The greater the variation in lung function, the more certain is the diagnosis of asthma. However, people with longstanding asthma may develop fixed airflow limitation. Airflow limitation can be transient and does not necessarily mean that the person has asthma e. Ideally, airflow limitation should be confirmed when the patient does not have a respiratory tract infection.
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Reduction in lung function during a respiratory tract infection with improvement in lung function after its resolution, commonly occurs in people with asthma, but can also be seen in patients with COPD or in healthy people without either asthma or COPD. National Asthma Council Australia. Recommendation types Quick Reference Guide. Home Populations Adolescents and young adults Management.
Assessing and managing asthma in adolescents and young adults. Recommendations By mid-adolescence around 14—16 years , consider applying asthma management guidance for adults in most situations.
How this recommendation was developed Consensus Based on clinical experience and expert opinion informed by evidence, where available. Confirming the diagnosis of asthma in a person using preventer treatment Opens in a new window Please view and print this figure separately: Confirming the diagnosis of asthma in a person using preventer treatment Confirming the diagnosis of asthma in a person using preventer treatment. Clinical profile Lung function Interpretation or action Typical variable respiratory symptoms Variable airflow limitation demonstrated Consistent with asthma diagnosis.
Variable airflow limitation not demonstrated Obtain historical documentation of variable airflow limitation if possible. If not available, test again either of: If diagnosis still not confirmed, consider bronchial provocation challenge test. Consider referral to a specialist respiratory physician to confirm the diagnosis. Ask about age at onset of symptoms and whether there were typical asthma symptoms earlier in life.
If not available, consider back-titrating preventer by one step: If still no evidence of variable airflow limitation, consider stopping preventer treatment with close monitoring and repeating spirometry another 2—3 weeks later. Withholding times vary between medicines: 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: Risk factors for adverse asthma outcomes in adults and adolescents Opens in a new window Please view and print this figure separately: Risk factors for adverse asthma outcomes in adults and adolescents Risk factors for adverse asthma outcomes in adults and adolescents.
For those in mid-to-late adolescence, follow the guidance for adults Figure. Stepped approach to adjusting asthma medication in children Opens in a new window Please view and print this figure separately: Stepped approach to adjusting asthma medication in children Stepped approach to adjusting asthma medication in children. Before considering stepping up, check symptoms are due to asthma, inhaler technique is correct, and adherence is adequate.
Consider stepping up if good control is not achieved. When asthma is stable and well controlled for more than 3 months, consider stepping down e. Stepped approach to adjusting asthma medication in adults Opens in a new window Please view and print this figure separately: Stepped approach to adjusting asthma medication in adults Stepped approach to adjusting asthma medication in adults. Before considering stepping up, check symptoms are due to asthma, inhaler technique is correct, and adherence is adequate Consider stepping up if good control is not achieved.
When asthma is stable and well controlled for 2—3 months, consider stepping down e. This combination is not classed as a reliever when used in a maintenance-only regimen. If adherence to preventer medicines is inadequate, explore barriers and motivating factors. Assess and manage comorbid conditions, lifestyle and psychosocial factors that could affect asthma: Interrelated psychosocial risk factors for poor asthma control in adolescents Poor adherence to treatment Denying or disregarding asthma symptoms Avoiding regular review appointments Life events new school, moving house, family disruption, absent parent Family problems e.
Boulet, 8 Rao et al. More information Diagnostic difficulties when investigating asthma-like symptoms in adolescents Asthma is commonly misdiagnosed in young people presenting with exercise-related symptoms or cough. Investigation and management of exercise-induced bronchoconstriction Close Physiological and psychological changes Stress, anxiety and extreme emotions Some patients report asthma flare-ups and asthma symptoms in response to stress and extreme emotions.
Investigating asthma-like symptoms in adolescents and young adults Laughter Laughing is a common trigger for wheeze in infants. Managing asthma during pregnancy Sexual activity Sexual activity may trigger asthma symptoms possibly due to physical exertion exercise-induced bronchoconstriction , heightened emotion, or a combination of these factors. Investigation and management of exercise-induced bronchoconstriction Close Impact of puberty on asthma In the past, it was thought that children typically 'outgrew' asthma due to maturation of the autonomic and central nervous systems under the effect of sex steroids during puberty.
