History:

Giovanni Battista Morgagni, credited with having first described lung trauma without chest wall traumaIn 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century.

It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hoo

ker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.
Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries.These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, Buford and Burbank described what they called "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it.

They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.

During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion.

For example, positive pressure ventilation was used to stabilize the flail segment from within the chest. It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion.Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion.

Prognosis:

This CT scan, taken 22 days after pulmonary contusion with major chest trauma, shows that the contusion has completely resolved.Pulmonary contusion usually resolves itself without causing permanent complications; however it may also have long-term ill effects on respiratory function. Most contusions resolve in five to seven days after the injury. Signs detectable by radiography are usually gone within 10 days after the injury—when they are not, other conditions, such as pneumonia, are the likely cause. Chronic lung disease correlates with the size of the contusion and can interfere with an individual's ability to return to work. Fibrosis of the lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced functional residual capacity for as long as six years after the injury.

As late as four years post-injury, decreased functional residual capacity has been found in most pulmonary contusion patients studied. During the six months after pulmonary contusion, up to 90% of people suffer difficulty breathing. In some cases, dyspnea persists for an indefinite period. Contusion can also permanently reduce the compliance of the lungs.

Complications:

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.

A chest X-ray showing acute respiratory distress syndromePneumonia, 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. T

he 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.

Fluid therapy:

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.

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. 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.

Supportive care:

Retaining secretions in the airways can worsen hypoxia and lead to infections. Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways. Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs. People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation.

Inadequate pulmonary toilet can result in pneumonia. People who do develop infections are given antibiotics. No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit. However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged. For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.

Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways.] Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful.Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood. Analgesics (pain medications) can be given to reduce pain.] Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can.

Fluid therapy:

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.

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. 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.

Supportive care:

Retaining secretions in the airways can worsen hypoxia and lead to infections. Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways. Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs. People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation. Inadequate pulmonary toilet can result in pneumonia.

People who do develop infections are given antibiotics. No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit. However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged. For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.

Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways.] Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful.Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood. Analgesics (pain medications) can be given to reduce pain.] Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can.

Classification:

The alveoliPulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung,while the latter does not. When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue. Contusion involves hemorrhage in the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of blood not interspersed with lung tissue. A collapsed lung can result when the pleural cavity (the space outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemopneumothorax).

These conditions do not inherently involve damage to the lung tissue itself, but they may be associated with it. Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of the ribcage is detached from the rest of the chest wall and moves independently.

Signs and symptoms:

Presentation may be subtle; people with mild contusion may have no symptoms at all. However, pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective states), including those indicative of the lung injury itself and of accompanying injuries. Because gas exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly associated. Dyspnea (painful breathing or difficulty breathing) is commonly seen, and tolerance for exercise may be lowered.

Rapid breathing and a rapid heart rate are other signs. With more severe contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling sound in the chest accompanying breathing) may be present. People with severe contusions may have bronchorrhea (the production of watery sputum). Wheezing and coughing are other signs.Coughing up blood or bloody sputum is present in up to half of cases. Cardiac output (the volume of blood pumped by the heart) may be reduced,and hypotension (low blood pressure) is frequently present. The area of the chest wall near the contusion may be tender or painful due to associated chest wall injury.

Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial presentation. The more severe the injury, the more quickly symptoms become apparent. In severe cases, symptoms may occur as quickly as three or four hours after the trauma. Hypoxemia (low oxygen concentration in the arterial blood) typically becomes progressively worse over 24–48 hours after injury. In general, pulmonary contusion tends to worsen slowly over a few days, but it may also cause rapid deterioration or death if untreated.

Causes:

Motor vehicle accidents are the most common cause of pulmonary contusion.Pulmonary contusion, which occurs in 25–35% of all blunt chest trauma, is usually caused by the rapid deceleration that results when the moving chest strikes a fixed object. About 70% of cases result from motor vehicle collisions, most often when the chest strikes the inside of the car.Falls, assaults, and sports injuries are other causes.

Pulmonary contusion can also be caused by explosions; the organs most vulnerable to blast injuries are those that contain gas, such as the lungs. Blast lung is severe pulmonary contusion, bleeding, or edema with damage to alveoli and blood vessels, or a combination of these. This is the primary cause of death among people who initially survive an explosion.

In addition to blunt trauma, penetrating trauma can cause pulmonary contusion. Contusion resulting from penetration by a rapidly moving projectile usually surrounds the path along which the projectile traveled through the tissue. The pressure wave forces tissue out of the way, creating a temporary cavity; the tissue readily moves back into place, but it is hurt. Pulmonary contusions that accompany gun and knife wounds are not usually severe enough to have a major effect on outcome;penetrating trauma causes less widespread lung damage than does blunt trauma. An exception is shotgun wounds, which can seriously damage large areas of lung tissue through a blast injury mechanism.

