/FVC<lower limit of normal).
Overall, there is no clear consensus on the definition of clinical phenotypes for asthma. However, in severe asthma these phenotypes are generally evaluated in clinical practice as follows5:
- Early-onset allergic phenotype
- Late-onset obese phenotype
- Late-onset eosinophilic phenotype
From a pragmatic clinical point of view the following features should be systematically described.
- Early/late onset asthma? (Onset of asthma symptoms in childhood or in adulthood)
- Evidence of Type 2 (T2) inflammation
- Evidence of eosinophilic airway inflammation (current and/or historical)
- Blood eosinophil count ≥0.3 x109 cells/L19,20
- Sputum eosinophil count ≥3% (only available in some specialised asthma centres)21
- FeNO >25 ppb*22
- Evidence of eosinophilic airway inflammation (current and/or historical)
In patients with no evidence of eosinophilic airway inflammation, consider repeating blood eosinophilic count and FeNO several times, and if possible perform induced sputum or consider bronchoscopy with cell counts in BAL before assuming non-T2 asthma.
*FeNO >50 ppb indicates high likelihood of eosinophilic airway inflammation. Whereas, FeNO <25 indicates low likelihood of eosinophilia22.
- IgE mediated allergy?
- Positive skin prick test, elevated specific IgE (>0.35 kU/L) for aeroallergens with relevant symptoms? 23
- Fixed airflow obstruction (FEV1<80% and FEV1/FVC <0.7)?
- Obesity (BMI >30kg/m2)
- Smoking history?
Identification of factors that impede the delivery of asthma medication to the airways, including non-adherence to treatment and incorrect inhaler technique, is crucial. A diagnosis of severe asthma presupposes that medication is taken as prescribed, but non-adherence is unfortunately common, even in patients on high-dose treatment5,8. If adherence is not systematically evaluated in patients with poor symptom control despite high dose treatment, non-adherent patients are likely to be misclassified as having severe asthma. This potentially leads to an inappropriate intensification of treatment including commencement of OCS (with the risk of systemic side-effects24) or expensive biological therapies25–27.
- Poor adherence to ICS in patients with difficult asthma is common (40-65 %)28–30 and is related to poor asthma outcomes including higher use of SABA, poor quality of life, lower FEV1, exacerbations and asthma related hospital admissions29,31. Consequently, we recommend that adherence be routinely assessed
- There is no clear consensus on the cut-off describing non-adherence. However, if using electronic registries for prescription fillings, patients are often considered adherent if ≥80% of ICS prescriptions are filled9,28,30,32
- See Table 4 for more details
Poor inhaler technique in patients with difficult asthma is common (20-60 %)9,28,30 and leads to poor asthma control and increased risk of exacerbations33. It is a particular challenge that these patients often have multiple inhalers each requiring different techniques to ensure correct administration. Consequently, we recommend inhaler technique to be thoroughly taught and checked at each new prescription, and systematically evaluated during each visit to the outpatient clinic. At every visit to the outpatient clinic, patients should demonstrate inhaler technique. Thus, ensuring that critical errors are systematically identified and corrected.
- More details are listed in Table 4
- Patients need a minimum set of skills to manage their disease adequately and optimise asthma control. Asthma patients need a basic understanding of their disease. This includes knowledge of triggers and comorbidities. They need to understand how their different medications work and their respective side effects. Additionally they need to be able to recognize the advent of exacerbations and how to handle them.34. Asthma education and guidance have shown to improve quality of life and reduce hospital admissions
- Written action plans: guidance on maintenance therapy, recognition and management of exacerbations
- Self-management education by specialised asthma nurses
The identification and management strategies of treatment barriers are shown in Table 4
Fillings of prescription for asthma medication in electronic registries (if available).
· Strength: objective assessment
· Limitation: Do not necessarily reveal short-term changes in adherence
Self-reported adherence: e.g. “How many times the previous week have you taken
· Strength: easy to use, inexpensive
· Limitation: Tendency of over-estimation 36
Check dates on inhalers
1. Identify causes of non-adherence:
· Side-effects or fear of side effects to treatment
· Perception that treatment is unnecessary
· Due to forgetfulness
· Misunderstanding of instructions
· Cost of medication
· Requires an empathic discussion with the patients regarding pros and cons or their treatment
· Consider simplifying the treatment to a more feasible regime such as once daily dosing
· Recommend systematic intake of asthma medication: e.g. before brushing teeth or reminders to use of inhalers.
