Air in subcutaneous tissue does not usually pose a lethal threat; small amounts of air are reabsorbed by the body. Once the pneumothorax or pneumomediastinum that causes the subcutaneous emphysema is resolved, with or without medical intervention, the subcutaneous emphysema will usually clear. However, spontaneous subcutaneous emphysema can, in rare cases, progress to a life-threatening condition, and subcutaneous emphysema due to mechanical ventilation may induce ventilatory failure.

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.

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

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.

Infliximab, an immune-suppressing antibody, has been tested in COPD; there was a possibility of harm with no evidence of benefit.

Roflumilast, cilomilast, and phosphodiesterase 4 inhibitors act as a bronchodilator and as an anti-inflammatory. They show promise in decreasing the rate of exacerbations, but do not appear to change a persons quality of life. Roflumilast and cilomilast may be associated with side effects such as gastrointestinal issues and weight loss. Sleep disturbances and mood disturbances related to roflumilast have also been reported.

Several new long-acting agents are under development. Treatment with stem cells is under study. While there is tentative data that it is safe, and the animal data is promising, there is little human data as of 2017. The human data has shown poor results.

A procedure known as target lung denervation, which involves decreasing the parasympathetic nervous system supply of the lungs, is being studied but does not have sufficient data to determine its use. The effectiveness of alpha-1 antitrypsin augmentation treatment for people who have alpha-1 antitrypsin deficiency is unclear.

Research continues into the use of telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely may reduce the number of emergency-room visits and improve the person's quality of life.

The tissues in the mediastinum will slowly resorb the air in the cavity so most pneumomediastinums are treated conservatively. Breathing high flow oxygen will increase the absorption of the air.

If the air is under pressure and compressing the heart, a needle may be inserted into the cavity, releasing the air.

Surgery may be needed to repair the hole in the trachea, esophagus or bowel.

If there is lung collapse, it is imperative the affected individual lies on the side of the collapse, although painful, this allows full inflation of the unaffected lung.

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.

Supplemental oxygen is recommended in those with low oxygen levels at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%). In this group of people, it decreases the risk of heart failure and death if used 15 hours per day and may improve people's ability to exercise. In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life. A risk of fires and little benefit exist when those on oxygen continue to smoke. In this situation, some recommend against its use. During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes. In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%.

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.

It is most commonly caused by:

- Oesophageal rupture, for example in Boerhaave syndrome

- Asthma or other conditions leading to alveolar rupture

- Bowel rupture, where air in the abdominal cavity tracts up into the chest.

It has also been associated with:

- "Mycoplasma pneumoniae" pneumonia

- obesity

It can be induced to assist thoracoscopic surgery. It can be caused by a pulmonary barotrauma resulting when a person moves to or from a higher pressure environment, such as when a SCUBA diver, a free-diver or an airplane passenger ascends or descends.

In rare cases, pneumomediastinum may also arise as a result of blunt chest trauma (e.g. car accidents, fights, over pressure of breathing apparatus), while still evolving in the same fashion as the spontaneous form.

Pneumomediastinum is most commonly seen in otherwise healthy young male patients and may not be prefaced by a relevant medical history of similar ailments.

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.

If left untreated, the condition can progress to a point where the blood accumulation begins to put pressure on the mediastinum and the trachea, effectively limiting the amount that the heart's ventricles are able to fill. The condition can cause the trachea to deviate, or move, toward the unaffected side.

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

Respiratory disease is a medical term that encompasses pathological conditions affecting the organs and tissues that make gas exchange possible in higher organisms, and includes conditions of the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of breathing. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities like bacterial pneumonia, pulmonary embolism, acute asthma and lung cancer.

The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.

Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airways disease (COAD) or chronic airflow limitation (CAL), is a group of illnesses characterised by airflow limitation that is not fully reversible. The flow of air into and out of the lungs is impaired. This can be measured with breathing devices such as a peak flow meter or by spirometry. The term COPD includes the conditions emphysema and chronic bronchitis although most patients with COPD have characteristics of both conditions to varying degrees. Asthma being a reversible obstruction of airways is often considered separately, but many COPD patients also have some degree of reversibility in their airways.

In COPD, there is an increase in airway resistance, shown by a decrease in the forced expiratory volume in 1 second (FEV1) measured by spirometry. COPD is defined as a forced expiratory volume in 1 second to forced vital capacity ratio (FEV1/FVC) that is less than 0.7. The residual volume, the volume of air left in the lungs following full expiration, is often increased in COPD, as is the total lung capacity, while the vital capacity remains relatively normal. The increased total lung capacity (hyperinflation) can result in the clinical feature of a "barrel chest" - a chest with a large front-to-back diameter that occurs in some individuals with COPD. Hyperinflation can also be seen on a chest x-ray as a flattening of the diaphragm.

The most common cause of COPD is cigarette smoking. COPD is a gradually progressive condition and usually only develops after about 20 pack-years of smoking. COPD may also be caused by breathing in other particles and gases.

The diagnosis of COPD is established through spirometry although other pulmonary function tests can be helpful. A chest x-ray is often ordered to look for hyperinflation and rule out other lung conditions but the lung damage of COPD is not always visible on a chest x-ray. Emphysema, for example can only be seen on CT scan.

The main form of long term management involves the use of inhaled bronchodilators (specifically beta agonists and anticholinergics) and inhaled corticosteroids. Many patients eventually require oxygen supplementation at home. In severe cases that are difficult to control, chronic treatment with oral corticosteroids may be necessary, although this is fraught with significant side-effects.

