Cardiac Trauma
Gary A. Smith
Timothy F. Feltes
Traumatic injury to the heart occurs when energy is transferred to the heart in amounts or at rates that exceed the tissue’s threshold to withstand it, resulting in structural damage or functional abnormality. The transfer of injurious energy is most commonly associated with blunt trauma, penetrating trauma, or contact with electrical current. Most medical knowledge about cardiac trauma in children is extrapolated from studies of adults. Relatively little direct information is available regarding cardiac injuries in children.
Blunt Cardiac Injury
Blunt trauma accounts for the vast majority of injuries to children and is the chief cause of cardiac trauma in the pediatric age group. The incidence of cardiac injury in blunt trauma among children has been reported to be from 0% to 43% (1). Blunt cardiac injuries are often unsuspected injuries associated with multiple system trauma. Clinical manifestations of cardiac trauma vary depending on the location of injury. They are often nonspecific and include shock, cardiovascular instability, dysrhythmias, chest pain, and changes in mentation. In victims of multiple trauma, all of these findings can be easily attributed to other serious injuries to the head, abdomen, or extremities.
Parmley et al. (2) performed autopsies on a large series of motor vehicle crash victims and found that blunt cardiac injury was one of the most frequently missed diagnoses. This finding has been corroborated by others. Having a high level of suspicion for blunt cardiac injury is necessary for early diagnosis and intervention. The autopsy series of Parmley et al. (2) described various mechanisms of nonpenetrating cardiovascular injury (Table 27.1).
Most blunt cardiac injuries from direct chest impact among children are the result of motor vehicle crashes (3). Blunt blows with weapons, fists, and animal kicks; blunt collisions during sports; and falls from heights also cause direct-impact cardiac injuries.
Because the heart is suspended from the great vessels, acceleration–deceleration injuries occur as the heart moves like a pendulum in the thorax. Traction on the great vessels can cause tears at their points of fixation.
Compression of the chest can crush the heart or cause damage through increased intrathoracic and intracardiac pressures. Cardiac rupture is more likely if compression occurs during maximum filling of the chambers. Rib fractures and contusions of the chest wall are not always seen, especially in children owing to their highly compliant chest walls. Abdominal and lower extremity compression also can force blood back to the heart, causing damage through a hydraulic ram effect.
Commotio cordis is a specific form of cardiac trauma that has become an increasingly recognized cause of sudden cardiac death in otherwise healthy young athletes (4). While the National Commotio Cordis Registry in Minneapolis lists almost 250 cases of commotio cordis, the frequency of such cases is most certainly underestimated (5). Commotio cordis is a form of nonpenetrating chest trauma insufficient to result in significant myocardial or chest wall injury. The most likely mode of death appears to be an induction of a malignant arrhythmia (i.e., ventricular fibrillation) due to the transfer of concentrated mechanical energy (concussion) to the heart resulting in electrical instability. The two critical components appear to be precordial impact location and the timing of the impact occurring during the upstroke of the T wave (6,7,8). The impact site for victims of commotio cordis is specifically located at or near to the center of the cardiac silhouette. Recent animal model studies suggest that the trauma must occur within an electrical vulnerability period during the cardiac cycle, namely, within 20 ms of the T-wave upstroke.
As reported recently by Maron and Estes (4), commotio cordis is seen most frequently in the second decade of life, peaking at 15 years of age. Baseball is the most common sport in which commotio cordis is observed followed by softball, hockey, and football. It is more commonly experienced during organized sporting events but by no means exclusively. In younger victims (<10 years of age) commotio cordis may occur during activities unrelated to sports.
TABLE 27.1 Mechanisms of Blunt Cardiac Trauma | ||||||||
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TABLE 27.2 Differential Features of Cardiac Concussion and Contusion | |||||||||||||||||||||||||||
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Victims of commotio cordis most commonly experience instantaneous cardiovascular collapse but in approximately 20% of cases victims are able to stay erect for several seconds after the trauma occurs. Survival from resuscitative efforts is low but has increased to 35% in recent years most likely due to increasing availability of automatic external defibrillators and bystanders knowledgeable in the use of these devices.
According to data from the above-mentioned national registry, nearly one-third of cases of commotio cordis that occurred during competitive sports were victims who were wearing a commercially available chest protector. Many of these devices were not designed to prevent commotio cordis and either expose the precordium or do not adequately absorb the impact from a projectile (9). Efforts have been made to create safer baseballs (aka “safety” baseballs) with some evidence of effectiveness. Some sports now require protective equipment (10). See Table 27.2 for features differentiating cardiac concussion from cardiac contusion (11). It is important that the public and organizers of sporting events be aware of the risk of commotio cordis.