· Consider the costs of medications before prescribing.
Ask the patient to show you how they use their inhalers at each clinic visit
Use inhaler-specific-checklists (Direct link)
Choose the optimal device for the individual patient. If different options are available try to include the patients in the decision making 6
Consider spacers for pMDI inhalers
Avoid different types of inhalers whenever possible
When prescribing a new inhaler, physically demonstrate the use of the inhaler with a placebo inhaler and ask the patient to demonstrate the inhaler use afterwards 6
Frequently reassess inhaler technique, as errors often reappear 6
Identification of comorbidities and exposures are central to the systematic evaluation of patients with possible severe asthma.
Asthma symptoms can be aggravated by several external triggers or irritants including allergens, smoking, pollution and certain drugs6,37. Assessment requires a detailed history including smoking history, exposure to different allergens, drugs and occupational exposure and is listed in Table 5.
Table 5: Potential asthma triggers including evaluation and management
Indoor allergens: Pets (cats, dogs), house dust mites, moulds, cockroaches, rodents
· SPT, specific IgE for aeroallergens (incl. Aspergillus fumigatus)
Evaluate the correlation to symptoms. If sensitised to pets, consider avoidance of pets. Remediation of dampness.
Antihistamines, nasal steroids, LTRA
Outdoor allergens: pollen, mould
· SPT, specific IgE for aeroallergens (incl. Aspergillus fumigatus)
Antihistamines, nasal steroids, LTRA
Tobacco smoke (active – passive)
Drugs: ASA, NSAID, Beta-blockers, ACE-inhibitors
· Samter’s triad: severe eosinophilic asthma, nasal polyposis and NSAID-exacerbated respiratory disease?
· ACE-inhibitors: cough
Avoid ACE-inhibitors and non-selective systemic beta-blockers
Symptoms aggravate with exposure at workplace*
· Flour, grain: bakers/farmers
· Isocyanates: painters, automotive industry workers, foam plastic production, insulation, polyurethane foam use
· Formaldehyde: health care workers, hairdressers, cosmetic workers
· Wood dusts: carpenters
· Platinum salts: dentists, chemist, photographers, electricians
· Animal allergens: farmers, veterinarians, animal breeders
Consider referral to specialists in occupational medicine
*NB: Severe asthma may develop many years after an exposure
ACE: angiotensin converting enzyme; ASA: acetylsalicylic acid; NSAID: non-steroidal anti-inflammatory drug; LTRA: leukotriene antagonist; SPT: skin prick test
Comorbidities in patients with difficult or severe asthma are common12,16,28,38,39. Some comorbidities can mimic asthma symptoms and others are associated with poor asthma outcomes 38,40. Consequently, by identifying and managing comorbidities, potential overtreatment of asthma may be avoided and a correct diagnosis of severe asthma ensured39,41. The most common and important comorbidities and their respective symptoms, diagnostic tests and management are listed in Table 6. A detailed description of comorbidities in severe asthma is available in the original “Nordic consensus statement on the systematic assessment and management of possible severe asthma in adults”1.
Table 6: Common comorbidities in severe asthma
Chronic rhinosinuitis /nasal polyps (CRSwNP) (50%)42
Nasal obstruction, rhinorrhoea, facial congestion,headache, anosmial 43
(CT of sinuses)
Allergic rhinoconjuctivitis (70%42*)
(*Positive skin prick test to aeroallergens)
Rhinorrhoea, sneezing, nasal obstruction, nasal, eye itching 23
History + skin prick test/ specific IgE
History incl. smoking
Dysfunctional Breathing (30%)28,40
Heterogeneous symptoms: Hyperventilation, breathlessness, deep sighing,
Nijmegen questionnaire 46
Physiotherapy – breathing retraining 45,48
Shortness of breath, dyspnoea, stridor rather than wheezing during attacks, hoarseness during attacks41
Screening with Pittsburgh VCD-index51
Continuous laryngoscopy under attacks
Anxiety, depression symptoms
HADS questionnaire Psychiatric assessment
Snoring, day time sleepiness, obesity, Night-time awakenings with breathing difficulty without asthmatic signs 54
Screening with STOP-BANG/Berlin questionnaire 55, Screening for daytime sleepiness with Epworth Sleepiness scale56
Polysomnography/ respiratory polygraphy
BMI >30 kg/m2
Dietician, weight loss57
Gastro-esophageal reflux (17-74%)3,16,42,58
Heartburn, acid regurgitation, cough, laryngeal symptoms
3 months of empiric PPI
24-hours pH monitoring
Cough, recurrent pulmonary infections
HRCT, sputum cultures,
Physiotherapy, long term mucoactive treatment, low-dose macrolides41,62
Poor asthma control, often chronic mucus hyper secretion41
Total IgE, IgE and IgG to Aspergillus fumigatus, blood eosinophilia, HRCT (bronchiectasis)
Prednisolone. Anti-fungal treatment. Omalizumab may be considered in some cases.