Mechanism:

The physical processes behind pulmonary contusion are poorly understood. However, it is known that lung tissue can be crushed when the chest wall bends inward on impact. Three other possible mechanisms have been suggested: the inertial effect, the spalling effect, and the implosion effect.

In the inertial effect, the lighter alveolar tissue is sheared from the heavier hilar structures, an effect similar to diffuse axonal injury in head injury. It results from the fact that different tissues have different densities, and therefore different rates of acceleration or deceleration.In the spalling effect, lung tissue bursts or is sheared where a shock wave meets the lung tissue, at interfaces between gas and liquid. The alveolar walls form such a gas-liquid interface with the air in the alveoli. The spalling effect occurs in areas with large differences in density; particles of the denser tissue are spalled (thrown) into the less dense particles.

The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas: the bubbles first implode, then rebound and expand beyond their original volume. The air bubbles cause many tiny explosions, resulting in tissue damage; the overexpansion of gas bubbles stretches and tears alveoli. This effect is thought to occur microscopically when the pressure in the airways increases sharply.

Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury, a contrecoup contusion may occur at the site opposite the impact as well. A blow to the front of the chest may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. (A similar mechanism may occur at the front of the lungs when the back is struck.)

The amount of energy transferred to the lung is determined in a large part by the compliance (flexibility) of the chest wall.Children's chests are more flexible because their ribs are more elastic and there is less ossification of their intercostal cartilage. Therefore, their chest walls bend, absorbing less of the force and transmitting more of it to the underlying organs.

An adult's more bony chest wall absorbs more of the force itself rather than transmitting it.Thus children commonly get pulmonary contusions without fractures overlying them, while elderly people are more likely to suffer fractures than contusions. One study found that pulmonary contusions were accompanied by fractures 62% of the time in children and 80% of the time in adults.

Pathophysiology:

Normally, oxygen and carbon dioxide diffuse across the capillary and alveolar membranes and the interstitial space (top). Fluid impairs this diffusion, resulting in less oxygenated blood (bottom).Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened and lose its normal elasticity. The water content of the lung increases over the first 72 hours after injury, potentially leading to frank pulmonary edema in more serious cases. As a result of these and other pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient oxygen).

Bleeding and edema:

In contusions, torn capillaries leak fluid into the tissues around them. The membrane between alveoli and capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung. With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli. Pulmonary contusion is characterized by microhemorrhages (tiny bleeds) that occur when the alveoli are traumatically separated from airway structures and blood vessels.Blood initially collects in the interstitial space, and then edema occurs by an hour or two after injury. An area of bleeding in the contused lung is commonly surrounded by an area of edema.

In normal gas exchange, carbon dioxide diffuses across the endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in the other direction. Fluid accumulation interferes with gas exchange, and can cause the alveoli to fill with proteins and collapse due to edema and bleeding. The larger the area of the injury, the more severe respiratory compromise will be.

Consolidation and collapse:

Pulmonary contusion can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial or total lung collapse) to occur. Consolidation occurs when the parts of the lung that are normally filled with air fill with material from the pathological condition, such as blood. Over a period of hours after the injury, the alveoli in the injured area thicken and may become consolidated. A decrease in the amount of surfactant produced also contributes to the collapse and consolidation of alveoli; inactivation of surfactant increases their surface tension. Reduced production of surfactant can also occur in surrounding tissue that was not originally injured.

Inflammation of the lungs, which can result when components of blood enter the tissue due to contusion, can also cause parts of the lung to collapse. Macrophages, neutrophils, and other inflammatory cells and blood components can enter the lung tissue and release factors that lead to inflammation, increasing the likelihood of respiratory failure.

In response to inflammation, excess mucus is produced, potentially plugging parts of the lung and leading to their collapse. Even when only one side of the chest is injured, inflammation may also affect the other lung. Uninjured lung tissue may develop edema, thickening of the septa of the alveoli, and other changes. If this inflammation is severe enough, it can lead to dysfunction of the lungs like that seen in acute respiratory distress syndrome.

Ventilation/perfusion mismatch:

Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli (ventilation) is about equal to that of blood in the capillaries around them (perfusion). This ratio is reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the hemoglobin, and the blood leaves the lung without being fully oxygenated. Insufficient inflation of the lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest, can also contribute to the ventilation/perfusion mismatch.

As the mismatch between ventilation and perfusion grows, blood oxygen saturation is reduced. Pulmonary hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in pulmonary contusion. The vascular resistance increases in the contused part of the lung, leading to a decrease in the amount of blood that flows into it, directing blood to better-ventilated areas. Although reducing blood flow to the unventilated alveoli is a way to compensate for the fact that blood passing unventilated alveoli is not oxygenated, the oxygenation of the blood remains lower than normal.

