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Commotio Cordis

A Deadly Consequence of Chest Trauma

G. Michael Vincent, MD; Heather McPeak

THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 11 - NOVEMBER 2021


In Brief: Commotio cordis is arrhythmia or sudden death from low-impact, blunt trauma to the chest without apparent heart injury. Ventricular fibrillation is the most common associated arrhythmia, and heart block, bundle branch block, and ST-segment elevation are also seen. Commotio cordis occurs most commonly in baseball but has also been reported in hockey, softball, and several other sports. Approximately two to four cases are reported each year, but the true incidence is uncertain. Survival is low, even when resuscitation is performed. Preventive measures include education of participants and coaches, chest protection, and softer baseballs. Other considerations include having external automatic defibrillators and trained personnel at youth sporting events.

Commotio cordis (cardiac concussion) refers to blunt, nonpenetrating, precordial chest impact that causes arrhythmia or sudden death without evidence of heart injury at autopsy. Absence of morphologic cardiac injury distinguishes concussion from contusion (contusio cordis) and other more severe injuries such as rupture. Commotio cordis occurs primarily in youth, with the highest incidence in baseball, softball, and ice hockey. Cases have also been described in football, lacrosse, basketball, cricket, martial arts, boxing, fights, and vehicular accidents (table 1) (1-10). Death is usually from ventricular fibrillation.


TABLE 1. Cases of Commotio Cordis in Sports and Other Activities (1,7-9)

Sports-Related (No.)

Baseball (40)
Softball (7)
Ice hockey (7)
Football (3)
Soccer (3)
Rugby (2)
Karate (2)
Lacrosse (1)
Boxing (1)
Other sports (4)

Other Causes (No.)
Fights (2) 8
Vehicular accidents (3) 8,9
Child abuse (1) 7

All data from Maron et al (1) unless otherwise noted.


Origins, Incidence, and Clinical Profile

A Victorian disorder. Kohl (11) has outlined investigations of blunt trauma to the chest by German investigators during the late 1800s. What is now called commotio cordis may have been reported as early as 1879 by Meola (12), who described the sudden death of one of his patients who expired after being hit in the sternum with a thrown stone. Several subsequent clinical and experimental studies (13-16) emphasized the differentiation of blunt chest injury without structural cardiac damage from that which occurs with injury, reportedly to assist disputes about claims for occupational accident compensation and pension determinations in Germany.

In their extensive experimental studies of chest trauma, Schlomka and colleagues (17,18) first used the phrase commotio cordis or cardiac concussion to define the condition of induced arrhythmias without visible cardiac injury. The differentiation between commotio cordis and contusio cordis was further defined later by Hediger (19). Subsequently, many additional investigations provided more detail (20-27). Recent studies by Maron et al (6) and Link et al (28) added important new information on the clinical course and the pathophysiology of the disorder and renewed interest in the subject. Although not a comprehensive review, these reports show that commotio cordis, a rare and relatively unknown condition, has a long history and has been the subject of extensive investigation.

Epidemiology. The incidence of commotio cordis is not known with certainty. Because the condition may be unrecognized, it is probably underreported. Statistics compiled by the US Consumer Products Safety Commission (29) indicate that in the 5- to 14-year-old age-group, more fatalities occurred from baseball than any other sport. From 1973 to 1995, there were 88 deaths related to baseball in this age-group. Sixty-eight deaths were caused by impacts from the ball, and 56% (38/68) were from chest impacts. Thirteen deaths occurred from players being struck by a bat, and 7 others were from other or unknown causes. From 1973 to 120210, 17 baseball- or softball-related deaths occurred from nonpenetrating chest trauma, an average of 2.1 deaths per year. From 120216 through 1990, there were 16 baseball- or softball-related cardiac deaths, an average of 3.3 per year.

