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.

The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary. A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition. Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary. For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it. Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock. Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.

No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive. Attempts are made to discover injuries accompanying the contusion, to prevent additional injury, and to provide supportive care while waiting for the contusion to heal. Monitoring, including keeping track of fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the patient's condition may progressively worsen. Monitoring for complications such as pneumonia and acute respiratory distress syndrome is of critical importance. Treatment aims to prevent respiratory failure and to ensure adequate blood oxygenation. Supplemental oxygen can be given and it may be warmed and humidified. When the contusion does not respond to other treatments, extracorporeal membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it and removes carbon dioxide prior to pumping it back in.

Treatment typically is supportive and includes monitoring and observation.

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.

Treatment of TBI varies based on the location and severity of injury and whether the patient is stable or having trouble breathing, but ensuring that the airway is patent so that the patient can breathe is always of paramount importance. Ensuring an open airway and adequate ventilation may be difficult in people with TBI. Intubation, one method to secure the airway, may be used to bypass a disruption in the airway in order to send air to the lungs. If necessary, a tube can be placed into the uninjured bronchus, and a single lung can be ventilated. If there is a penetrating injury to the neck through which air is escaping, the trachea may be intubated through the wound. Multiple unsuccessful attempts at conventional (direct) laryngoscopy may threaten the airway, so alternative techniques to visualize the airway, such as fiberoptic or video laryngoscopy, may be employed to facilitate tracheal intubation. If the upper trachea is injured, an incision can be made in the trachea (tracheotomy) or the cricothyroid membrane (cricothyrotomy, or cricothyroidotomy) in order to ensure an open airway. However, cricothyrotomy may not be useful if the trachea is lacerated below the site of the artificial airway. Tracheotomy is used sparingly because it can cause complications such as infections and narrowing of the trachea and larynx. When it is impossible to establish a sufficient airway, or when complicated surgery must be performed, cardiopulmonary bypass may be used—blood is pumped out of the body, oxygenated by a machine, and pumped back in. If a pneumothorax occurs, a chest tube may be inserted into the pleural cavity to remove the air.

People with TBI are provided with supplemental oxygen and may need mechanical ventilation. Employment of certain measures such as Positive end-expiratory pressure (PEEP) and ventilation at higher-than-normal pressures may be helpful in maintaining adequate oxygenation. However, such measures can also increase leakage of air through a tear, and can stress the sutures in a tear that has been surgically repaired; therefore the lowest possible airway pressures that still maintain oxygenation are typically used. Mechanical ventilation can also cause pulmonary barotrauma when high pressure is required to ventilate the lungs. Techniques such as pulmonary toilet (removal of secretions), fluid management, and treatment of pneumonia are employed to improve pulmonary compliance (the elasticity of the lungs).

While TBI may be managed without surgery, surgical repair of the tear is considered standard in the treatment of most TBI. It is required if a tear interferes with ventilation; if mediastinitis (inflammation of the tissues in the mid-chest) occurs; or if subcutaneous or mediastinal emphysema progresses rapidly; or if air leak or large pneumothorax is persistent despite chest tube placement. Other indications for surgery are a tear more than one third the circumference of the airway, tears with loss of tissue, and a need for positive pressure ventilation. Damaged tissue around a rupture (e.g. torn or scarred tissue) may be removed in order to obtain clean edges that can be surgically repaired. Debridement of damaged tissue can shorten the trachea by as much as 50%. Repair of extensive tears can include sewing a flap of tissue taken from the membranes surrounding the heart or lungs (the pericardium and pleura, respectively) over the sutures to protect them. When lung tissue is destroyed as a result of TBI complications, pneumonectomy or lobectomy (removal of a lung or of one lobe, respectively) may be required. Pneumonectomy is avoided whenever possible due to the high rate of death associated with the procedure. Surgery to repair a tear in the tracheobronchial tree can be successful even when it is performed months after the trauma, as can occur if the diagnosis of TBI is delayed. When airway stenosis results after delayed diagnosis, surgery is similar to that performed after early diagnosis: the stenotic section is removed and the cut airway is repaired.

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

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.

Usually the sequestration is removed after birth via surgery. In most cases this surgery is safe and effective; the child will grow up to have normal lung function.

In a few instances, fetuses with sequestrations develop problematic fluid collections in the chest cavity. In these situations a Harrison catheter shunt can be used to drain the chest fluid into the amniotic fluid.

In rare instances where the fetus has a very large lesion, resuscitation after delivery can be dangerous. In these situations a specialized delivery for management of the airway compression can be planned called the EXIT procedure, or a fetal laser ablation procedure can be performed. During this minimally invasive fetal intervention, a small needle is inserted into the sequestration, and a laser fiber is targeted at the abnormal blood vessel going to the sequestration. The goal of the operation is to use laser energy to stop the blood flow to the sequestration, causing it to stop growing. Ideally, after the surgery, the sequestration steals less blood flow from the fetus, and the heart and lungs start growing more normally as the sequestration shrinks in size and the pleural effusion goes away.

The treatment for this is a wedge resection, segmentectomy, or lobectomy via a VATS procedure or thoracotomy.

Pulmonary sequestrations usually get their blood supply from the thoracic aorta.

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.