If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result from trauma.

Diagnosis:

To diagnose pulmonary contusion, health professionals use clues from a physical examination, information about the event that caused the injury, and radiography. Laboratory findings may also be used; for example, arterial blood gasses may show insufficient oxygen and excessive carbon dioxide even in someone receiving supplemental oxygen. However, blood gas levels may show no abnormality early in the course of pulmonary contusion.

X-ray:

A chest X-ray showing right sided pulmonary contusion associated with rib fractures and subcutaneous emphysemaChest X-ray is the most common method used for diagnosis, and may be used to confirm a diagnosis already made using clinical signs. Consolidated areas appear white on an X-ray film. Contusion is not typically restricted by the anatomical boundaries of the lobes or segments of the lung.

The X-ray appearance of pulmonary contusion is similar to that of aspiration, and the presence of hemothorax or pneumothorax may obscure the contusion on a radiograph. Signs of contusion that progress after 48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS.

Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect the condition early after the injury. In a third of cases, pulmonary contusion is not visible on the first chest radiograph performed. It takes an average of six hours for the characteristic white regions to show up on a chest X-ray, and the contusion may not become apparent for 48 hours. When a pulmonary contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan might reveal other injuries that were missed with X-ray.

Computed tomography:

A chest CT scan revealing pulmonary contusions, pneumothorax, and pseudocystsComputed tomography (CT scanning) is a more sensitive test for pulmonary contusion, and it can identify abdominal, chest, or other injuries that accompany the contusion. In one study, chest X-ray detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in 31.2% of the same people. Unlike X-ray, CT scanning can detect the contusion almost immediately after the injury. However, in both X-ray and CT a contusion may become more visible over the first 24–48 hours after trauma as bleeding and edema into lung tissues progress. CT scanning also helps determine the size of a contusion, which is useful in determining whether a patient needs mechanical ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that ventilation will be needed. CT scans also help differentiate between contusion and pulmonary hematoma, which may be difficult to tell apart otherwise. However, pulmonary contusions that are visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment.

Ultrasound:

An ultrasound image showing early pulmonary contusion, at this moment not visible on radiography. Interstitial syndromes are expressed with the vertical white lines, the "B-lines".Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis for pulmonary contusion. Its use is still not widespread, being limited to facilities which are comfortable with its use for other applications, like pneumothorax, airway management, and hemothorax. Accuracy has been found to be comparable to CT scanning.

Prevention:

Prevention of pulmonary contusion is similar to that of other chest trauma. Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision, and by distributing forces involved in the crash more evenly across the body. However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned when it deploys. Child restraints such as carseats protect children in vehicle collisions from pulmonary contusion. Equipment exists for use in some sports to prevent chest and lung injury; for example, in softball the catcher is equipped with a chest protector. Athletes who do not wear such equipment, such as basketball players, can be trained to protect their chests from impacts. Protective garments can also prevent pulmonary contusion in explosions.Although traditional body armor made from rigid plates or other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary contusion, because it does not prevent the blast's shock wave from being transferred to the lung. Special body armor has been designed for military personnel at high risk for blast injuries; these garments can prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers from blast lung injuries.These garments alternate layers of materials with high and low acoustic impedance (the product of a material's density and a wave's velocity through it) in order to "decouple" the blast wave, preventing its propagation into the tissues.

Treatment:

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.

Incidence:

Commotio cordis is a very rare event, but nonetheless is often considered when an athlete presents with sudden cardiac death. Some of the sports which have a risk for this cause of trauma are baseball, soccer, ice hockey, polo, rugby, cricket, softball, pelota, fencing, lacrosse, boxing, karate, kung fu and other martial arts. Children are especially vulnerable, possibly[citation needed] due to the mechanical properties of their thoracic skeleton. From 1996 to spring 2007, the USA National Commotio Cordis Registry had 188 cases recorded, with about half occurring during organized sports Almost all (96%) of the victims were male, the mean age of the victims during that period was 14.7 years, and fewer than 1 in 5 survived the incident.

Other situations:

Commotio cordis may also occur in other situations, such as in children who are punished with blows over the precordium, cases of torture, frontal collisions of motor vehicles (the impact of the steering wheel against the thorax, although this has decreased substantially with the use of safety belts and air bags).

Cases of commotio cordis have been recorded in people who were shot by firearms over the precordium and were using body armour, thus stopping the bullet but causing a mechanical impact to the thorax (the so-called Behind Armour Blunt Trauma or BABT); or after being hit by less-lethal crowd control firearm shots using rubber bullets or plastic bullets.

