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For adolescents who have persistent asthma and use maintenance drugs, the short-acting drug is used as a quick-relief, or rescue, medication to treat asthma attacks. It may also be used to prevent asthma symptoms triggered by exercise. Your doctor may recommend allergy shots immunotherapy if an allergy induces asthma attacks and if the allergen cannot be avoided.

This treatment may be particularly useful for an allergy to pets, dust mites or pollens. The purpose of allergy shots is to build up a tolerance by gradually increasing exposure to an allergen. Shots are administered once or twice a week in increasing doses, usually for three to six months.

A maintenance dose is administered every two to four weeks for a period of three to five years. Most asthma medications are given with a device that allows a child to breathe medication directly into the lungs. Talk to your doctor about the proper use of a device, the delivery options for your child's medication and the appropriate device for your child's needs. Treating asthma requires adherence to an ongoing treatment plan, regular monitoring, adjustments in the plan as needed and self-care.

Some studies have shown that asthma management creates a particular set of challenges among adolescents, who are seeking greater autonomy, developing socially and emotionally, and experiencing changes in their relationships with friends and family. The task of managing a chronic medical condition or taking medication in front of peers may cause embarrassment or self-consciousness. The routine may seem like a burden to greater independence, or there may be denial about the severity of asthma. Adolescents with asthma may be at greater risk of depression and anxiety, and these psychological factors may result in poorer asthma management.

Your doctor can work with you and your adolescent to create a written action plan that outlines self-monitoring and care. You should share the plan with other family members, friends, teachers, coaches and school administrators. A thorough plan includes such things as the following:.

Acute Bronchitis

Your doctor will likely ask your child to use a peak flow meter at home. This hand-held device measures how well air flows from the lungs when exhaling. It can monitor the effectiveness of your ongoing treatment and assess lung function after using a rescue medication. You can work with your adolescent to keep a record of peak flow measurements, symptoms and treatment schedule to share with your doctor.

These records can help your doctor determine if the long-term treatment plan is effective and make adjustments to the plan. Keep appointments as recommended by your doctor to review records and adjust the action plan as necessary. Depending on the triggers for your child's asthma, make adjustments as much as possible at home, school and other environments to minimize your child's exposure to triggers. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission.

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Most cases of acute bronchitis do not require medical treatment. People diagnosed with acute bronchitis will be told to rest and drink plenty of fluids to keep the mucus thin, watery and easy to cough up. Warm, moist air also can loosen sputum and make coughing and breathing easier. Because of that, many physicians recommend at least one of the following for people with bronchitis:.

Asthma and Bronchitis (By Appointment Only) - Health Facts

Breathing in the steam from a sink or pot filled with hot water. You can catch more of the steam by tenting a towel over your head while bending over the water. For safety reasons, do not breathe from a pot of boiling water that is still on the stove. If you have a fever, most physicians will recommend taking aspirin , ibuprofen Advil , Motrin and others or acetaminophen Tylenol to reduce fever. However, aspirin should not be given to children under age 19 to avoid the risk of Reye's syndrome, a rare but serious, potentially fatal illness that can occur when a child with a fever takes aspirin.

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If bronchitis is caused by a bacterial infection and doesn't get better on its own, an antibiotic may be prescribed. Antibiotics will be given only when there is a strong suspicion that the bronchitis is caused by a bacterial infection. That's because of rising concerns about antibiotic resistance, in which bacteria evolve in ways that allow them to survive antibiotics. This problem is increasing and is caused, in part, by antibiotics being used incorrectly and when they are not needed.

In some cases, doctors may prescribe a bronchodilator, an inhaled medication that helps the airways to open. These are the same medications used by some people with asthma to ease breathing during an asthma attack. Make an appointment with your health care provider if a mild cough gets worse after a week or if you have a cough that produces thick, bloody, foul-smelling or green-colored phlegm.

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You should call your doctor if:. You have a high fever that does not come down after taking a fever-relieving medication, such as acetaminophen or aspirin. Any time you have chest pain, you should call your doctor for advice. Chest pain can come from the heart as well as the lungs. People at high risk of complications from acute bronchitis — such as infants, the elderly or people with chronic lung or heart disease — should call a physician at the first signs of bronchitis.