Vehicle occupants who wear seat belts have a lower incidence of TBI after a motor vehicle accident. However, if the strap is situated across the front of the neck (instead of the chest), this increases the risk of tracheal injury. Design of medical instruments can be modified to prevent iatrogenic TBI, and medical practitioners can use techniques that reduce the risk of injury with procedures such as tracheotomy.

Since the mechanism behind chylothorax is not well understood, treatment options are limited. Drainage of the fluid out of the pleural space is essential to obviate damage to organs, especially the inhibition of lung function by the counter pressure of the chyle. Another treatment option is pleuroperitoneal shunting (creating a communication channel between pleural space and peritoneal cavity). By this surgical technique loss of essential triglycerides that escape the thoracic duct can be prevented. Omitting fat (in particular FFA) from the diet is essential. Either surgical or chemical pleurodesis are options: the leaking of lymphatic fluids is stopped by irritating the lungs and chest wall, resulting in a sterile inflammation. This causes the lung and the chest wall to be fused together which prevents the leaking of lymphatic fluids into the pleural space. The medication octreotide has been shown to be beneficial and in some cases will stop the chylothorax after a few weeks.

In animals, the most effective form of treatment until recently has been surgical ligation of the thoracic duct combined with partial pericardectomy. There is at least one case report (in a cat) of clinical response to treatment with rutin.

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.

There are two situations when an inferior vena cava filter is considered advantageous, and those are if anticoagulant therapy is contraindicated (e.g. shortly after a major operation), or a person has a pulmonary embolus in spite of being anticoagulated. In these instances, it may be implanted to prevent new or existing DVTs from entering the pulmonary artery and combining with an existing blockage. In spite of the device's theoretical advantage of preventing pulmonary emboli, there is a lack of evidence supporting its effectiveness.

Inferior vena cava filters should be removed as soon as it becomes safe to start using anticoagulation. Although modern filters are meant to be retrievable, complications may prevent some from being removed. The long-term safety profile of permanently leaving a filter inside the body is not known.

Anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, may be required. People are often admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until the INR has reached therapeutic levels. Increasingly, however, low-risk cases are managed at home in a fashion already common in the treatment of DVT. Evidence to support one approach versus the other is weak.

The standard and most important treatment is to descend to a lower altitude as quickly as possible, preferably by at least 1000 metres. Oxygen should also be given if possible. Symptoms tend to quickly improve with descent, but more severe symptoms may continue for several days. The standard drug treatments for which there is strong clinical evidence are dexamethasone and nifedipine. Phosphodiesterase inhibitors such as sildenafil and tadalafil are also effective but may worsen the headache of mountain sickness.

Corticosteroids are the mainstay of treatment of IPH, though they are controversial and lack clear evidence in their favour. They are thought to decrease the frequency of haemorrhage, while other studies suggest that they do not have any effect on the course or prognosis of this disease. In either case, steroid therapy has significant side effects. Small trials have investigated the use of other medications, but none has emerged as a clear standard of care. This includes immune modulators such as hydroxychloroquine, azathioprine, and cyclophosphamide. 6-mercaptopurine as a long-term therapy may prevent pulmonary haemorrhage. A 2007 scientific letter. reports preliminary success in preventing pulmonary haemorrhage with the anti-oxidant N-acetylcysteine.

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.

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.

The dual (ET and ET) endothelin receptor antagonist bosentan was approved in 2001. Sitaxentan (Thelin) was approved for use in Canada, Australia, and the European Union, but not in the United States. In 2010, Pfizer withdrew Thelin worldwide because of fatal liver complications. A similar drug, ambrisentan is marketed as Letairis in the U.S. by Gilead Sciences.

The U.S. FDA approved sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), for the treatment of PAH in 2005. It is marketed for PAH as Revatio. In 2009, they also approved tadalafil, another PDE5 inhibitor, marketed under the name Adcirca. PDE5 inhibitors are believed to increase pulmonary artery vasodilation, and inhibit vascular remodeling, thus lowering pulmonary arterial pressure and pulmonary vascular resistance.

Tadalafil is taken orally, as well as sildenafil, and it is rapidly absorbed (serum levels are detectable at 20 minutes). The T (biological half-life) hovers around 17.5 hours in healthy subjects. Moreover, if we consider pharmacoeconomic implications, patients that take tadalafil would pay two-thirds of the cost of sildenafil therapy. However, there are some adverse effects of this drug such as headache, diarrhea, nausea, back pain, dyspepsia, flushing and myalgia.

Standard medical treatment consists of anticoagulants (blood thinners), diuretics, and oxygen. Lifelong anticoagulation is recommended, even after PEA. Routine inferior vena cava filter placement is not recommended.

In patients with non-operable CTEPH or persistent/recurrent PH after PEA, there is evidence for benefit from pulmonary vasodilator drug treatment. The microvascular disease component in CTEPH has provided the rationale for off-label use of drugs approved for PAH. Currently, only riociguat (a stimulator of soluble guanylate cyclase) is approved for treatment of adults with inoperable CTEPH or persistent or recurrent CTEPH after surgical treatment. Other drug trials are ongoing in patients with inoperable CTEPH, with macitentan recently proving efficacy and safety in MERIT

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.

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

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.