In contrast, the precordial thump (hard blows given over the precordium with a closed fist in order to revert cardiac arrest) is a sanctioned procedure for emergency resuscitation by trained health professionals witnessing a monitored arrest when no equipment is at hand, endorsed by the latest guidelines of the International Liaison Committee on Resuscitation.

It has been discussed controversially, as - in particular in severe hypoxia - it may cause the opposite effect (i.e., a worsening of rhythm - commotio cordis). In a normal adult, the energy range involved in the precordial thump is 5-10 times below that associated with commotio cordis.

Mechanism of injury:

Electrocardiogram schematic tracing, showing the period of vulnerability to stretch-induced ventricular fibrillation which occurs in commotio cordisThe following factors influence the chance of commotio cordis:
Direction of impact over the precordium (precise area, angle of impact) Total applied energy (area of impact versus energy, i.e., the mass of the projectile multiplied half the square of its velocity) Impact occurring within a specific 10-30 millisecond portion of the cardiac cycle. This period occurs in the ascending phase of the T wave, when the ventricular myocardium is repolarizing, moving from systole to diastole (relaxation).

The small window of vulnerability explains why it is a rare event. Considering that the total cardiac cycle has a duration of 1000 milliseconds (for a base cardiac frequency of 60 beats per minute), the probability of a mechanical trauma within the window of vulnerability is 1 to 3% only. That also explains why the heart becomes more vulnerable when it is physically strained by sports activities:
The increase in heart rate (exercise tachycardia) may double the probability above (e.g., with 120 beats per minute the cardiac cycle shortens to 500 milliseconds without fundamentally altering the window-of-vulnerability's size); Relative exercise-induced hypoxia and acceleration of the excito-conductive system of the heart make it more susceptible to stretch-induced ventricular fibrillation. The cellular mechanisms of commotio cordis are still poorly understood, but probably related to the activation of mechano-sensitive proteins, ion channels.

It is estimated that impact energies of at least 50 joules are required to cause cardiac arrest, when applied in the right time and spot of the precordium of an adult. Impacts of up to 130 joules have already been measured with hockey pucks and lacrosse balls, 450 joules in karate punches and 1028 joules in boxer Rocky Marciano's punch. The 50 joules threshold, however, can be considerably lowered when the victim's heart is under ischemic conditions, such as in coronary artery insufficiency.

There is also an upper limit of impact energy applied to the heart; too much energy will create structural damage to the heart muscle as well as causing electrical upset. This condition is referred to as contusio cordis (from Latin for bruising of the heart). On isolated guinea pig hearts, as little as 5 mJ was needed to induce release of creatine kinase, a marker for muscle cell damage. Obviously one should take into account that this figure does not include the dissipation of energy through the chest wall, and is not scaled up for humans, but it is indicative that relatively small amounts of energy are required to reach the heart before physical damage is done.

Outcome and treatment:

Fulminant death is the most common outcome, because cardiopulmonary resuscitation requires quick action by a specialized medical team, using a defibrillator and cardioactive drugs, and these are rarely on hand in sports arenas. Due to the significant danger to children (death by commotio cordis is the leading cause of fatalities in youth baseball in the US, with 2 to 3 deaths per year), it has been recommended that "communities and school districts reexamine the need for accessible automatic defibrillators and cardiopulmonary resuscitation-trained coaches at organized sporting events for children.

Prevention:

Equipment and dress used in several sports. clearly demonstrating the lack of protection against chest concussion. From left to right, top to bottom: boxing, field hockey, baseball, karate, cricket, woman's lacrosse and soccer.The mandatory use of heavily padded special vests in front of the thorax is generally sufficient to prevent high energy impacts to the precordium. The problem with many sports such as soccer, baseball and karate is that, despite the danger posed by a multitude of punches, kicks, pads, mallets, bats, pucks and balls moving at high speeds, etc., their dress codes represent an obstacle to the use of mechanical protection to the precordium for all players, or at least for goalkeepers, batters, ball catchers, etc. For example, boxing traditionally requires a naked chest, cricket gear protects the legs but not the chest, and soccer has practically no protection gear at all; although the ball weighs only 450 grams, it can reach speeds of 30 meters per second, and barrier defenses actually encourage the player to block the ball with his chest.

Parents of children active in these sports are advised to adopt simple protective measures, particularly in informal "backyard" games, which are often much more dangerous than formal ones, which require some protection.

Legal issues:

Several people have been convicted of involuntary manslaughter in cases involving insufficient and slow medical help to athletes who underwent commotio cordis during sports events, as well as in cases of intentional delivery of contusive blows. In one such case, a man was sentenced to 18 years of prison for killing his own son with a blow to the chest.