Two other mechanisms of blunt cardiac injury have been described: blast injury and a combination injury, which involves more than one of the above mechanisms.
The types of anatomic injuries resulting from these various mechanisms in blunt cardiac trauma include pericardial injury, myocardial contusion, cardiac rupture, septal disruption, ventricular aneurysm, injury to the heart valves and supporting structures, and injury to the great vessels, brachiocephalic arteries, venae cavae, and coronary arteries (Table 27.3).
Pericardial Injury
Blunt pericardial injuries range from contusion to rupture and are usually associated with myocardial injury. Isolated pericardial injuries are rare. Pericardial lacerations and pericardial rupture are rarely significant injuries unless cardiac herniation occurs through a pericardial tear. Cardiac herniation can result in severe circulatory compromise and rapid death. Cardiac tamponade is a common complication of myocardial injury but is not likely with isolated pericardial injury.
Traumatic pericarditis can develop after pericardial contusion. A chronic pericarditis after cardiac trauma can last 1 to 4 weeks. The clinical features are single or recurrent pericardial or pleural effusions, similar to the postpericardiotomy syndrome.
The frequency of pericardial injury associated with blunt chest trauma is unknown. Asymptomatic pericardial effusions have been demonstrated by cardiac ultrasonographic examination following blunt chest trauma. Pericardial lacerations were frequently found in dogs following sublethal blunt chest trauma. The most frequent manifestations of traumatic pericarditis include pericardial friction rub and nonspecific electrocardiographic (ECG) ST-T wave changes and diffuse low voltages.
Traumatic cardiac tamponade rarely presents with all the classic Beck triad features of hypotension, distant heart sounds, and elevated central venous pressure with neck vein distension. An echocardiogram is the most sensitive diagnostic test for cardiac tamponade and can be used in the emergency department for selected trauma patients. A diagnostic and therapeutic pericardiocentesis also can be used for patients with suspected cardiac tamponade. However, false-negative pericardiocentesis results have been observed in 25% to 80% of patients who have blood in the pericardium (12).
Treatment of traumatic pericarditis is based on symptoms. If pericardial effusion or associated pleural effusions are clinically significant, pericardiocentesis or thoracocentesis is indicated. Chronic pericarditis or postpericardiotomy syndrome is treated with anti-inflammatory agents.
TABLE 27.3 Types of Blunt Cardiac Injuries | ||||||
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Most pericardial lacerations are incidentally found during thoracotomy being performed for other indications and are not repaired unless the defect is large enough to pose a risk of cardiac herniation. Large pericardial lacerations that are difficult to repair may be managed by pericardiectomy.
Myocardial Contusion
Myocardial contusion in the general population is most often a result of direct blunt force to the chest during motor vehicle crashes, industrial injuries, farm injuries, or sports injuries. The reported incidence of myocardial contusion associated with major trauma varies between 3% and 76% depending on the study population and the diagnostic criteria (13,14). Approximately one-third of children with cardiac contusion may have no external evidence of chest injury. ECG abnormalities and dysrhythmias are less common in these children than in adults who have cardiac contusion.
The first reported case of autopsy-proven myocardial contusion was in 1764; it described a boy struck in the chest by a plate (15). Recognition of cardiac contusion is difficult because of nonspecific clinical findings and lack of an accurate diagnostic test (3). The findings of cardiac contusion are easily attributed to other serious injuries that are often present. Predicting which cases will be clinically significant has not been possible, thus complicating the discussion about appropriate management of myocardial contusion. The diagnosis of myocardial contusion should be considered in any child with significant blunt chest or multiple system trauma.
Most cases of myocardial contusion are mild and asymptomatic, and go unrecognized, but complications can be serious. Complications of myocardial contusion include dysrhythmias, conduction disturbances, cardiac failure, aneurysms, pseudoaneurysms, myocardial wall thinning, cardiac rupture, and cardiac arrest. Most are late findings. Underlying cardiac disease, including ischemia, cardiomyopathy, or congenital heart disorders, increases the risk of complications from blunt cardiac injury. The pathologic findings of myocardial contusion include myocardial hemorrhage, myocardial fiber necrosis, and, later, fibrous scar formation.
