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.

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning upright may relieve symptoms. Loop diuretics such as furosemide or bumetanide are administered, often together with morphine or diamorphine to reduce respiratory distress. Both diuretics and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate.

Continuous positive airway pressure and bilevel positive airway pressure (BIPAP/NIPPV) has been demonstrated to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary edema, and may reduce mortality.

It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed.

The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics.

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.

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.

Patients with single aspergillomas generally do well with surgery to remove the aspergilloma, and are best given pre-and post-operative antifungal drugs. Often, no treatment is necessary. However, if a patient coughs up blood (haemoptysis), treatment may be required (usually angiography and embolisation, surgery or taking tranexamic acid). Angiography (injection of dye into the blood vessels) may be used to find the site of bleeding which may be stopped by shooting tiny pellets into the bleeding vessel.

For chronic cavitary pulmonary aspergillosis and chronic fibrosing pulmonary aspergillosis, lifelong use of antifungal drugs is usual. Itraconazole and voriconazole are first and second-line anti fungal agents respectively. Posaconazole can be used as third-line agent, for patients who are intolerant of or developed resistance to the first and second-line agents. Regular chest X-rays, serological and mycological parameters as well as quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these drugs.

Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. By themselves, they have no effect on overall one-year mortality. Whether they affect the progression of the disease is unknown. When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone. Inhaled steroids are associated with increased rates of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.

Inhaled bronchodilators are the primary medications used, and result in a small overall benefit. The two major types are β agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.

In those with mild disease, short-acting agents are recommended on an as needed basis. In those with more severe disease, long-acting agents are recommended. Long-acting agents partly work by improving hyperinflation. If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added. With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable. Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. While both may be used at the same time, any benefit is of questionable significance.

Several short-acting β agonists are available, including salbutamol (albuterol) and terbutaline. They provide some relief of symptoms for four to six hours. Long-acting β agonists such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited while others view the evidence of benefit as established. Long-term use appears safe in COPD with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks. Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β agonist drugs that require twice-daily dosing for people with stable COPD.

Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life, and tiotropium provides those benefits better than ipratropium. It does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke. Aclidinium, another long acting agent, reduces hospitalizations associated with COPD and improves quality of life. Aclinidinium has been used as an alternative to tiotropium, but which drug is more effective is not known.

There should also be a "care plan" in case of future exacerbations. Patients may watch for symptoms, such as shortness of breath, change in character or amount of mucus, and start self-treatment as discussed with a health care provider. This allows for treatment right away until a doctor can be seen.

The symptoms of acute exacerbations are treated using short-acting bronchodilators. A course of corticosteroids, usually in tablet or intravenous rather than inhaled form, can speed up recovery. The IV and oral forms of steroids have been found to be equivalent. Antibiotics are often used but will only help if the exacerbation is due to an infection. Antibiotics are indicated when a patient notes increased sputum production, purulent sputum, increased dyspnea, has an elevated white count, or is febrile. Examples of first-line antibiotics are amoxicillin, doxycycline and co-trimoxazole.

Oxygen therapy should be initiated if there is significantly low blood oxygen. High flow oxygen may be harmful in those with an acute exacerbation of COPD. In the prehospital environment those given high flow O rather than titrating their O saturations to 88% to 92% had worse outcomes.

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.

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.

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.

Treatment options include

- gefitinib - epidermal growth factor receptor tyrosine kinase inhibitor

- indomethacin

- corticosteroids

- octreotide

- radiation therapy

- bronchoscopy as is often done in the post traumatic setting.

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.

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.

Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. There is tentative evidence that salbutamol may be useful in those with wheezing; however, it may result in nervousness and tremors. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms. Getting plenty of rest and fluids is also often recommended.

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.

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.

Management has generally been reported to be conservative, though deaths have been reported.

- Removal from water

- Observation

- Diuretics and / or Oxygen when necessary

- Episodes are generally self-limiting in the absence of other medical problems

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

In general, aspiration pneumonitis is treated conservatively with antibiotics indicated only for aspiration pneumonia. The choice of antibiotic will depend on several factors, including the suspected causative organism and whether pneumonia was acquired in the community or developed in a hospital setting. Common options include clindamycin, a combination of a beta-lactam antibiotic and metronidazole, or an aminoglycoside.

Corticosteroids are sometimes used in aspiration pneumonia, but there is limited evidence to support their effectiveness.