Some experts consider this in three phases: Inspire Foundation Go to: Relationships Australia Go to: Smarter than Smoking Go to: Overdiagnosis of asthma in obese and nonobese adults. Overtreatment with inhaled corticosteroids and diagnostic problems in primary care patients, an exploratory study. Confirmation of asthma in an era of overdiagnosis. How often is the diagnosis bronchial asthma correct?. British Guideline on the Management of Asthma. Ann Allergy Asthma Immunol.
Stress-induced breathlessness in asthma. Influence of comorbid conditions on asthma. Characteristics of perimenstrual asthma and its relation to asthma severity and control: Diagnosis and management of asthma in adolescents. As with very young children, school-age children treated with inhaled corticosteroids are at risk for decreased growth velocity.
In an analysis of adult height among participants in the Childhood Asthma Management Program clinical trial who were followed for an average of 4. It is not uncommon for asthma to develop during adolescence, particularly in females. Furthermore, as children with established asthma enter adolescence, symptoms can change significantly, in part due to hormonal and pubertal factors. When evaluating adolescents, it is important to consider that asthma misdiagnosis is common in patients who have exercise-induced dyspnea, which can occur as a result of normal or physiologic exercise limitations rather than as a result of asthma, especially in adolescents who are obese, smoke, or take acetaminophen regularly.
It is important for clinicians to consider that the transition from childhood to adolescence can be particularly challenging for patients with chronic diseases such as asthma. With increased depressive symptoms, adolescents are more likely to engage in risky, unhealthy behaviors, such as smoking and substance abuse, and to have a general disregard for health consequences. It is important to screen adolescents annually for signs of psychological distress and to encourage treatment adherence through education and formation of supportive patient-provider relationships. During the transition from adolescence to adulthood, it is important for healthcare providers to work with patients and their parents to develop an action plan that promotes gradual increases in patient responsibility for self-care.
So what can be done to bring down exacerbation rates? Biomarkers provide some clues. Which more effectively prevents acute asthma recurrence after ED discharge: Three questions on current issues in asthma treatment.
Asthma in children and adolescents
Lung function analysis in females Table 3b showed no significant difference between adolescent-onset and never-asthmatics at years. Female adolescent-onset asthmatics demonstrated lower gain in FEV 1 than never-asthmatics between 10 and years. Atopy did not differ significantly between the adolescent-onset and never-asthmatics at 4-years but was significantly higher in adolescent-onset asthmatics at 10 and years Table 4.
At years, analysis of DRS showed that adolescent-onset asthmatics had intermediate BHR, significantly less than for persistent-adolescent asthma but significantly greater than for never —asthma Figure 1a. Univariate analysis of potential associated factors Table E3 ; Online data supplement identified atopy at 10 and years, rhinitis at 10 and years, BHR at 10 and years, maternal history of asthma, and paracetamol use at 18 as having significant association with adolescent-onset asthma.
The factors included in the model were; gender, atopy at 10, rhinitis at 10, maternal asthma, social class I-III at birth, paracetamol use at 18, and proportion with BHR at Atopy, rhinitis and presence of BHR at years predicted subsequent development of adolescent-onset asthma. Among the environmental factors, only paracetamol use at age years showed independently significant association with adolescent-onset asthma. The early-adult newly diagnosed asthma characterised in the Tucson cohort 5 bears some similarity to the adolescent-onset asthma identified in the present study.
Optimizing Asthma Care at Different Stages of Life: Children and Adolescents
That is consistent with significant female predominance of new-onset adolescent asthma in studies from New Zealand 6 , Norway 7 , and Germany 8. Recent findings from the Netherlands 25 , while showing no significant gender difference in asthma prevalence at 16 years, showed greater adolescent incident asthma and less adolescent asthma remission in females. Although we found higher female prevalence of adolescent-onset asthma Another notable distinction is that we found significant association of adolescent-onset asthma with atopy at 10 and years whereas prior studies 6 — 8 mainly identified a non-atopic state.
We recently reported a considerable rise in rhinitis prevalence over adolescence from Rhinitis at years emerged as independently significant for adolescent-onset asthma in the present study. Rochat 9 reported a Relative Risk [RR] of 3. These relationships have been demonstrated in adult populations too. Shaaban 11 reported RR of 3. Rhinitis has also been identified as a risk factor for subsequent BHR We previously reported 12 substantial asymptomatic BHR at years, which we now show is a significant risk factor for adolescent-onset asthma.
