Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury. It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries. The estimated mortality rate of pulmonary contusion ranges from 14–40%, depending on the severity of the contusion itself and on associated injuries. When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion. One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries. Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with multiple injuries (polytrauma) who die. An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone.

Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions. As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion. Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.

Differences in the bodies of children and adults lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma in multiple body systems. Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and thus suffer from the injury more commonly. Pulmonary contusion has been found in 53% of children with chest injuries requiring hospitalization. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures. The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars as pedestrians. Some differences in children's physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.

Pulmonary contusion can result in respiratory failure—about half of such cases occur within a few hours of the initial trauma. Other severe complications, including infections and acute respiratory distress syndrome (ARDS) occur in up to half of cases. Elderly people and those who have heart, lung, or kidney disease prior to the injury are more likely to stay longer in hospital and have complications from the injury. Complications occur in 55% of people with heart or lung disease and 13% of those without. Of people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two additional injuries develop the condition. A larger contusion is associated with an increased risk. In one study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of people with less than 20% did so.

Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary contusion. Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to infection. Intubation and mechanical ventilation further increase the risk of developing pneumonia; the tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or sinuses into them. Also, intubation prevents coughing, which would clear bacteria-laden secretions from the airways, and secretions pool near the tube's cuff and allow bacteria to grow. The sooner the endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be put back in, the risk of pneumonia rises. People who are at risk for pulmonary aspiration (e.g. those with lowered level of consciousness due to head injuries) are especially likely to get pneumonia. As with ARDS, the chances of developing pneumonia increase with the size of the contusion. Children and adults have been found to have similar rates of complication with pneumonia and ARDS.

Studies reflecting international frequency demonstrated that 2-3% of all infants in NICUs develop pulmonary interstitial emphysema. When limiting the population studied to premature infants, this frequency increases to 20-30%, with the highest frequencies occurring in infants weighing fewer than 1000 g.

The prevalence of pulmonary interstitial emphysema widely varies with the population studied. In a 1987 study 3% of infants admitted to the neonatal intensive care unit (NICU) developed pulmonary interstitial emphysema.

SIPE is estimated to occur in 1-2% of competitive open-water swimmers, with 1.4% of triathletes, 1.8% of combat swimmers and 1.1% of divers and swimmers reported in the literature.

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.

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

A pulmonary laceration can cause air to leak out of the lacerated lung and into the pleural space, if the laceration goes through to it. Pulmonary laceration invariably results in pneumothorax (due to torn airways), hemothorax (due to torn blood vessels), or a hemopneumothorax (with both blood and air in the chest cavity). Unlike hemothoraces that occur due to pulmonary contusion, those due to lung laceration may be large and long lasting. However, the lungs do not usually bleed very much because the blood vessels involved are small and the pressure within them is low. Therefore, pneumothorax is usually more of a problem than hemothorax. A pneumothorax may form or be turned into a tension pneumothorax by mechanical ventilation, which may force air out of the tear in the lung.

The laceration may also close up by itself, which can cause it to trap blood and potentially form a cyst or hematoma. Because the lung is elastic, the tear forms a round cyst called a "traumatic air cyst" that may be filled with air, blood, or both and that usually shrinks over a period of weeks or months. Lacerations that are filled with air are called pneumatoceles, and those that are filled with blood are called pulmonary hematomas. In some cases, both pneumatoceles and hematomas exist in the same injured lung. A pneumatocele can become enlarged, for example when the patient is mechanically ventilated or has acute respiratory distress syndrome, in which case it may not go away for months. Pulmonary hematomas take longer to heal than simple pneumatoceles and commonly leave the lungs scarred.

Over time, the walls of lung lacerations tend to grow thicker due to edema and bleeding at the edges.

Pulmonary aspiration of particulate matter may result in acute airway obstruction which may rapidly lead to death from arterial hypoxemia.

Pulmonary aspiration of acidic material (such as stomach acid) may produce an immediate primary injury caused by the chemical reaction of acid with lung parenchyma, and a later secondary injury as a result of the subsequent inflammatory response.

The death rate of people with flail chest depends on the severity of their condition, ranging from 10 to 25%.

The incidence of clinical HAPE in unacclimatized travelers exposed to high altitude (~) appears to be less than 1%. The U.S. Army Pike's Peak Research Laboratory has exposed sea-level-resident volunteers rapidly and directly to high altitude; during 30 years of research involving about 300 volunteers (and over 100 staff members), only three have been evacuated with suspected HAPE.