Macrolide antibiotics, such as erythromycin, are an effective treatment for DPB when taken regularly over an extended period of time. Clarithromycin or roxithromycin are also commonly used. The successful results of macrolides in DPB and similar lung diseases stems from managing certain symptoms through immunomodulation (adjusting the immune response), which can be achieved by taking the antibiotics in low doses. Treatment consists of daily oral administration of erythromycin for two to three years, an extended period that has been shown to dramatically improve the effects of DPB. This is apparent when an individual undergoing treatment for DPB, among a number of disease-related remission criteria, has a normal neutrophil count detected in BAL fluid, and blood gas (an arterial blood test that measures the amount of oxygen and carbon dioxide in the blood) readings show that free oxygen in the blood is within the normal range. Allowing a temporary break from erythromycin therapy in these instances has been suggested, to reduce the formation of macrolide-resistant "P. aeruginosa". However, DPB symptoms usually return, and treatment would need to be resumed. Although highly effective, erythromycin may not prove successful in all individuals with the disease, particularly if macrolide-resistant "P. aeruginosa" is present or previously untreated DPB has progressed to the point where respiratory failure is occurring.

With erythromycin therapy in DPB, great reduction in bronchiolar inflammation and damage is achieved through suppression of not only neutrophil proliferation, but also lymphocyte activity and obstructive mucus and water secretions in airways. The antibiotic effects of macrolides are not involved in their beneficial effects toward reducing inflammation in DPB. This is evident because the treatment dosage is much too low to fight infection, and in DPB cases with the occurrence of macrolide-resistant "P. aeruginosa", erythromycin therapy still reduces inflammation.

A number of factors are involved in suppression of inflammation by erythromycin and other macrolides. They are especially effective at inhibiting the proliferation of neutrophils, by diminishing the ability of interleukin 8 and leukotriene B4 to attract them. Macrolides also reduce the efficiency of adhesion molecules that allow neutrophils to stick to bronchiolar tissue linings. Mucus production in the airways is a major culprit in the morbidity and mortality of DPB and other respiratory diseases. The significant reduction of inflammation in DPB attributed to erythromycin therapy also helps to inhibit the production of excess mucus.

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.

In 2001 the American Thoracic Society, drawing on the work of the British and Canadian Thoracic Societies, established guidelines for the management of adult CAP dividing patients into four categories based on common organisms:

- Healthy outpatients without risk factors: This group (the largest) is composed of otherwise-healthy patients without risk factors for DRSP, enteric gram-negative bacteria, "pseudomonas" or other, less-common, causes of CAP. Primary microoganisms are viruses, atypical bacteria, penicillin-sensitive "streptococcus pneumoniae" and "haemophilus influenzae". Recommended drugs are macrolide antibiotics, such as azithromycin or clarithromycin, for seven to ten days.

- Outpatients with underlying illness or risk factors: Although this group does not require hospitalization, patients have underlying health problems (such as emphysema or heart failure) or are at risk for DRSP or enteric gram-negative bacteria. They are treated with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin) or a β-lactam antibiotic (such as cefpodoxime, cefuroxime, amoxicillin or amoxicillin/clavulanic acid) and a macrolide antibiotic, such as azithromycin or clarithromycin, for seven to ten days.

- Hospitalized patients without risk for "pseudomonas": This group requires intravenous antibiotics, with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin), a β-lactam antibiotic (such as cefotaxime, ceftriaxone, ampicillin/sulbactam or high-dose ampicillin plus a macrolide antibiotic (such as azithromycin or clarithromycin) for seven to ten days.

- Intensive-care patients at risk for "pseudomonas aeruginosa": These patients require antibiotics targeting this difficult-to-eradicate bacterium. One regimen is an intravenous antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an IV antipseudomonal fluoroquinolone such as levofloxacin. Another is an IV antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an aminoglycoside such as gentamicin or tobramycin, plus a macrolide (such as azithromycin) or a nonpseudomonal fluoroquinolone such as ciprofloxacin.

For mild-to-moderate CAP, shorter courses of antibiotics (3–7 days) seem to be sufficient.

Some patients with CAP will be at increased risk of death despite antimicrobial treatment. A key reason for this is the host's exaggerated inflammatory response. On one hand it is required to control the infection but on the other, it leads to bystander tissue damage. As a consequence of this recent research focuses on immunomodulatory therapy that can modulate the immune response to reduce injury to the lung and other affected organs such as the heart. Although the evidence for these agents has not resulted in their routine use, there potential benefits are highly promising.