General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.

A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.

Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.

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.

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.

Treatment consists of humidified oxygen, bronchodilators, suction, endotracheal tube and chest physiotherapy. There is no role for routine treatment of smoke inhalation with either antibiotics or steroids. Treatment depends on the severity of the smoke inhalation.

Inhalation therapy with nebulized heparin and acetylcysteine is usually started and continued for five to seven days during the hospital stay.

Broadspectrum antibiotic to cover mixed flora is the mainstay of treatment. Pulmonary physiotherapy and postural drainage are also important. Surgical procedures are required in selective patients for drainage or pulmonary resection.

There is no standardized treatment for indium lung disease. Treatment options include pulmonary lavage and corticosteroid therapy. Prognostic factors were a matter of research as of 2012, but preliminary evidence suggests that duration of employment and reported use of respiratory protection are not prognostic factors, but the serum level of indium may be a prognostic factor - higher levels of serum indium have been associated with worse prognoses. Indium lung disease has been fatal in several cases.

Lung cancer may be related to indium lung disease, though indium is not a known carcinogen.

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.

Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:

- Treatment options for idiopathic pulmonary fibrosis are very limited. Though research trials are ongoing, there is no evidence that any medications can significantly help this condition. Lung transplantation is the only therapeutic option available in severe cases. Since some types of lung fibrosis can respond to corticosteroids (such as prednisone) and/or other medications that suppress the body's immune system, these types of drugs are sometimes prescribed in an attempt to slow the processes that lead to fibrosis.

- Two pharmacological agents intended to prevent scarring in mild idiopathic fibrosis are pirfenidone, which reduced reductions in the 1-year rate of decline in FVC. Pirfenidone also reduced the decline in distances on the 6-minute walk test, but had no effect on respiratory symptoms. The second agent is nintedanib, which acts as antifibrotic, mediated through the inhibition of a variety of tyrosine kinase receptors (including platelet-derived growth factor, fibroblast growth factor, and vascular endothelial growth factor). A randomized clinical trial showed it reduced lung-function decline and acute exacerbations.

- Anti-inflammatory agents have only limited success in reducing the fibrotic progress. Some of the other types of fibrosis, such as non-specific interstitial pneumonia, may respond to immunosuppressive therapy such as corticosteroids. However, only a minority of patients respond to corticosteroids alone, so additional immunosuppressants, such as cyclophosphamide, azathioprine, methotrexate, penicillamine, and cyclosporine may be used. Colchicine has also been used with limited success. There are ongoing trials with newer drugs such as IFN-γ and mycophenolate mofetil..

- Hypersensitivity pneumonitis, a less severe form of pulmonary fibrosis, is prevented from becoming aggravated by avoiding contact with the causative material.

- Oxygen supplementation improves the quality of life and exercise capacity. Lung transplantation may be considered for some patients.

Flock worker's lung can be prevented with engineering controls that protect workers from inhaling flock. Engineering controls to prevent inhalation of flock can include using guillotine cutters rather than rotary cutters, and ensuring that blades are sharp, since dull blades shear off more respirable particles. Flocking plants have also implemented medical surveillance programs for workers to diagnose cases at an earlier stage. Another technique for preventing flock worker's lung is cleaning the workplace with alternatives to compressed air in order to avoid resuspending particulates in the air.

Most cases respond to antibiotics and prognosis is usually excellent unless there is a debilitating underlying condition. Mortality from lung abscess alone is around 5% and is improving.

Flock worker's lung is generally treated by removing the individual from the environment where they are inhaling flock. Symptoms generally improve within days to weeks after stopping exposure. The benefits of glucocorticoid therapy are unclear.

Flock worker's lung may raise the risk for lung cancer, but the connection is a topic of research as of 2015. The disease can be subacute or develop over long periods of exposure.

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.

The National Institute of Occupational Safety and Health, Japan (JNIOSH) set limits for acceptable exposure at 0.0003 mg/m after the discovery of indium lung. Methods for reducing indium exposure are thought to be the best mode of protection. Medical surveillance of indium workers is also a method of prevention.

Hypoxia caused by pulmonary fibrosis can lead to pulmonary hypertension, which, in turn, can lead to heart failure of the right ventricle. Hypoxia can be prevented with oxygen supplementation.

Pulmonary fibrosis may also result in an increased risk for pulmonary emboli, which can be prevented by anticoagulants.

Many people with this condition have no symptoms. Treatment is aimed at the health problems causing the lung problem and the complications caused by the disorder.