Approximately 1 out of 13 people admitted to the hospital with fractured ribs are found to have flail chest.

Individual susceptibility to HAPE is difficult to predict. The most reliable risk factor is previous susceptibility to HAPE, and there is likely to be a genetic basis to this condition, perhaps involving the gene for angiotensin converting enzyme (ACE). Recently, scientists have found the similarities between low amounts of 2,3-BPG (also known as 2,3-DPG) with the occurrence of HAPE at high altitudes. Persons with sleep apnea are susceptible due to irregular breathing patterns while sleeping at high altitudes.

Injury to the lung may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include:

- Inhalation of hot or toxic gases

- Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)

- Aspiration, e.g., gastric fluid

- Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.

- Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation

- Swimming induced pulmonary edema also known as immersion pulmonary edema

- Transfusion Associated Circulatory Overload (TACO) occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time.

- Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the donor, such as anti-HLA or anti-neutrophil antibodies.

- Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS.

Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above.

- Arteriovenous malformation

- Hantavirus pulmonary syndrome

- High altitude pulmonary edema (HAPE)

- Envenomation, such as with the venom of Atrax robustus

For individuals who survive the initial crush injury, survival rates are high for traumatic asphyxia.

"Flash pulmonary edema" ("FPE"), is rapid onset pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures. Treatment of FPE should be directed at the underlying cause, but the mainstays are ensuring adequate oxygenation, diuresis, and decrease of pulmonary circulation pressures.

Recurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of recurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

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.

A pulmonary hematoma is a collection of blood within the tissue of the lung. It may result when a pulmonary laceration fills with blood. A lung laceration filled with air is called a pneumatocele. In some cases, both pneumatoceles and hematomas exist in the same injured lung. Pulmonary hematomas take longer to heal than simple pneumatoceles and commonly leave the lungs scarred. A pulmonary contusion is another cause of bleeding within the lung tissue, but these result from microhemorrhages, multiple small bleeds, and the bleeding is not a discrete mass but rather occurs within the lung tissue. An indication of more severe damage to the lung than pulmonary contusion, a hematoma also takes longer to clear. Unlike contusions, hematomas do not usually interfere with gas exchange in the lung, but they do increase the risk of infection and abscess formation.

Pulmonary diseases may also impact newborns, such as pulmonary hyperplasia, pulmonary interstitial emphysema (usually preterm births), and infant respiratory distress syndrome,

Death may occur rapidly with acute, massive pulmonary bleeding or over longer periods as the result of continued pulmonary failure and right heart failure. Historically, patients had an average survival of 2.5 years after diagnosis, but today 86% may survive beyond five years.

Less than 5 to 10% of symptomatic PEs are fatal within the first hour of symptoms.

There are several markers used for risk stratification and these are also independent predictors of adverse outcome. These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevated cardiac enzymes. Some ECG changes including S1Q3T3 also correlate with worse short-term prognosis. There have been other patient-related factors such as COPD and chronic heart failure thought to also play a role in prognosis.

Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter and some deficits may be permanent. There is controversy over whether small subsegmental PEs need treatment at all and some evidence exists that patients with subsegmental PEs may do well without treatment.

Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year.

Mortality from untreated PEs was said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan, which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

Pulmonary emboli occur in more than 600,000 people in the United States each year. It results in between 50,000 and 200,000 deaths per year in the United States. The risk in those who are hospitalized is around 1%. The rate of fatal pulmonary emboli has declined from 6% to 2% over the last 25 years in the United States.

The sudden impact on the thorax causes an increase in intrathoracic pressure. In order for traumatic asphyxia to occur, a Valsalva maneuver is required when the traumatic force is applied. Exhalation against the closed glottis along with the traumatic event causes air that cannot escape from the thoracic cavity. Instead, the air causes increased venous back-pressure, which is transferred back to through the right atrium, to the superior vena cava and to the head and neck veins and capillaries.

There is still much debate to whether pulmonary sequestration is a congenital problem or acquired through reccurent pulmonary infection. It is widely believed that extralobar pulmonary sequestrations are a result of prenatal pulmonary malformation while intralobar pulmonary sequestrations can develop due to reccurent pulmonary infections in adolescents and young adults.