Beta2-adrenergic agonists are recommended for bronchospasm.

- Short acting (SABA)

- Terbutaline

- Salbutamol

- Levosalbutamol

- Long acting (LABA)

- Formoterol

- Salmeterol

- Others

- Dopamine

- Norepinephrine

- Epinephrine

Interventions include intravenous (IV) medications (e.g. magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g., albuterol or ipratropium bromide/salbutamol), and positive-pressure therapy, including mechanical ventilation. Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways. Intravenous corticosteroids and methylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such as ketamine or propofol, have bronchodilating properties. According to a new randomized control trial ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy.

The neurotransmitter acetylcholine is known to decrease sympathetic response by slowing the heart rate and constricting the smooth muscle tissue. Ongoing research and successful clinical trials have shown that agents such as diphenhydramine, atropine and Ipratropium bromide (all of which act as receptor antagonists of muscarinic acetylcholine receptors) are effective for treating asthma and COPD-related symptoms .

Status asthmaticus is slightly more common in males and is more common among people of African and Hispanic origin. The gene locus glutathione dependent S-nitrosoglutathione (GSNOR) has been suggested as one possible correlation to development of status asthmaticus.

Medication challenge tests, such as the methacholine challenge test, have a lower sensitivity for detection of exercise-induced bronchoconstriction in athletes and are also not a recommended first-line approach in the evaluation of exercise-induced asthma.

Mannitol inhalation has been recently approved for use in the United States.

It should be noted, however, that a relatively recent review of the literature has concluded that there is currently insufficient available evidence to conclude that either mannitol inhalation or eucapnic voluntary hyperventilation are suitable alternatives to exercise challenge testing to detect exercise-induced bronchoconstriction and that additional research is required.

The treatment of EIB has been extensively studied in asthmatic subjects over the last 30 years, but not so in EIB. Thus, it is not known whether athletes with EIB or ‘sports asthma’ respond similarly to subjects with classical allergic or nonallergic asthma. However, there is no evidence supporting different treatment for EIB in asthmatic athletes and nonathletes.

The most common medication used is a beta agonist taken about 20 minutes before exercise. Some physicians prescribe inhaled anti-inflammatory mists such as corticosteroids or leukotriene antagonists, and mast cell stabilizers have also proven effective. A randomized crossover study compared oral montelukast with inhaled salmeterol, both given two hours before exercise. Both drugs had similar benefit but montelukast lasted 24 hours.

Three randomized double-blind cross-over trials have examined the effect of vitamin C on EIB. Pooling the results of the three vitamin C trials indicates an average 48% reduction in the FEV1 decline caused by exericise (Figure). The systematic review concluded that "given the safety and low cost of vitamin C, and the positive findings for vitamin C administration in the three EIB studies, it seems reasonable for physically active people to test vitamin C when they have respiratory symptoms such as cough associated with exercise." It should be acknowledged that the total number of subjects involved in all three trials was only 40.

Figure: This forest plot shows the effect of vitamin C (0.5–2 g/day) on post-exercise decline in FEV1 in three studies with asthmatic participants. Constructed from data in Fig. 4 of Hemilä (2013).

The three horizontal lines indicate the three studies, and the diamond shape at the bottom indicates the pooled effect of vitamin C: decrease in the post-exercise decline in FEV1 by 48% (95%CI: 33 to 64%).

In May 2013, the American Thoracic Society issued the first treatment guidelines for EIB.

Underlying disease must be controlled to prevent exacerbation and worsening of ABPA, and in most patients this consists of managing their asthma or CF. Any other co-morbidities, such as sinusitis or rhinitis, should also be addressed.

Hypersensitivity mechanisms, as described above, contribute to progression of the disease over time and, when left untreated, result in extensive fibrosis of lung tissue. In order to reduce this, corticosteroid therapy is the mainstay of treatment (for example with prednisone); however, studies involving corticosteroids in ABPA are limited by small cohorts and are often not double-blinded. Despite this, there is evidence that acute-onset ABPA is improved by corticosteroid treatment as it reduces episodes of consolidation. There are challenges involved in long-term therapy with corticosteroids—which can induce severe immune dysfunction when used chronically, as well as metabolic disorders—and approaches have been developed to manage ABPA alongside potential adverse effects from corticosteroids.