The diagnosis of myocardial contusion can generally be made in patients with blunt chest trauma if the ECG demonstrates a dysrhythmia or changes compatible with ischemia or contusion, the creatine phosphokinase–muscle band (CPK-MB) fraction is >5% of the total CPK, and the echocardiogram is abnormal (16). However, ECG findings in cardiac contusion are nonspecific, and false-positive results can occur. Because CPK-MB is also present in skeletal muscle, pancreas, and bowel, extensive skeletal muscle or abdominal trauma can cause elevation of CPK-MB. In addition, CPK-MB has been shown to have a low sensitivity and specificity for cardiac injury in some studies (17,18). Measurement of lactate dehydrogenase (LDH) isoenzymes and serum glutamic oxalotransaminse (SGOT) is of no value in the diagnosis of cardiac contusion. Troponin I and T have been shown to be accurate indicators of myocardial injury that may aid in the diagnosis of myocardial contusion (19,20,21). In adult studies, the positive predictive value of elevated cardiac troponin T ranges from 20% to 100% and the negative predictive value ranges from 74% to 100% (22,23). Diagnostic sensitivity may be improved by use of recently developed highly sensitive cardiac troponin assays, but validation studies have not yet been reported (24).
The echocardiogram may be more useful than serial ECGs or cardiac isoenzyme measurements in evaluating blunt cardiac injuries because it can detect pericardial effusion, valvular dysfunction, septal defects, enlarging chambers, and wall motion abnormalities and can be used to determine ejection fraction. Echocardiographic abnormalities are detected in 20% to 47% of patients following blunt trauma (25). Transesophageal echocardiography may offer advantages over transthoracic echocardiography, especially in obese patients. The proximity of the esophagus to the thoracic aorta and atrioventricular (AV) valves allows clearer visualization of injuries to these structures. In the absence of ECG abnormalities or cardiac isoenzyme elevation, cardiac dysmotility on echocardiogram is not associated with adverse patient outcome (26).
Gated radionuclide angiography is a useful method for detecting abnormalities of cardiac function. It has been applied in the evaluation of blunt cardiac trauma to detect diminished ejection fractions, hypokinetic wall segments, and ventricular aneurysms. The most common finding identified in adult patients with blunt chest trauma was mild hypokinesis of the right ventricular wall with diminished ejection fraction. Unfortunately, gated radionuclide angiography is not predictive of morbidity and mortality in cardiac contusion.
Following blunt chest trauma, patients with abnormal ECGs require admission, continuous cardiac monitoring, and evaluation of cardiac isoenzymes. Cardiac monitoring should continue until abnormal ECGs have reverted to normal for at least 24 hours, cardiac isoenzymes have normalized, and stabilization of other major injuries has been achieved. The main treatment goal is avoidance of death caused by dysrhythmias or hemodynamic compromise.
Cardiac Rupture
Although an uncommon injury, cardiac rupture is estimated to cause 10% to 15% of adult motor vehicular crash fatalities. Two-thirds of deaths owing to cardiac rupture occur at the scene (27). Cardiac rupture occurs most commonly in young male drivers suffering precordial steering wheel impact during a crash (28). Ventricular rupture is more common than atrial rupture, and the thin-walled anteriorly positioned right ventricle is more commonly ruptured than the left ventricle. Multiple chamber rupture is not uncommon in these cases, as is combined cardiac rupture and aortic rupture, reflecting the large amount of force involved in these injuries (2).
Ventricular rupture can result from direct cardiac compression or from an indirect hydraulic ram effect that occurs during abdominal or extremity compression. During late diastole, compressing a distended noncompliant ventricle can tear AV valves, chambers, septa, and other cardiac structures. Atrial rupture appears to involve compression of the filled chamber as well as torsion when the AV valves are closed and the chamber is filled during late systole. The atrial appendages are the thinnest portions and most prone to atrial rupture. Delayed ruptures are extremely rare and may follow infarction associated with trauma and gradual softening of the ischemic tissues or rupture of a myocardial aneurysm or pseudoaneurysm (28).
The clinical manifestation of myocardial rupture is usually tamponade, although approximately one-third of patients will have exsanguinating hemorrhage through associated pericardial lacerations. The association of cardiac tamponade with cardiac rupture limits the rate of exsanguination and increases the chances of survival for these patients.
The first surgical repair of blunt cardiac rupture was reported by Des Forges et al. (29) in 1955 involving a 4-cm right atrial laceration. Until then, cardiac rupture had been considered universally lethal. Surviving ventricular rupture secondary to blunt chest trauma is rare. In 1990, the first pediatric survivor was preceded by only three reported adult cases (30).
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