ABPA: allergic bronchopulmonary aspergillosis; BMI: body mass index; CPAP: continuous Positive Airway Pressure; ILO: Inducible laryngeal obstruction; HRCT: high resolution computed tomography;
Overall, the management of severe asthma can be divided into three domains as shown in Figure 3: Non-pharmacological management, pharmacological treatments and management of comorbidities.
The principles of asthma treatment presented in this guide are mostly based on the 2019 GINA guidelines6 with some modifications (Figure 4).
We propose a stepwise approach according to the inflammatory phenotype when managing severe asthma (Figure 5).
Patients with severe asthma are per definition treated with high-dose ICS and a second controller. Before considering biological treatments, regular asthma therapy should be optimized. Potential contributing factors must be addressed and managed, such as external triggers, comorbidities and treatment barriers.
- Consider optimising inhalers: from metered-dose inhalers (pMDI) to dry powder inhalers (DPI) or vice versa according to patients/treating specialists preference, consider spacers if using pMDI
- Consider additional controllers as add-on treatments
- LAMA: especially in patients with exacerbations 64,65
- LTRA: consider in patients with AERD or allergic rhinitis 6
- Consider reliever treatments: as needed ICS-formoterol is preferred in patients with exacerbations66
- In patients, who are not well-controlled on high dose ICS-LABA, consider referral to a severe asthma specialist/centre1,5
Further treatment opportunities according to the inflammatory phenotype (Figure 5):
Evidence of T2 inflammation
- Reconsider adherence!
- Consider increasing ICS6 – be aware of side effects!
- Consider low-dose macrolides:
- Conflicting results, however there is some evidence that treatment with azithromycin 250-500 mg three times a week reduces exacerbations in patients with eosinophilic as well as non-eosinophilic airway inflammation67,68
- Be aware of: prolonged QTc, hearing loss/tinnitus and potential bacterial resistance 67
- Consider low dose OCS:
- Low evidence, therefore the lowest dose for as short time as possible.
- Be aware of side-effects: diabetes, hypertension, peptic ulcers, osteoporosis24,69,70
- Consider ABPA: Specific IgE/IgG against Aspergillus fumigatus, total IgE, blood eosinophils, bronchiectasis (HRCT)71
- Consider biological therapies (according to eosinophilic or allergic predominance):
- Allergic asthma:
- Perennial atopy combined with allergen induced symptoms+ exacerbations + total IgE within dose range* 72–74
- Reduces exacerbations, improves symptom control and lung function 72,75,76
- Predictors of treatment response: see Figure 6
- Allergic asthma:
- Eosinophilic asthma:
- Exacerbations + blood eosinophil count ≥ 0.3 x 109/L (lower if patients on long-term OCS)*6,19
- Reduces exacerbations 19,77,78
- Less effect on symptoms and lung function 78–80.
- OCS sparing effect 81,82
- Effect on chronic rhinosinusitis with nasal polyps 83
- Predictors of treatment response: see Figure 6
- Eosinophilic asthma:
Exacerbations + blood eosinophil count ≥ 0.15 x 109 / FeNO≥25 ppb (lower if patients are on long-term OCS)* 6,84
- Reduces exacerbations, increases lung function and symptom control 84
- OCS sparing effect 85
- Effect on chronic rhinosinusitis with nasal polyps 86 and atopic dermatitis 87
- Predictors of treatment response: See Figure 6
*Check local eligibility criteria for the different biological treatments, as these may vary from those listed.
At present, no direct comparisons between any of the biological therapies exist.
