When eosinophilic pneumonia is related to an illness such as cancer or parasitic infection, treatment of the underlying cause is effective in resolving the lung disease. When due to AEP or CEP, however, treatment with corticosteroids results in a rapid, dramatic resolution of symptoms over the course of one or two days. Either intravenous methylprednisolone or oral prednisone are most commonly used. In AEP, treatment is usually continued for a month after symptoms disappear and the x-ray returns to normal (usually four weeks total). In CEP, treatment is usually continued for three months after symptoms disappear and the x-ray returns to normal (usually four months total). Inhaled steroids such as fluticasone have been used effectively when discontinuation of oral prednisone has resulted in relapse.

Because EP affects the lungs, individuals with EP have difficulty breathing. If enough of the lung is involved, it may not be possible for a person to breathe without support. Non-invasive machines such as a bilevel positive airway pressure machine may be used. Otherwise, placement of a breathing tube into the mouth may be necessary and a ventilator may be used to help the person breathe.

Eosinophilic pneumonia due to cancer or parasitic infection carries a prognosis related to the underlying illness. AEP and CEP, however, have very little associated mortality as long as intensive care is available and treatment with corticosteroids is given. CEP often relapses when prednisone is discontinued; therefore, some people with CEP require lifelong therapy. Chronic prednisone is associated with many side effects, including increased infections, weakened bones, stomach ulcers, and changes in appearance.

PAP 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.

Most patients recover with corticosteroid therapy. A standardized approach to dosing starting at 0.75 mg/kg and weaning over 24 weeks has been shown to reduce total corticosteroid exposure without affecting outcome.

About two thirds of patients recover with corticosteroid therapy: the usual corticosteroid administered is prednisolone in Europe and prednisone in the USA; these differ by only one functional group and have the same clinical effect. The corticosteroid is initially administered in high dosage, typically 50 mg per day tapering down to zero over a six-month to one-year period. If the corticosteroid treatment is halted too quickly the disease may return. Other medications must be taken to counteract side effects of the steroid.

The first advance in the treatment of pulmonary alveolar proteinosis came in November 1960, when Dr. Jose Ramirez-Rivera at the Veterans' Administration Hospital in Baltimore applied repeated "segmental flooding" as a means of physically removing the accumulated alveolar material.

The standard treatment for PAP is whole-lung lavage, in which the lung is filled with sterile fluid with subsequent removal of the fluid along with the abnormal surfactant material. This is generally effective at improving PAP symptoms, often for a prolonged period of time. Since the mouse discovery noted above, the use of GM-CSF injections has also been attempted, with variable success. Lung transplantation can be performed in refractory cases.

"N"-Acetylcysteine (NAC) is a precursor to glutathione, an antioxidant. It has been hypothesized that treatment with high doses of NAC may repair an oxidant–antioxidant imbalance that occurs in the lung tissue of patients with IPF. In the first clinical trial of 180 patients (IFIGENIA), NAC was shown in previous study to reduce the decline in VC and DLCO over 12 months of follow-up when used in combination with prednisone and azathioprine (triple therapy).

More recently, a large randomized, controlled trial (PANTHER-IPF) was undertaken by the National Institutes of Health (NIH) in the USA to evaluate triple therapy and NAC monotherapy in IPF patients. This study found that the combination of prednisone, azathioprine, and NAC increased the risk of death and hospitalizations and the NIH announced in 2012 that the triple-therapy arm of the PANTHER-IPF study had been terminated early.

This study also evaluated NAC alone and the results for this arm of the study were published in May 2014 in the New England Journal of Medicine, concluding that "as compared with placebo, acetylcysteine offered no significant benefit with respect to the preservation of FVC in patients with idiopathic pulmonary fibrosis with mild-to-moderate impairment in lung function".

A Cochrane review comparing pirfenidone with placebo, found a reduced risk of disease progression by 30%. FVC or VC was also improved, even if a mild slowing in FVC decline could be demonstrated only in one of the two CAPACITY trials. A third study, which was completed in 2014 found reduced decline in lung function and IPF disease progression. The data from the ASCEND study were also pooled with data from the two CAPACITY studies in a pre-specified analysis which showed that pirfenidone reduced the risk of death by almost 50% over one year of treatment.

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.

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.

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo), is a recombinant human IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase-III clinical trials after an open-label, early-phase trial showed a 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

Regardless of cause, UIP is relentlessly progressive, usually leading to respiratory failure and death without a lung transplant. Some patients do well for a prolonged period of time, but then deteriorate rapidly because of a superimposed acute illness (so-called "accelerated UIP"). The outlook for long-term survival is poor. In most studies, the median survival is 3 to 4 years. Patients with UIP in the setting of rheumatoid arthritis have a slightly better prognosis than UIP without a known cause (IPF).

Non-specific interstitial pneumonia (NSIP) is a form of idiopathic interstitial pneumonia.

It has been suggested that idiopathic nonspecific interstitial pneumonia has an autoimmune mechanism, and is a possible complication of undifferentiated connective tissue disease.