While BHR declined across all groupings during adolescence in our study, the BHR dose-response slope for adolescent-onset asthmatics shifted during adolescence towards the greater levels of persistent-adolescent asthmatics. Asymptomatic BHR has been linked to enhanced airway inflammation and remodelling 13 , accelerated decline in FEV 1 14 and subsequent asthma Laprise 13 demonstrated that airway changes in subjects with asymptomatic BHR became more exaggerated once symptoms develop.
We found significant sputum eosinophilia and raised FeNO in our adolescent-onset asthmatics at years, indicating that symptoms, BHR and airway inflammation go hand in hand in this group. We found that at years, male adolescent-onset asthmatics had evidence of impaired lung function while pre-symptomatic. This may reflect more pronounced effects of subclinical disease on lung function in males at that age on account of naturally smaller relative airway calibre in preadolescent males who have yet to enter their growth spurt.
By contrast, we detected reduced lung function in female but not male adolescent-onset asthmatics at years. These findings need to be interpreted with caution given the small sample sizes involved. However, if replicated elsewhere, the cause of such gender differences are worthy of speculation. Females have a shorter period of adolescent growth that stops at menarche while male growth continues longer The only adolescent factor significantly associated with adolescent-onset asthma was paracetamol use at The role of paracetamol as a risk factor for asthma via enhanced oxidative airway damage is gaining increasing scrutiny 17 , However it is worth noting that we did not detect any association of other potent oxidative effects such as tobacco smoke with adolescent-onset asthma which may cast doubt over that mechanism as an explanation for any relationship with paracetamol.
We did not adopt categorical cut-offs to define paracetamol consumption as there is no clear evidence of clinically relevant cut-offs in that context. A limitation of our study is lack of precise data on dosage and indication for use of paracetamol. Therefore these findings should be viewed as demonstrating an association rather than causative relationship.
Confounding by indication cannot be excluded and reverse causation remains a potential explanation of our reported association of paracetamol exposure with adolescent-onset asthma. We did not identify evidence of early-life environment predisposing to adolescent-onset asthma. By contrast tobacco exposures, in early life and adolescence, have previously been implicated as risk factors for incident airways disease 15 , 16 , However smoking-related incident disease may reflect various wheezing phenotypes not all of which receive an asthma diagnosis.
This may reflect that heredity is more significant for some asthma phenotypes than others. Our study has several strengths. The prospective nature of our work enables better accuracy in assessing temporal relationships and risk factors. Recall bias maybe problematic in longitudinal studies of disease development. However, the high rate of cohort follow-up strengthens the reliability of our findings. We used standardised study materials including ISAAC questionnaires, validated in diverse populations, to ensure comparability with other populations.
We defined adolescent-onset asthma as that absent at years but present at years. To counter this we excluded 17 cases of recurrent childhood asthma in adolescence.
Optimizing Asthma Care at Different Stages of Life: Children and Adolescents
The remaining 56 cases of adolescent-onset asthma had no evidence of earlier childhood asthma from prospectively collected data. We did not exclude 17 cases with isolated episodes of wheezing in the first few years of life, as early life wheezing may not represent asthma.
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It is impossible to exclude a few cases of disease recurrence amongst incident asthma in our study, though as cited by the Tucson group in a similar study 5 we can be confident that all our incident asthma cases represent first expression of disease severe enough to obtain an asthma diagnosis. An important implication of our characterisation of adolescent-onset asthma is that we identified potentially modifiable risk factors, present at a pre-symptomatic stage. Treatment of childhood rhinitis, with anti-inflammatory drugs or allergen specific immunotherapy might offer an avenue to reduce adolescent-onset asthma.
Evidence to support that notion is limited but one observational study 27 noted remission of asymptomatic BHR when rhinitis was treated with nasal steroids. Immunotherapy has been shown to reduce asthma in children with allergic rhinitis 33 and may prove beneficial in reducing adolescent-onset asthma risk in such children. In conclusion, adolescent-onset asthma is associated with pre-existing atopy, rhinitis and asymptomatic BHR plus adolescent behaviour such as paracetamol use. Awareness of potentially modifiable influences may reduce the impact of this disease state and should stimulate future work.
The authors gratefully acknowledge the cooperation of the children and parents who have participated in this study. Finally we would like to highlight the role of the late Dr David Hide in starting this study. This is a PDF file of an unedited manuscript that has been accepted for publication.
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