The most commonly described technique, known as sparing, involves using an antifungal agent to clear spores from airways adjacent to corticosteroid therapy. The antifungal aspect aims to reduce fungal causes of bronchial inflammation, whilst also minimising the dose of corticosteroid required to reduce the immune system’s input to disease progression. The strongest evidence (double-blinded, randomized, placebo-controlled trials) is for itraconazole twice daily for four months, which resulted in significant clinical improvement compared to placebo, and was mirrored in CF patients. Using itraconazole appears to outweigh the risk from long-term and high-dose prednisone. Newer triazole drugs—such as posaconazole or voriconazole—have not yet been studied in-depth through clinical trials in this context.

Whilst the benefits of using corticosteroids in the short term are notable, and improve quality of life scores, there are cases of ABPA converting to invasive aspergillosis whilst undergoing corticosteroid treatment. Furthermore, in concurrent use with itraconazole, there is potential for drug interaction and the induction of Cushing syndrome in rare instances. Metabolic disorders, such as diabetes mellitus and osteoporosis, can also be induced.

In order to mitigate these risks, corticosteroid doses are decreased biweekly assuming no further progression of disease after each reduction. When no exacerbations from the disease are seen within three months after discontinuing corticosteroids, the patient is considered to be in complete remission. The exception to this rule is patients who are diagnosed with advanced ABPA; in this case removing corticosteroids almost always results in exacerbation and these patients are continued on low-dose corticosteroids (preferably on an alternate-day schedule).

Serum IgE can be used to guide treatment, and levels are checked every 6–8 week after steroid treatment commences, followed by every 8 weeks for one year. This allows for determination of baseline IgE levels, though it’s important to note that most patients do not entirely reduce IgE levels to baseline. Chest X-ray or CT scans are performed after 1–2 months of treatment to ensure infiltrates are resolving.

Patients with plastic bronchitis that is being caused due to a co-morbid condition generally have a good prognosis once the underlying disease is treated.

Patients, families, and caregivers are encouraged to join the NIH Rare Lung Diseases Consortium Contact Registry. This is a privacy protected site that provides up-to-date information for individuals interested in the latest scientific news, trials, and treatments related to rare lung diseases.

Bronchial hyperresponsiveness (or other combinations with airway or hyperreactivity) is a state characterised by easily triggered bronchospasm (contraction of the bronchioles or small airways).

Bronchial hyperresponsiveness can be assessed with a bronchial challenge test. This most often uses products like methacholine or histamine. These chemicals trigger bronchospasm in normal individuals as well, but people with bronchial hyperresponsiveness have a lower threshold.

Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people suffering from chronic obstructive pulmonary disease (COPD). In the Lung Health Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other factors. In asthma it tends to be reversible with bronchodilator therapy, while this is not the case in COPD.

Bronchial hyperresponsiveness has been associated with gas cooking among subjects with the "GSTM1" null genotype.

Reactive airways dysfunction syndrome (RADS) is a term proposed by Stuart M. Brooks and colleagues in 1985

It can also manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal, and can even create long-term airway damage depending on the amount of exposure and the concentration of chlorine. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects.

Recovery is directly dependent on the duration and level of exposure to the causative agent. Depending on the severity of the case, the condition of the patient can improve dramatically during the first year after removal from exposure.

Three basic types of procedures are used for treating the affected workers: reducing a worker's exposure, removing a worker from the environment with the asthma-causing agent, and treatment with asthma medications. Completely stopping exposure is more effective treatment than reducing exposure. By reducing exposure, the probability of suffering another reaction is lowered. Methods of reducing exposure include transferring an affected worker to a position without the relevant asthmagen, use of respiratory protection, and engineering controls. In 1984 innovator David Cornell discovered and invented effective control equipment in the UK for the removal of many harmful workplace fumes. 'BOFA' extraction products are now found in over 100 countries worldwide.

People affected by occupational asthma that occurred after a latency period, whether a few months or years, should be immediately removed from exposure to the causative agent. However, this can entail severe socio-economic consequences for the worker as well as the employer due to loss of job, unemployment, compensation issues, quasi-permanent medical expenditures, and hiring and re-training of new personnel. This can be mitigated by transferring the worker within a company.