Respiratory disease is a common and significant cause of illness and death around the world. In the US, approximately 1 billion "common colds" occur each year. A study found that in 2010, there were approximately 6.8 million emergency department visits for respiratory disorders in the U.S. for patients under the age of 18. In 2012, respiratory conditions were the most frequent reasons for hospital stays among children.

In the UK, approximately 1 in 7 individuals are affected by some form of chronic lung disease, most commonly chronic obstructive pulmonary disease, which includes asthma, chronic bronchitis and emphysema.

Respiratory diseases (including lung cancer) are responsible for over 10% of hospitalizations and over 16% of deaths in Canada.

In 2011, respiratory disease with ventilator support accounted for 93.3% of ICU utilization in the United States.

Bronchiolitis obliterans organizing pneumonia (BOOP), also known as cryptogenic organizing pneumonia, is a form of non-infectious pneumonia; more specifically, BOOP is an inflammation of the bronchioles (bronchiolitis) and surrounding tissue in the lungs. It is often a complication of an existing chronic inflammatory disease such as rheumatoid arthritis, dermatomyositis, or it can be a side effect of certain medications such as amiodarone. BOOP was first described by Gary Epler in 1985.

Some authors have recommended the use of an alternate name, cryptogenic organizing pneumonia (COP), to reduce confusion with bronchiolitis obliterans, a distinct and unrelated disease.

The clinical features and radiological imaging resemble infectious pneumonia. However, diagnosis is suspected after there is no response to multiple antibiotics, and blood and sputum cultures are negative for organisms.

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.

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage. But in interstitial lung disease, the repair process goes awry and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.

To date, no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in adult ARDS.

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.

Usual interstitial pneumonia (UIP) is a form of lung disease characterized by progressive scarring of both lungs. The scarring (fibrosis) involves the supporting framework (interstitium) of the lung. UIP is thus classified as a form of interstitial lung disease. The term "usual" refers to the fact that UIP is the most common form of interstitial fibrosis. "Pneumonia" indicates "lung abnormality", which includes fibrosis and inflammation. A term previously used for UIP in the British literature is cryptogenic fibrosing alveolitis, a term that has fallen out of favor since the basic underlying pathology is now thought to be fibrosis, not inflammation.

In immunocompromised patients, prophylaxis with co-trimoxazole (trimethoprim/sulfamethoxazole), atovaquone, or regular pentamidine inhalations may help prevent PCP.

Antipneumocystic medication is used with concomitant steroids in order to avoid inflammation, which causes an exacerbation of symptoms about four days after treatment begins if steroids are not used. By far the most commonly used medication is trimethoprim/sulfamethoxazole, but some patients are unable to tolerate this treatment due to allergies. Other medications that are used, alone or in combination, include pentamidine, trimetrexate, dapsone, atovaquone, primaquine, pafuramidine maleate (under investigation), and clindamycin. Treatment is usually for a period of about 21 days.

Pentamidine is less often used as its major limitation is the high frequency of side effects. These include acute pancreatic inflammation, kidney failure, liver toxicity, decreased white blood cell count, rash, fever, and low blood sugar.

Acute eosinophilic pneumonia is the acute-onset form of eosinophilic pneumonia, a lung disease caused by the buildup of eosinophils, a type of white blood cell, in the lungs. It is characterized by a rapid onset of shortness of breath, cough, fatigue, night sweats, and weight loss. Though the underlying cause is unknown, it can be triggered by a change in medication or tobacco smoking. It is treated with corticosteroids and has a favorable prognosis.

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.

Treatment is directed at correcting the underlying cause. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. One method is continuous positive airway pressure, which delivers pressurized air or oxygen through a nose or face mask to help ensure that the alveoli do not collapse, even at the end of a breath. This is helpful, as partially inflated alveoli can be expanded more easily than collapsed alveoli. Sometimes additional respiratory support is needed with a mechanical ventilator.

The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. Antibiotics are given for an infection. Chronic atelectasis is often treated with antibiotics because infection is almost inevitable. In certain cases, the affected part of the lung may be surgically removed when recurring or chronic infections become disabling or bleeding is significant. If a tumor is blocking the airway, relieving the obstruction by surgery, radiation therapy, chemotherapy, or laser therapy may prevent atelectasis from progressing and recurrent obstructive pneumonia from developing.

Alveolar lung disease may be divided into acute or chronic. Causes of acute alveolar lung disease include pulmonary edema (cardiogenic or neurogenic), pneumonia (bacterial or viral), pulmonary embolism, systemic lupus erythematosus, bleeding in the lungs (e.g., Goodpasture syndrome), idiopathic pulmonary hemosiderosis, and granulomatosis with polyangiitis.

Chronic alveolar lung disease can be caused by pulmonary alveolar proteinosis, alveolar cell carcinoma, mineral oil pneumonia, sarcoidosis (alveolar form), lymphoma, tuberculosis, metastases, or desquamative interstitial pneumonia.