Symptoms of acute bronchitis are often similar to symptoms of mild asthma. EB has an established place in asthma where it contributes to airway hyperresponsiveness AHR , asthma symptoms, and airway remodelling. Anti-inflammatory agents such as inhaled corticosteroids are used successfully to treat EB in asthma. The implications of eosinophilic airway inflammation in disorders other than asthma and the potential role of the asthma treatment paradigm in those disorders with EB is the subject of this review.

Eosinophils are typically absent in sputum samples from normal subjects. The main cell seen is the macrophage, followed by a smaller proportion of neutrophils. The upper normal limit of sputum eosinophils in adults and children is 2. For example, Rytila et al found the upper limit to be 0. Asthma is defined as episodic respiratory symptoms occurring in association with variable airflow obstruction which may be demonstrated by bronchodilator responsiveness, increased diurnal variability of peak expiratory flow PEF , or the demonstration of AHR.

Interleukin IL -5 is a key cytokine associated with the development of eosinophilia in various tissue sites in the body. IL-5 promotes the growth and differentiation of eosinophil precursors, prolongs their lifespan in tissue by inhibition of apoptosis, and can activate tissue eosinophils. It is likely that other mediators also contribute to the pathogenesis of EB. Cytokines and enzymes such as the matrix metalloproteinases that participate in tissue remodelling are also increased during eosinophilic airway inflammation.

The subepithelial fibrosis that characterises asthma is one manifestation of tissue remodelling that is also reported to occur in allergic rhinitis with EB. The place of airway remodelling in non-asthmatic EB is not clearly defined. Changes in eosinophilic airway inflammation are a well established cause of increased airway responsiveness in asthma. Airway responsiveness is also modified by eosinophilic inflammation, even when this is in the non-asthmatic range.

Similarly, corticosteroid treatment reduces eosinophilic inflammation and improves airway responsiveness in both the asthmatic 2, 3 and non-asthmatic range. Consequently, EB cannot be equated with AHR but is an important modifier of the degree of airway responsiveness. Airway inflammation with eosinophils can be caused by exposure to allergens and occupational sensitisers.

The triggers that cause EB without asthma are similar to the triggers of EB in asthma. Exposure to allergens, 15— 18 occupational chemicals, 19 and drugs 20 are all reported to cause EB with cough. Some patients with chronic cough and EB have associated gastro-oesophageal reflux GOR , raising the possibility that this may also induce eosinophilic airway inflammation.

EB responds well to anti-inflammatory treatment with inhaled corticosteroids. Eosinophilic bronchitis is a key feature of asthma where it forms part of the current definition 32 and is believed to be responsible for AHR and asthma symptoms. EB is not a universal feature of asthma, however. Eosinophilic bronchitis may be absent during exacerbations of asthma 33, 34 and also in stable disease.

Prevalence and consequences of eosinophilic bronchitis in different clinical syndromes. In asthma EB is a determinant of severity, increases during exacerbations of the disease, and is the focus of preventive treatment. The development of airway wall remodelling is a characteristic feature of asthma that may result from chronic eosinophilic inflammation, so the focus of asthma treatment is directed at controlling eosinophilic airway inflammation.

Inhaled corticosteroids are administered on a daily basis and generally for long periods in order to suppress symptoms and exacerbations. Increasingly, the trends in treatment are to introduce corticosteroids earlier in the course of the disease and to continue treatment during asymptomatic periods to prevent the adverse effects of eosinophilic airway inflammation—namely, exacerbations and remodelling. Patients with seasonal allergic rhinitis and atopic subjects without asthma may have EB demonstrated either by sputum analysis 38— 41 or in bronchial biopsy samples.

Cough variant asthma CVA is characterised by eosinophilia in sputum, 48— 51 bronchoalveolar lavage BAL fluid, 21, 52 and in bronchial biopsy specimens. In addition, there can be thickening of the subepithelial basement membrane, a feature of airway wall remodelling. Isolated chronic cough is a common clinical problem.