Additional data are available from the United States Commotio Cordis Registry in Minneapolis (1), in which 70 cases of commotio cordis had been reported as of June 192021. The most common sports involved (see table 1) were youth baseball (40 cases), followed by softball and ice hockey (7 cases each). Seventy percent of victims (49/70) were less than 16 years of age, 99% male (69/70), and 87% white (61/70). Approximately half of the cases occurred during organized competitive sports. The rest occurred in various activities, including informal sports at home, the playground, or at school. Commotio cordis may have legal implications in cases that occur as a consequence of a fist or other blow to the chest during fighting or child abuse (7,20).

Clinical profile. In most cases the blow occurs to the precordial area, but cases of left lateral chest trauma have been described (5). When death occurs, it is immediate in about half of the cases, while in the others there is a brief period of consciousness before collapse. Various possible physiologic mechanisms underlie these different sequences. The rate of successful resuscitation is low (1,6): Only 10% of the 70 patients reported by the commotio cordis registry (1) survived chest impacts. Fifty-two (74%) were known to have had timely cardiopulmonary resuscitation, often by trained personnel. An organized heart rhythm was restored in 11 patients, 7 of whom survived. In 6 of the 7 survivors, resuscitation had been initiated within 1 minute, presumably influencing the successful outcome. No signs of cardiac injury are evident at autopsy, although trauma to the chest wall is often identified by a bruise or abrasion, providing insight into the location of the chest blow.

What We Know About Pathophysiology and Mechanisms

The pathophysiology and electrophysiology of the condition are not completely defined. Both the physical aspects of the chest blow and the physiologic consequences of the blow need to be considered.

Chest wall biomechanics. In young athletes, the narrower anteroposterior (AP) diameter of the thorax and greater compliance of the chest wall are thought to play an important role in commotio cordis. In addition, the slower reflexes in younger athletes, less awareness of risk, and the limited training and use of protective gear in young athletes compared with collegiate or professional athletes are among other reasons suggested for the greater incidence in the young.

Biomechanical aspects were given consideration early by Schlomka et al (17,18), who determined the risk of commotio cordis to be proportional to both the speed and force of the impact and inversely proportional to the size of the contact area. Much later, Bir and Viano (30) reviewed studies that evaluated the biomechanical response of the thorax to blunt trauma; factors investigated included the magnitude of chest compression, rate of chest deformation, and the viscous criterion (VC) as predictors of the degree of cardiac injury. Review showed that the VC (an index of the magnitude of chest wall deflection plus the velocity of deflection, normalized for AP thickness) was the best predictor of commotio cordis (30). The VC was proportional to the likelihood of an adverse cardiac effect. Mechanisms considered to produce the cardiac effect include abrupt deceleration of the heart as it strikes the sternum or spine (7,31), a direct concussive effect from chest wall impact (5), and, in more severe chest blows such as those occurring in vehicular accidents, a crush injury as the heart is compressed between the sternum and the spine (7,31).

Object physical properties. The only studies we found on the physical aspects of the object striking the chest concerned the physical properties of baseballs. Softer-core baseballs have been developed in an attempt to decrease the likelihood of commotio cordis. Janda et al (32) examined the effect of baseball hardness on the VC in a surrogate chest wall model. They compared nine softer-core balls with the regulation ball. In general, softer balls produced lower VCs than the regulation ball, though results varied. One softer-core ball produced the lowest VC, but another one produced the highest VC.

The authors concluded that softer-core baseballs may not differ from standard baseballs with respect to the risk of fatal chest impact, and they noted that ball hardness is just one factor involved in commotio cordis. They raised an additional concern that using softer balls might give young players a false sense of security, encouraging them to take more risks. Their findings indicate that the softest and lightest balls likely reduce magnitude of chest deformation, may reduce the risk of cardiac injury, and should be used in conjunction with education of players and coaches to reduce the incidence of commotio cordis.

