History and exam
Your Organizational Guidance
ebpracticenet urges you to prioritize the following organizational guidance:
Astma bij volwassenen: diagnose en monitoring in de eerste lijnPublished by: Werkgroep Ontwikkeling Richtlijnen Eerste Lijn (Worel)Last published: 2020Asthme chez l’adulte : diagnostic et surveillance en soins de santé primairesPublished by: Groupe de Travail Développement de recommmandations de première ligneLast published: 2020Key diagnostic factors
common
recent upper respiratory tract infection
With a recent sinusitis or common cold, symptoms are typically exacerbated and may lead to prolonged cough and respiratory symptoms.
dyspnea
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with strong emotions, such as stress/anxiety.
May wake the patient from sleep.
cough
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with strong emotions, such as stress/anxiety.
May wake the patient from sleep.
expiratory wheezes
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with strong emotions, such as stress/anxiety.
Polyphonic, high-pitched expiratory wheezes are typical of asthma.
Auscultation sounds: Polyphonic wheeze
Auscultation sounds: Expiratory wheeze
nasal polyposis
Appear as single or multiple polyps in the nasal cavity.
Risk factors
strong
family history
A parental history of asthma is a major risk factor for early development of asthma.[1]
gene polymorphisms and epigenetics
Multiple genes and gene polymorphisms have been implicated in the development of asthma or airway hyperresponsiveness to environmental triggers.[12][15][16][17] These have been observed to affect nitric oxide synthase (NOS), cytokines (e.g., IL-13, IL-4,IL-4R, TNF-α), beta-2 adrenergic receptor (ADRB2), thymic Stromal Lymphopoietin (TSLP), and the vitamin D receptor (VDR).[12][14][16][17][18][19][20]
Genetic risk factors likely interact with environmental exposures in early childhood (e.g., allergens, viral infections, pollution, and tobacco smoke) to increase the risk of asthma, possibly by triggering differential methylation.[11][12][13][14]
allergen/irritant exposure
Exposure and sensitization to aeroallergens and certain foods is a recognized risk factor for developing asthma (e.g., based on positive skin-prick tests). Common allergens/irritants include cats, dogs, cockroaches, house dust mites, fungal spores, environmental tobacco smoke, pollens (e.g., tree, weed, and grass), and fumes from chemicals (e.g., bleach).[55] Sensitization to multiple allergens in early life has been associated with reduced lung function growth.[56]
occupational exposure
Workers commonly affected by occupational allergens include bakers, farmers, carpenters, and people involved in manufacturing plastics, foams, and glues. See Occupational asthma.
air pollution
Outdoor air pollution is associated with an increased risk of both asthma and loss of asthma control, especially exposure to traffic-related air pollution, including NO₂, particulate matter ≤2.5 micrometers (PM2.5), and black carbon.[11][32][57][58]
Indoor air pollutants linked to an asthma diagnosis and both increased symptoms and exacerbations include particulate matter (e.g., from wood burning, natural gas, cooking, smoking, candles) and evaporative volatile organic compounds (e.g., household cleaning agents, glue, personal care products, formaldehyde).[32][33][34][35][36]
Prenatal exposure to traffic-related air pollution, particularly from the second trimester, has been associated with an increased risk of asthma development among children and adolescents.[32]
Workers may be affected by occupational triggers. See Occupational asthma.
atopic disease history
History of eczema, atopic dermatitis, and allergic rhinitis is strongly associated with the development of asthma.[27][59] The progression from eczema/atopic dermatitis to allergic rhinitis to subsequent asthma has been termed the "allergic or atopic march."[60] Association is possibly due to genetic variants in shared susceptibility genes.[27][60]
obesity
High body mass index (BMI) is a leading risk factor for asthma-attributed disability adjusted life years globally.[5] A high BMI increases the likelihood of developing asthma, and significant weight loss can improve asthma control.[38][39][40] Obesity also affects the time-to-first exacerbation in patients with moderate-to-severe asthma, independent of drug therapy.[41]
Patients with obesity have higher use of all asthma drugs and higher inhaled corticosteroid doses than their healthy-weight peers, despite lower lung function parameters.[42][61] Evidence suggests a female-predominant obese asthma phenotype in which patients are less responsive to typical asthma drugs and have a poorer prognosis.[38][39][62]
Postulated mechanisms include reduced lung and tidal volume (promoting airway narrowing), low-grade systemic inflammation, effect of comorbidities, or a common etiology.[43][63][64]
cigarette smoking
Smoking increases the risk of developing asthma and is associated with a worse prognosis.[26][55][65] Patients with asthma who smoke have been found to have elevated levels and activation of neutrophils compared with nonsmoking patients with asthma.[26] Smoking is a leading risk factor for asthma-attributed disability adjusted life years.[5]
Passive exposure to cigarette smoke is also an important risk factor for asthma.