The course of treatment of fire breather's pneumonia remains controversial. Administration of bronchodilators, corticosteroids, and prophylactic antibiotics to prevent secondary infection, is a common course of treatment. Some studies suggest that steroids may improve outcomes in severely affected individuals, yet these data are only based on a limited number of patients. The use of gastric decontamination to prevent subsequent pulmonary injury from hydrocarbon ingestion is controversial. It may have potential benefit in large (> 30 cc), intentional ingestion of compounds with systemic toxicity.

Prognosis after peak symptoms is typically good, with most patients making a full recovery in weeks to months.

Prevention of occupational asthma can be accomplished through better education of workers, management, unions and medical professionals. This will enable them to identify the risk factors and put in place preventive measures, including respiratory protection and exposure limits.

There are limited national and international studies into the burden of ABPA, made more difficult by a non-standardized diagnostic criteria. Estimates of between 0.5–3.5% have been made for ABPA burden in asthma, and 1–17.7% in CF. Five national cohorts, detecting ABPA prevalence in asthma (based on GINA estimates), were used in a recent meta-analysis to produce an estimate of the global burden of ABPA complicating asthma. From 193 million asthma sufferers worldwide, ABPA prevalence in asthma is estimated between the extremes of 1.35–6.77 million sufferers, using 0.7–3.5% attrition rates. A compromise at 2.5% attrition has also been proposed, placing global burden at around 4.8 million people affected. The Eastern Mediterranean region had the lowest estimated prevalence, with a predicted case burden of 351,000; collectively, the Americas had the highest predicted burden at 1,461,000 cases. These are likely underestimates of total prevalence, given the exclusion of CF patients and children from the study, as well as diagnostic testing being limited in less developed regions.

This disease is irreversible and severe cases often require a lung transplant. Transplant recipients are at risk for re-developing the disease, as bronchiolitis obliterans is a common complication of chronic rejection. Evaluation of interventions to prevent bronchiolitis obliterans relies on early detection of abnormal spirometry results or unusual decreases in repeated measurements.

A multi-center study has shown the combination of inhaled fluticasone propionate, oral montelukast, and oral azithromycin may be able to stabilize the disease and slow disease progression. This has only been studied in patients who previously underwent hematopoietic stem cell transplantation.

Treatment is with corticosteroids and possibly intravenous immunoglobulins.

In order to prevent bronchiectasis, children should be immunized against measles, pertussis, pneumonia, and other acute respiratory infections of childhood. While smoking has not been found to be a direct cause of bronchiectasis, it is certainly an irritant that all patients should avoid in order to prevent the development of infections (such as bronchitis) and further complications.

Treatments to slow down the progression of this chronic disease include keeping bronchial airways clear and secretions weakened through various forms of pneumotherapy. Aggressively treating bronchial infections with antibiotics to prevent the destructive cycle of infection, damage to bronchial tubes, and more infection is also standard treatment. Regular vaccination against pneumonia, influenza and pertussis are generally advised. A healthy body mass index and regular doctor visits may have beneficial effects on the prevention of progressing bronchiectasis. The presence of hypoxemia, hypercapnia, dyspnea level and radiographic extent can greatly affect the mortality rate from this disease.

ILD is not a single disease, but encompasses many different pathological processes. Hence treatment is different for each disease.

If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued.

Many cases due to unknown or connective tissue-based causes are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant treatment. Patients with a low level of oxygen in the blood may be given supplemental oxygen.

Pulmonary rehabilitation appears to be useful. Lung transplantation is an option if the ILD progresses despite therapy in appropriately selected patients with no other contraindications.

On October 16, 2014, the Food and Drug Administration approved a new drug for the treatment of Idiopathic Pulmonary Fibrosis (IPF). This drug, Ofev (nintedanib), is marketed by Boehringer Ingelheim Pharmaceuticals, Inc. This drug has been shown to slow the decline of lung function although the drug has not been shown to reduce mortality or improve lung function. The estimated cost of the drug per year is approximately $94,000.