T2 low inflammation
- Reconsider important comorbidities/alternative diagnosis: e.g. VCD, DB, COPD, bronchiectasis, obesity etc. (Table 3, Table 6): consider HRCT, lung volumes, DLCO, induced sputum if not done
- Add LAMA if not yet in use (especially if FEV1 <80% and exacerbations)
- Consider low-dose macrolides:
- Conflicting results, however there is some evidence that treatment with azithromycin 250-500 mg three times a week reduces exacerbations in patients with non-eosinophilic as well as eosinophilic airway inflammation67,68
- Be aware of: prolonged QTc, hearing loss/tinnitus and potential bacterial resistance (sputum cultures should be obtained if bronchiectasis is present)67
- Consider bronchial thermoplasty
- Reduces long-term exacerbations, but is associated with increased risk of exacerbations in relation to the procedure 88
- Contraindications: bronchiectasis, FEV1<50%
- Lack of long-term follow up data 5
Patients with difficult asthma should undergo a detailed systematic assessment according to the three evaluation steps described earlier in this document (Figure 2)
- Diagnosis & phenotype
- Identification of treatment barriers
- Identification and management of exposures and comorbidities
Before commencing a biological drug, we advocate that at minimum the following to be evaluated and managed including reviewing response to management after approximately 3-6 months to ensure a true diagnosis of severe refractory asthma, as illustrated in Figure 7.
Figure 7: Recommended minimum assessment before commencing T2-targeted biological therapies for severe asthma.
Consider referral if
- Difficult and persistent uncontrolled asthma (low lung function, poor symptom control or frequent exacerbations) on GINA step 5 treatments (high dose ICS + second controller) despite good adherence, correct inhaler therapy and attempts to optimise therapy with different inhalers and add-on therapies
- Treatment with maintenance OCS
Content in referral letter to a severe asthma centre is illustrated in Box 2
1. Difficult asthma (high dose ICS + second controller)? (Y/N)
2. Asthma control:
Exacerbations last 12 months (n):
3. Asthma diagnosis confirmed (Y/N), if yes, which test and when?
4. Current medications
5. Results of any treatment trials (LAMA, LTRA, oral steroids etc)
6. Inhalation technique checked and correct?
7. Adherence checked and acceptable? (Including how adherence is assessed –prescriptions fillings, self-reported)
8. Exposures (work history, possible exposure to allergens (home, hobbies, at work) and other exposures)?
9. Information on concomitant diseases (allergic rhinitis, chronic rhinosinusitis, obesity, OSAS, GERD, bronchiectasis, COPD etc.)
10. Test results: include most recent evaluations of respiratory and asthma (including X-ray, spirometry, peak flow follow-ups, bronchial challenge tests, FeNO, blood eosinophil counts, total IgE)
*If proper diagnostic evaluation have not been done, relevant diagnostic work-up should be performed be the treating generalist or respiratory specialist before referring the patient to a severe asthma centre.
ABPA Allergic bronchopulmonary aspergillosis
ACE Angiotensin-converting enzyme
ACT Asthma Control Test
ACQ Asthma Control Questionnaire
AHR Airway hyperresponsiveness
ASA acetylsalicylic acid
ATS American Thoracic Society
COPD Chronic obstructive pulmonary disease
CPAP Continuous Positive Airway Pressure
CT Computed tomography
DB Dysfunctional breathing
DLCO Diffusing capacity for carbon monoxide
DPI Dry powder inhaler
ERS European Respiratory Society
FEV1 Forced expiratory volume in 1 second
FVC Forced vital capacity
FeNO Fractional exhaled nitric oxide
GERD Gastroesophageal reflux disease
GINA Global Initiative for Asthma
GSRS Gastrointestinal Symptom Rating Scale
HADS Hospital Anxiety and Depression Scale
HRCT High resolution computed tomography
ICS Inhaled corticosteroids
ILO Inducible laryngeal obstruction
LABA Long-acting beta-agonist
LAMA Long-acting muscarinic antagonist
LTRA Leukotriene antagonist
MDI Metered-dose Inhaler
NSAID Nonsteroidal anti-inflammatory drug
NSAN Nordic Severe Asthma Network
NORA Nordic Respiratory Academy
OCS Oral corticosteroids
OSAS Obstructive sleep apnea syndrome
PEF Peak expiratory flow
SABA Short-acting beta-agonist
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