Fast-acting drugs for RA include aspirin and corticosteroids, which alleviate pain and reduce inflammation. Slow-acting drugs termed disease modifying antirheumatic drugs (DMARDs), include gold, methotrexate and hydroxychloroquine (Plaquenil), which promote disease remission and prevent progressive joint destruction. In patients with less severe RA, pain relievers, anti-inflammatory drugs and physical rest are sufficient to improve quality of life. In patients with joint deformity, surgery is the only alternative for recovering articular function.

Prognosis is related to the underlying disorder and the type and severity of lung disease. In severe cases, lung transplantation can be considered. This is more common in cases of bronchiolitis obliterans, pulmonary fibrosis, or pulmonary hypertension. Most complications are not fatal, but does reduce life expectancy to an estimated 5 to 10 years.

Preventing alveolar overdistension – Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation.

Preventing cyclic atelectasis (atelectotrauma) – Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis.

Open lung ventilationn – Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).

High frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury.

Permissive hypercapnia and hypoxaemia allow the patient to be ventilated at less aggressive settings and can thererfore mitigate all forms of ventilator associated lung injury

There are no current guidelines available on the investigation and management of GLILD and evidence is restricted to retrospective case series. Because of the association with poorer outcomes, and because some patients develop advanced lung disease, most specialists now recommend treatment in early disease, but this is always an individual decision between patient and health-care team. Many centres screen for the development of GLILD (and other lung complications) using regular lung function tests and CT scans.

Studies of GLILD have been conducted in patients on background immunoglobulin replacement. In a cohort of 59 CVID patients with granulomatous disease, 30 (51%) of whom had lung involvement, complete remission of disease was obtained in 5 of 25 attempts using corticosteroids (three patients), methotrexate (1 patient) and cyclophosphamide (1 patient). Partial responses were also seen with rituximab and hydroxychloroquine. In contrast, a second report suggested poor response to corticosteroids alone, but a good response to 18-months treatment with rituximab and azathioprine in seven patients. Bone marrow transplantation has been attempted. Immunosuppression has been associated with development of opportunistic infection and other predictable side effects, and the balance of risks and benefits of therapy must be carefully weighed in each case. This may be best achieved by joint working between immunology, respiratory, radiology and pathology specialists, working as part of a multi-professional team with the patient.

There is very little information written by, and for patients with GLILD. However, interest in the condition is increasing and multi-centre studies such as STILPAD are in progress.

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.

Full recovery is common with proper treatment. Pulmonary laceration usually heals quickly after a chest tube is inserted and is usually not associated with major long-term problems. Pulmonary lacerations usually heal within three to five weeks, and lacerations filled with air will commonly heal within one to three weeks but on occasion take longer. However, the injury often takes weeks or months to heal, and the lung may be scarred. Small pulmonary lacerations frequently heal by themselves if material is removed from the pleural space, but surgery may be required for larger lacerations that do not heal properly or that bleed.

As with other chest injuries such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the chest cavity. A thoracostomy tube can be used to remove blood and air from the chest cavity. About 5% of cases require surgery, called thoracotomy. Thoracotomy is especially likely to be needed if a lung fails to re-expand; if pneumothorax, bleeding, or coughing up blood persist; or in order to remove clotted blood from a hemothorax. Surgical treatment includes suturing, stapling, oversewing, and wedging out of the laceration. Occasionally, surgeons must perform a lobectomy, in which a lobe of the lung is removed, or a pneumonectomy, in which an entire lung is removed.

VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.

Fire breather's pneumonia, also known as fire breather's lung or fire-eater's lung, is a distinct type of exogenous—that is, originating outside the body—lipoid pneumonia (chemical pneumonitis) that results from inhalation or aspiration of hydrocarbons of different types, such as lamp oil. Accidental inhalation of hydrocarbon fuels can occur during fire breathing, fire eating, or other fire performance, and may lead to pneumonitis.

Symptoms can vary significantly among individuals, ranging from asymptomatic to a severe, life-threatening disease. Onset usually occurs within hours, though symptoms may not appear for several days. Lipoid pneumonia is a rare condition, but is an occupational hazard of fire performers.

"Fire-eater's lung" is an important variant of hydrocarbon pneumonitis, which typically involves adolescents or young adults who are exposed through mishap during flame-blowing performances using a variety of different flammable materials. The substances used overlap with some of the pediatric exposures (kerosene, gasoline) but can also include other hydrocarbons such as jet fuel and, in France, an aromatic hydrocarbon enriched petroleum-distillate called "kerdan". There has also been a case of citronella oil aspiration in a fire-eater. As with hydrocarbon pneumonitis in children, fire-eater's lung can also be complicated by pneumatocele. Although the term "acute lipoid pneumonia" has been used to refer to the "fire-eater's lung" syndrome, this is a misnomer.