Link et al (28) studied the effect of ball hardness in a swine model, in which they compared the effect of three softer-core balls with the regulation ball on electrocardiographic changes and induction of ventricular arrhythmias in 48 pigs. They also found variability in the impact of the softer-core balls. Ventricular fibrillation occurred in 8% of impacts with the softest ball, significantly lower than the 29% observed in impacts with the least-soft safety ball, and the 35% with the regulation ball. The medium-soft and least-soft baseballs produced a lower, but not statistically significant, incidence of ventricular fibrillation than the regulation ball. Thus, these data agree with those of Janda et al (32); softer-core balls do not prevent all instances of commotio cordis, but they may reduce the risk.

Evidence From Animal Models and Human Survivors

Animal models. Ventricular arrhythmias and conduction defects have been demonstrated in several animal models. Recently, Link et al (28) studied the effects of standardized, low-energy impacts to the chest wall in a swine model. Wooden projectiles the size and weight of baseballs were propelled at the pigs' chest walls at 30 mph and synchronized with the cardiac cycle. The results provided the very important observation that the risk and type of arrhythmia induced depended on when the impact occurred during the cardiac electrical cycle. Impacts that occurred 15 to 30 msec before the T-wave peak (the vulnerable period or the time of greatest heterogeneity of repolarization) produced ventricular fibrillation in 9 of 10 impacts, whereas fibrillation was not induced at any other time in the cycle. Ventricular fibrillation occurred immediately in this model. Impacts during the QRS complex produced transient heart block in 4 of 10 impacts, and those during the QRS and ST segments produced ST-segment elevation and left bundle branch block as well.

More limited data are available on the hemodynamic and angiographic effects of chest trauma unassociated with morphologic damage (23,24,28). Liedtke et al (23) used a canine model of chest trauma without morphologic injury. In one set of experiments, they found alterations of intracardiac pressures and cardiac output, and in a second set identified abnormalities of coronary flow, left ventricular pressure, and left ventricular wall motion (24). They postulated that such abnormalities were caused by transient changes in coronary vasomotion—presumably vasoconstriction—and that the coronary flow disturbance might be involved in arrhythmia pathogenesis.

Link et al (28) also evaluated results of coronary arteriography, myocardial perfusion with technetium-99m sestamibi, and left ventriculography or echocardiography in their swine model. Coronary arteriography, performed immediately after impact in 13 test pigs and 4 control animals, was normal. Myocardial perfusion imaging revealed defects in 3 of 12 pigs who were struck, including 2 of 5 resuscitated from ventricular fibrillation, but no defects in control pigs. On echocardiogram or left ventricular angiogram, 9 of the test pigs showed a regional wall motion defect, while none of the control animals did. Histologic examination revealed that 2 of 18 test animals and 1 of 4 controls showed moderate hemorrhage of the anterior left ventricle.

Additional study of the conduction system was performed in 6 of the 18 test animals. One of the 2 pigs with heart block from the impact showed marked hemorrhage of the atrioventricular bundle and bundle branches. In each of the animals with ventricular fibrillation, mild hemorrhage in the approaches to the sinus node was present, and 1 pig also had mild hemorrhage in the periphery of the left bundle branch.

Observations in humans. Only a few survivors of commotio cordis have been reported. Ventricular fibrillation is the most common rhythm identified (2,4), but complete heart block (5) and idioventricular rhythm (33) have also been reported (5,34,35). ST-segment elevation was present in three of these seven survivors (28,35), a finding similar to some experimental animal models (23,28,35).

In one patient studied shortly after resuscitation, echocardiography and left ventriculography revealed an anteroapical regional wall motion defect in addition to the prominent ST-segment elevation (figure 1: not shown) (35). Normal coronary angiography excluded fixed obstruction but not prior epicardial or small-vessel spasm. The wall motion defect resolved within 24 hours.