EB may occur in patients with chronic cough who are subsequently diagnosed as having CVA, EB without asthma, 14 or atopic cough. Atopic cough was described by Fujimura et al in It appears that there is considerable overlap between the atopic cough described by Fujimura et al and EB without asthma as described by Gibson and others. Some correspondents have suggested that chronic cough with EB or atopic cough should be considered a form of asthma. Does cough with EB cause chronic airway obstruction? A single case report suggests this can occur. How should cough with EB be treated? Either until symptoms are suppressed or continuously and early as in asthma?

There is also an important issue of diagnosing cough with EB. Patients presenting with episodic respiratory symptoms of cough, wheeze, chest tightness, dyspnoea, and sputum production but whose lung function measurements do not fulfil the criteria for asthma are often left without a diagnosis and without effective treatment. Bronchodilator response, PEF variability, and airway responsiveness to histamine or 4. The clinical course and treatment requirements for these patients are not well defined.

The high incidence of subsequent asthma in patients with EB without asthma suggests that this condition may be a precursor of subsequent asthma. The same issues arise for EB with respiratory symptoms as for cough. In addition to the typical IL-8 mediated neutrophil influx, 69 some patients with COPD have eosinophilic inflammation detected in sputum, bronchial washings, BAL fluid, and bronchial biopsy specimens table 1.

COPD can develop in patients who do not smoke. The mechanisms of chronic airflow obstruction in these patients are poorly characterised, but it is important to note that EB without asthma has progressed to chronic airflow obstruction in the absence of smoking. The prevalence of asthma is increasing in western countries, predominantly in atopic subjects. The conditions that precede the development of asthma are not well defined, but may represent an opportunity to intervene and reduce the rise in asthma prevalence.

Cough variant asthma with EB may be a precursor of typical asthma with wheeze, and allergic rhinitis with EB may be a precursor for cough with EB, and also for episodic respiratory symptoms without AHR. Much work is being directed at interventions in infancy to prevent the development of atopic disease. Another approach could be to prevent the development of symptomatic asthma by targeting EB without asthma.

If EB is a precursor for asthma, then intervention at this stage could reduce the rising prevalence of asthma.

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Since cough is an early feature of EB, the recognition and effective treatment of cough with EB may reduce asthma prevalence. The studies reviewed establish that EB occurs not only in asthma, but also in chronic cough, COPD, and allergic rhinitis. The mechanisms and causal factors that operate in EB without asthma are similar to EB with asthma. The optimal treatment and prognosis of EB need to be considered, especially in the context of the rising prevalence of asthma and the development of chronic airflow obstruction. The prognosis for EB in the various clinical syndromes needs to be established by longitudinal observational studies.

In particular, is EB a risk factor for subsequent asthma, for airway remodelling, or for the development of chronic airflow obstruction? What is the optimal treatment for EB without asthma? Should inhaled corticosteroids be given only to control symptoms, or should they be continued during asymptomatic periods in order to reduce exacerbations and prevent disease progression? Are other treatments effective, in particular nasal corticosteroids or histamine H 1 antagonists, especially if there is atopy or nasal disease present?

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It will be important to examine the effectiveness of these treatments in controlled studies and to investigate their effects on eosinophilic airway inflammation. How can the recognition of EB be incorporated into clinical practice?

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Based on the prevalence of EB in various syndromes and after clinical assessment and assessment for variability of airflow, patients can be stratified according to their likelihood of having EB. The ADP has been used to establish the diagnosis and treatment for patients presenting with chronic cough. The assessment of EB is not part of this protocol. Induced sputum analysis would also allow corticosteroid treatment to be commenced with a reasonably high chance of success and would provide an objective marker of treatment response.

This is in contrast to the ADP where a diagnosis can only be reached retrospectively after the cough resolves, based upon treatment in an uncontrolled treatment trial and without objective markers of response. It seems likely that assessment of induced sputum for EB could be included in the ADP after assessment for variable airflow obstruction.