Current smoking status increases the risk of exacerbation in patients with moderate-to-severe asthma, independent of drug therapy.[41]
vaping
The potential harms of vaping were first highlighted by an outbreak of e-cigarette or vaping use-associated lung injury (EVALI) in 2019.[66]
Vaping (i.e., electronic nicotine delivery system or e-cigarette use) has since been associated with higher rates of asthma and asthma exacerbations, independent of combustible cigarette or cannabis use.[30][67][68][69][70]
Ever use of e-cigarettes is associated with obstructive lung function impairment after adjusting for traditional smoking and other covariates.[28][29][30]
early life respiratory viral infection and viral wheeze
Infection with human respiratory syncytial virus (RSV) or human rhinovirus in early life increases the likelihood of developing asthma in those at risk.[21] Long-term follow-up in a prospective cohort of 49 patients revealed that over half (n=26) who had been hospitalized for viral wheezing episodes in early childhood had asthma in young adulthood.[71]
Viral infection may be detected in up to 58% of patients with an asthma exacerbation.[72]
nasal polyposis
The prevalence of chronic rhinosinusitis with nasal polyps is higher in patients with asthma compared with the general population, and is associated with greater disease severity.[73][74] The two conditions share pathophysiologic processes including airway remodeling and eosinophilia.[74] Chronic rhinosinusitis with nasal polyps is more commonly associated with adult early- or late-onset versus childhood asthma.[73]
aspirin and nonsteroidal anti-inflammatory drug (NSAID) use
low socioeconomic status
Socioeconomic status (SES), as defined by an individual’s education and income, can affect health outcomes in asthma. People from a lower SES are more likely to live in areas with the poorest air quality and worst housing conditions, to be exposed to more psychosocial stressors, and to have poorer diets.[44] SES also affects access to health care, with a lower SES consistently associated with increased secondary health care utilization, including emergency department attendance.[75] Black and Hispanic people are disproportionately affected by lower SES in the US.[44] Factors associated with lower SES increase the risks of asthma, poor asthma control, and acute exacerbations.
weak
gastroesophageal reflux
Prevalent in patients with poorly controlled asthma.[76] The link between gastroesophageal reflux disease (GERD) and the development of asthma remains unclear, but could be related to chronic irritation and inflammation of the airways following exposure to gastric contents.[77][78] A Cochrane review found that treatment for GERD moderately improved lung function and decreased the use of rescue drug in patients with moderate-to-severe asthma and comorbid GERD, but failed to show an effect on exacerbations and hospital utilization.[79] Another meta-analysis showed that treatment with proton-pump inhibitors had no effect on asthma symptoms in patients with symptomatic GERD.[80]
obstructive sleep apnea
The prevalence of obstructive sleep apnea (OSA) in patients with asthma is approximately two to three times higher than in the general population.[81] Both conditions share risk factors including obesity, rhinitis, and gastroesophageal reflux disease.[78][81] Patients with asthma should be screened for symptoms suggestive of OSA and, if positive, referred for sleep testing to confirm the diagnosis.[82]
sex
As children, boys have a higher prevalence of asthma compared with girls. This changes during adolescence and adulthood, when the prevalence of asthma is higher in women.[8] Sex hormones mediate this transition. Overall, however, female sex increases the risks of asthma in adults and the risk of exacerbation in patients with moderate-to-severe asthma.[8][41][83]
preterm birth
Preterm (gestational age <37 weeks) and early term (gestational age 37-38 weeks) birth are associated with increased risks of asthma from childhood to adulthood.[84][85] This risk is elevated after spontaneous and medically indicated preterm birth, with or without perinatal respiratory complications.[85]
polycystic ovary syndrome
vitamin D deficiency
Cross-sectional studies have suggested that suboptimal vitamin D status is associated with impaired lung function, higher exacerbation frequency, and reduced corticosteroid response.[90] Vitamin D supplementation may have a role in reducing the risk of asthma exacerbations and improving asthma control, but the available evidence is inconsistent. See Emerging treatments.[91][92][93][94] More evidence is needed to establish a clear correlation.
Use of this content is subject to our disclaimer