Specific pretreatments, drugs to prevent chemically induced lung injuries due to respiratory airway toxins, are not available. Analgesic medications, oxygen, humidification, and ventilator support currently constitute standard therapy. In fact, mechanical ventilation remains the therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. Positive end-expiratory pressure (PEEP) is used in mechanically ventilated patients with ARDS to improve oxygenation. Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions. Corticosteroids are sometimes administered, and bronchodilators to treat bronchospasms. Drugs that reduce the inflammatory response, promote healing of tissues, and prevent the onset of pulmonary edema or secondary inflammation may be used following severe injury to prevent chronic scarring and airway narrowing.

Although current treatments can be administered in a controlled hospital setting, many hospitals are ill-suited for a situation involving mass casualties among civilians. Inexpensive positive-pressure devices that can be used easily in a mass casualty situation, and drugs to prevent inflammation and pulmonary edema are needed. Several drugs that have been approved by the FDA for other indications hold promise for treating chemically induced pulmonary edema. These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is particularly appealing because it has an established safety record and can be easily administered as an initial intervention. Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the "AANA Journal" discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation. Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying pulmonary edema. Some of these potential drugs target the inflammatory response or the specific site(s) of injury. Others modulate the activity of ion channels that control fluid transport across lung membranes or target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may be instrumental in determining new targets for therapy. Mechanistic studies may also aid in the development of new diagnostic approaches. Some chemicals generate metabolic byproducts that could be used for diagnosis, but detection of these byproducts may not be possible until many hours after initial exposure. Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.

Currently there are no clinically approved agents that can reduce pulmonary and airway cell dropout and avert the transition to pulmonary and /or airway fibrosis.

Treatment of bronchiectasis includes controlling infections and bronchial secretions, relieving airway obstructions, removal of affected portions of lung by surgical removal or artery embolization and preventing complications. The prolonged use of antibiotics prevents detrimental infections and decreases hospitalizations in people with bronchiectasis, but also increases the risk of people becoming infected with drug-resistant bacteria.

Other treatment options include eliminating accumulated fluid with postural drainage and chest physiotherapy. Postural drainage techniques, aided by physiotherapists and respiratory therapists, are an important mainstay of treatment. Airway clearance techniques appear useful.

Surgery may also be used to treat localized bronchiectasis, removing obstructions that could cause progression of the disease.

Inhaled steroid therapy that is consistently adhered to can reduce sputum production and decrease airway constriction over a period of time, and help prevent progression of bronchiectasis. This is not recommended for routine use in children. One commonly used therapy is beclometasone dipropionate.

Although not approved for use in any country, mannitol dry inhalation powder, has been granted orphan drug status by the FDA for use in people with bronchiectasis and with cystic fibrosis.

Different treatments have been used to manage pulmonary interstitial emphysema with variable success. Admission/transfer to a neonatal intensive care unit (NICU) is common and expected for patients with PIE.

Treatments include:

- Lateral decubitus position with the affected side down

- High-frequency ventilation

- Lobectomy

- Selective Main Bronchial Intubation and Occlusion

Diagnosis of obstructive disease requires several factors depending on the exact disease being diagnosed. However one commonalty between them is an FEV1/FVC ratio less than 0.7, i.e. the inability to exhale 70% of their breath within one second.

Following is an overview of the main obstructive lung diseases. "Chronic obstructive pulmonary disease" is mainly a combination of chronic bronchitis and emphysema, but may be more or less overlapping with all conditions.

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

To date there have been no clinical trials to determine effective treatment for this disease. Some patients have been treated with somatostatin analogs. Although the cough associated with DIPNECH tends to diminish on this treatment, improvement in pulmonary function has not been clearly demonstrated. There are also reports of symptomatic treatment with long- and short-acting beta agonists. Although steroids, both oral and inhaled, have been used in the setting of DIPNECH, there is no clear improvement with this treatment.

It is not uncommon for typical carcinoids to arise within DIPNECH. Due to presence of these tumors, DIPNECH is classified as a pre-malignant condition. Although there have been reports of atypical carcinoids with local lymph node involvement, there are no reports of more aggressive neuroendocrine tumors, such as large cell neuroendocrine or small cell lung cancer, associated with DIPNECH. When isolated bronchial carcinoids are diagnosed, oncology guidelines recommend surgical resection with lymph node sampling. However, as multiple carcinoids may develop in the setting of DIPNECH, a more conservative approach is often considered to preserve lung function.