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.

Beta2-adrenergic agonists are recommended for bronchospasm.

- Short acting (SABA)

- Terbutaline

- Salbutamol

- Levosalbutamol

- Long acting (LABA)

- Formoterol

- Salmeterol

- Others

- Dopamine

- Norepinephrine

- Epinephrine

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 .

The best treatment is avoidance of conditions predisposing to attacks, when possible. In athletes who wish to continue their sport or do so in adverse conditions, preventive measures include altered training techniques and medications.

Some take advantage of the refractory period by precipitating an attack by "warming up," and then timing competition such that it occurs during the refractory period. Step-wise training works in a similar fashion. Warm up occurs in stages of increasing intensity, using the refractory period generated by each stage to reach a full workload.

Therapeutic interventions with medium-chain triglyceride-enriched low-fat diets, intratracheal heparin, inhaled tissue plasminogen activator, and steroids have also been reported and have met with variable success.

Inhaled mucolytics: Potassium iodide and acetylcysteine inhaled therapy are often used to help the patient cough up the casts by breaking down the thick mucus formations.

Inhaled and oral steroids: If PB is associated with asthma or an infection, inhaled and oral steroids have been shown to be effective.

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.

Acute therapy for PB is often focused on removal or facilitated expectoration of the casts. This is followed by short and long term efforts to identify and remediate the underlying condition resulting in the excessive airway leakage or inflammation that is causing the casts to form.

PB can present as a life threatening emergency when the casts obstruct the major airways resulting in acute respiratory distress. Intervention by a skilled physician experienced with foreign body removal from the lungs is essential. Evaluation by means of bronchoscopy can be difficult and time consuming and is best performed under general anesthesia.

Casts can be removed mechanically by bronchoscopy or physical therapy. High-frequency chest wall oscillation can also be used to vibrate the chest wall at a high frequency to try to loosen and thin the casts. Inhaled therapy using bronchodilators, corticosteroids or mucolytics can be used to try to disrupt the cast formation.

Recently, heavy T2-weighted MRI has revealed that occult lymphatic anomalies that represent developmental remnants or subclinical GLA are present in adults who present with expectoration of large multiantennary, branching casts. Intranodal lymphangiogram and dynamic contrast-enhanced MR lymphangiography have been used to more precisely image the leaks, and in the small number of patients who have been treated to date, embolization of the TD has been highly successful in controlling cast formation.

Cannulation of the thoracic duct followed by embolization should be considered in those patients who are shown to have leakage of lymphatic fluid into the airway.

Short-acting beta-agonists like salbutamol or terbutaline or long-acting beta-agonists like salmeterol and formoterol dilate airways which relieve the symptoms thus reducing the severity of the reaction. Some patients also use it just before work to avoid a drop in the FEV.

Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can also be used depending on the severity of the case.

Treatment is with corticosteroids and possibly intravenous immunoglobulins.

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.

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.

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.

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.

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

Treatment depends on the underlying cause. Treatments include iced saline, and topical vasoconstrictors such as adrenalin or vasopressin. Selective bronchial intubation can be used to collapse the lung that is bleeding. Also, endobronchial tamponade can be used. Laser photocoagulation can be used to stop bleeding during bronchoscopy. Angiography of bronchial arteries can be performed to locate the bleeding, and it can often be embolized. Surgical option is usually the last resort, and can involve, removal of a lung lobe or removal of the entire lung. Non–small-cell lung cancer can also be treated with erlotinib or gefitinib. Cough suppressants can increase the risk of choking.

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.

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.

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.

There is evidence to show that steroids given to babies less than 8 days old can prevent bronchopulmonary dysplasia. However, the risks of treatment may outweigh the benefits.

It is unclear if starting steroids more than 7 days after birth is harmful or beneficial. It is thus recommended that they only be used in those who cannot be taken off of a ventilator.

Pulmonary interstitial emphysema often resolves gradually and may take 2–3 weeks. For longer durations of PIE the length of time of mechanical ventilation needed may increase and the incidence of bronchopulmonary dysplasia becomes higher. Some infants may develop chronic lobar emphysema, which may require surgical lobectomies.

Subcutaneous emphysema is usually benign. Most of the time, SCE itself does not need treatment (though the conditions from which it results may); however, if the amount of air is large, it can interfere with breathing and be uncomfortable. It occasionally progresses to a state "Massive Subcutaneous Emphysema" which is quite uncomfortable and requires surgical drainage. When the amount of air pushed out of the airways or lung becomes massive, usually due to positive pressure ventilation, the eyelids swell so much that the patient cannot see. Also the pressure of the air may impede the blood flow to the areolae of the breast and skin of the scrotum or labia. This can lead to necrosis of the skin in these areas. The latter are urgent situations requiring rapid, adequate decompression. Severe cases can compress the trachea and do require treatment.

In severe cases of subcutaneous emphysema, catheters can be placed in the subcutaneous tissue to release the air. Small cuts, or "blow holes", may be made in the skin to release the gas. When subcutaneous emphysema occurs due to pneumothorax, a chest tube is frequently used to control the latter; this eliminates the source of the air entering the subcutaneous space. If the volume of subcutaneous air is increasing, it may be that the chest tube is not removing air rapidly enough, so it may be replaced with a larger one. Suction may also be applied to the tube to remove air faster. The progression of the condition can be monitored by marking the boundaries with a special pencil for marking on skin.

Since treatment usually involves dealing with the underlying condition, cases of spontaneous subcutaneous emphysema may require nothing more than bed rest, medication to control pain, and perhaps supplemental oxygen. Breathing oxygen may help the body to absorb the subcutaneous air more quickly.

First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.

Evidence does not support the general use of antibiotics in acute bronchitis. While some evidence suggests antibiotics speed up resolution of the cough by about 12 hours there is a greater risk of gastrointestinal problems and no change in longer term outcomes. Antibiotics use also leads to the promotion of antibiotic-resistant bacteria, which increase morbidity and mortality.

Most cases are self-limited and resolve themselves in a few weeks.