COPD is generally irreversible although lung function can partially recover if the patient stops smoking. Smoking cessation is an essential aspect of treatment. Pulmonary rehabilitation programmes involve intensive exercise training combined with education and are effective in improving shortness of breath. Severe emphysema has been treated with lung volume reduction surgery, with some success in carefully chosen cases. Lung transplantation is also performed for severe COPD in carefully chosen cases.

Alpha 1-antitrypsin deficiency is a fairly rare genetic condition that results in COPD (particularly emphysema) due to a lack of the antitrypsin protein which protects the fragile alveolar walls from protease enzymes released by inflammatory processes.

Barrel chest generally refers to a , deep chest found on a man. A man described as barrel chested will usually have a naturally large ribcage, very round torso, large lung capacity, and can potentially have great upper body strength. It can sometimes be a sign of acromegaly (a syndrome resulting from excess levels of human growth hormone (HGH) in the body). It is most commonly related to osteoarthritis as individuals age. Arthritis can stiffen the chest causing the ribs to become fixed in their most expanded position, giving the appearance of a barrel chest.

Barrel chest also refers to an increase in the anterior posterior diameter of the chest wall resembling the shape of a barrel, most often associated with emphysema. There are two main causes of the barrel chest phenomenon in emphysema:

1. Increased compliance of the lungs leads to the accumulation of air pockets inside the thoracic cavity.

2. Increased compliance of the lungs increases the intrathoracic pressure. This increase in pressure allows the chest wall to naturally expand outward.

Barrel chest occurs naturally in native people who live at altitudes of over 5500 m, e.g. the Himalayas or the Andes. These natives also have polycythemia and other accommodations for high altitude life.

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.

A hemothorax is managed by removing the source of bleeding and by draining the blood already in the thoracic cavity. Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called a tube thoracostomy. Generally, the thoracostomy tube is placed between the ribs in the sixth or seventh intercostal space at the mid-axillary line. Usually the lung will expand and the bleeding will stop after a chest tube is inserted.

The blood in the chest can thicken as the clotting cascade is activated when the blood leaves the blood vessels and comes into contact with the pleural surface, injured lung or chest wall, or with the chest tube. As the blood thickens, it can clot in the pleural space (leading to a retained hemothorax) or within the chest tube, leading to chest tube clogging or occlusion. Chest tube clogging or occlusion can lead to worse outcomes as it prevents adequate drainage of the pleural space, contributing to the problem of retained hemothorax. In this case, patients can be hypoxic, short of breath, or in some cases, the retained hemothorax can become infected (empyema).

Retained hemothorax occurs when blood remains in the pleural space, and is a risk factor for the development of complications, including the accumulation of pus in the pleural space and fibrothorax. It is treated by inserting a second chest tube or by drainage by video-assisted thoracoscopy. Fibrolytic therapy has also been studied as a treatment.

When hemothorax is treated with a chest tube, it is important that it maintain its function so that the blood cannot clot in the chest or the tube. If clogging occurs, internal chest tube clearing can be performed using an open or closed technique. Manual manipulation, which may also be called milking, stripping, or tapping, of chest tubes is commonly performed to maintain an open tube, but no conclusive evidence has demonstrated that any of these techniques are more effective than the others, or that they improve chest tube drainage.

In some cases bleeding continues and surgery is necessary to stop the source of bleeding. For example, if the hemothorax was caused by aortic rupture in high energy trauma, surgical intervention is mandatory.

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.

The pathogenesis of PMF is complicated, but involves two main routes - an immunological route, and a mechanical route.

Immunologically, disease is caused primarily through the activity of lung macrophages, which phagocytose dust particles after their deposition. These macrophages seek to eliminate the dust particle through either the mucociliary mechanism, or through lymphatic vessels which drain the lungs. Macrophages also produce an inflammatory mediator known as interleukin-1 (IL-1), which is part of the immune systems first line defenses against infecting particles. IL-1 is responsible for 'activation' of local vasculature, causing endothelial cells to express certain cell adhesion molecules, which help the cells of the bodies immune system to migrate into tissues. Macrophages exposed to dust have been shown to have markedly decreased chemotaxis. Production of inflammatory mediators - and the tissue damage that ensues as an effect of this, as well as reduced motility of cells, is fundamental to the pathogenesis of pneumoconiosis and the accompanying inflammation, fibrosis, and emphysema.

There are also some mechanical factors involved in the pathogenesis of Complex Pneumoconiosis that should be considered. The most notable indications are the fact that the disease tends to develop in the upper lobe of the lung - especially on the right, and its common occurrence in taller individuals.

Progressive Massive Fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis (usually in the upper lung zones), can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracitricial emphysema.

The disease arises firstly through the deposition of silica or coal dust (or other dust) within the lung, and then through the body's immunological reactions to the dust.

Pneumopericardium is a medical condition where air enters the pericardial cavity. This condition has been recognized in preterm neonates, in which it is associated with severe lung pathology, after vigorous resuscitation, or in the presence of assisted ventilation. This is a serious complication, which if untreated may lead to cardiac tamponade and death. Pneumomediastinum, which is the presence of air in the mediastinum, may mimic and also coexist with pneumopericardium.

It can be congenital, or introduced by a wound.

The mechanism responsible for pneumopericardium is the ‘Macklin effect’ – There is initially an increased pressure gradient between the alveoli and the interstitial space. Increased pressure leads to alveolar rupture, resulting in air getting through to the pericapillary interstitial pulmonary space. This space is continuous with the peribronchial and pulmonary perivascular sheaths. From here, the air tracks to the hilum of the lung and then to the mediastinum. In case of a pericardial tear, this air enters the pericardial cavity and pneumopericardium develops. The condition may remain asymptomatic or may progress to life-threatening conditions like tension pneumopericardium or cardiac tamponade.

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 .