Mechanical stimulation of the heart, such as during cardiac surgery and cardiac catheterization, can induce premature ventricular contractions and short runs of ventricular tachycardia. The mechanisms have been reviewed extensively elsewhere (36,37). However, ventricular fibrillation from such mechanical stimulation is rare in the normal heart, and quite uncommon even in patients with heart disease. Consequently, one would not expect the mechanical impact of a chest blow to induce ventricular fibrillation in young, healthy persons. Precipitation of ventricular fibrillation in commotio cordis victims, coupled with the experimental and clinical pathophysiologic data (summarized in table 2), suggest that some element of cardiac injury probably occurs in commotio cordis, even though it may not be apparent at autopsy.


TABLE 2. Evidence for Myocardial Injury in Commotio Cordis


ST-segment elevation in patients and animal models

Wall motion and myocardial perfusion defects

Complete heart block and bundle branch block

Low rate of successful resuscitation

Precipitation of ventricular fibrillation, when mechanical stimulation, including EPS studies, rarely does so in normal hearts


Preventive Measures

Recommendations for preventing sports injuries in general have been published (29,38,39). For baseball-related injuries they include use of chest protectors for catchers and possibly batters, elimination of the on-deck circle, and further evaluation of the use of National Operating Committee on Standards for Athletic Equipment (NOCSAE) softer-core safety baseballs; the last has also been recommended by others (3,5,32,39). Chest protection is being discussed for use in hockey, and helmets and protective eyewear in other sports are being considered as well.

Education of players and coaches must be an important part of the preventive strategy. They should be made aware of the risks, including the potential for death from commotio cordis, as well as the potential for serious harm to eyes, brain, and other body parts.

The increasing recognition of risk for sudden death in youth due to hypertrophic and other cardiomyopathies, long-QT syndrome, coronary artery anomalies, idiopathic ventricular fibrillation, as well as commotio cordis suggests that consideration might be given to having an automated external defibrillator and personnel trained in its use available for youth athletics' injuries (40).

SELECTED READINGS*

  • Abrunzo TJ: Commotio cordis: the single, most common cause of traumatic death in youth baseball. Am J Dis Child 1991;145(11):1279-1282
  • Kyle SB: Youth baseball protective equipment project final report. Washington, DC, US Consumer Product Safety Commission, 1996
  • Liedtke AJ, Allen RP, Nellis SH: Effects of blunt cardiac trauma on coronary vasomotion, perfusion, myocardial mechanics, and metabolism. J Trauma 120210;20(9):777-785
  • Liedtke AJ, Gault JH, Demuth WE: Electrocardiographic and hemodynamic changes following nonpenetrating chest trauma in the experimental animal. Am J Physiol 1974;226(2):377-382
  • Link MS, Ginsburg SH, Wang PJ, et al: Commotio cordis: cardiovascular manifestations of a rare survivor. Chest 192021;114(1):326-328
  • Link MS, Wang PJ, Pandian NG, et al: An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med 192021;338(25):1805-1811
  • Maron BJ, Link MS, Wang PJ, et al: Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol 1999;10(1):114-120
  • Maron BJ, Poliac L, Kaplan JA, et al: Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med 1995;333(6):337-342
  • Maron BJ, Strasburger JF, Kugler JD, et al: Survival following blunt chest impact-induced cardiac arrest during sports activities in young athletes. Am J Cardiol 1997;79(6):840-841
  • Viano DC, Andrzejak DV, Polley TZ, et al: Mechanism of fatal chest injury by baseball impact in children: development of an experimental model. Clin J Sport Med 1992;2(3):166-171

*A complete reference list will be available at www.physsportsmed.com beginning in December.

Dr Vincent is chairman of the department of medicine at the LDS Hospital and professor of medicine at the University of Utah School of Medicine in Salt Lake City. Ms McPeak is a certified exercise trainer and a research assistant at the LDS Hospital in Salt Lake City. Address correspondence to G. Michael Vincent MD, LDS Hospital, Physicians Office Tower, Suite 130, 324 10th Ave, Salt Lake City, UT 84143; e-mail to [email protected].


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