AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Sudden unexpected cardiac death in young people that occurs during sports participation is usually associated with previously diagnosed or undiagnosed structural or electrical cardiac abnormalities. Examples of such abnormalities include hypertrophic cardiomyopathy, anomalous origin of a coronary artery, arrhythmogenic right ventricular cardiomyopathy, and primary electrical disorders, such as congenital prolongation of the QTc interval and catecholaminergic ventricular tachycardia. Sudden death due to ventricular fibrillation may also occur when a baseball or other projectile strikes the precordium of an individual with no underlying cardiac disease. This is termed commotio cordis (CC).

Recent data from the registry of the Minneapolis Heart Institute Foundation show that CC is the second leading cause of sudden death in young athletes, behind hypertrophic cardiomyopathy.¹ However, CC is rarely described in the pediatric literature and is mentioned in very few current texts on critical care, emergency medicine, and pediatric cardiology.

CC typically involves young, predominantly male athletes in whom a sudden, blunt, nonpenetrating and innocuous-appearing trauma to the anterior chest results in immediate cardiac arrest and sudden death from ventricular fibrillation. Resuscitation is rare. Although CC usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard projectile or bodily contact caused impact to the person's precordium. More than 180 cases of CC have been reported to the US Commotio Cordis Registry (Minneapolis, Minn).² In all likelihood, CC remains significantly underdiagnosed and underreported.

Pathophysiology

Although reported more often in recent years, CC remains a rare event. This is based, in part, on the pathophysiology of the disorder, which requires precise synchronization of a number of relevant variables. In a series of studies using a swine model of CC, the critical timing and location of blunt chest trauma required to induce ventricular fibrillation and sudden death were demonstrated.

Ventricular fibrillation can be triggered by chest wall impact immediately over the heart and occurs most frequently with impact over the center of the left ventricle. Impact over other precordial sites causes ventricular fibrillation less often. Similarly, nonsustained polymorphic ventricular tachycardia, ST-segment elevation, transient complete heart block, left bundle-branch block, and left ventricular wall motion abnormalities occurred only following impact over the cardiac silhouette in the swine model. Chest wall impact that did not overlie the heart failed to produce ventricular fibrillation or any other ECG abnormalities.

During the experimental studies, when precordial impacts were timed to occur during various points in the cardiac cycle, the electrophysiologic consequences were determined to be critically dependent on impact timing. Consistently, 90% of low-energy precordial impacts, produced by striking the precordium with a wooden object similar in size and weight to a baseball, resulted in immediate ventricular fibrillation if the impact was delivered within a 15-millisecond window that occurred 15-30 milliseconds before the T-wave peak. This window represents only about 3% of the cardiac cycle in an individual engaged in activities who has a heart rate of 120 beats per minute. Ventricular fibrillation was not preceded by ventricular tachycardia, conduction abnormalities, or ischemic ST changes; this suggests that the mechanism was related to a primary electrical phenomenon, not to myocardial ischemia.

Impacts delivered outside this period of vulnerability on the T-wave upstroke or during other portions of the electrical cycle never resulted in ventricular fibrillation; however, such impacts occasionally caused polymorphic ventricular tachycardia, complete heart block, left bundle-branch block, or ST-segment elevation, all of which were transient. In vivo studies have suggested that impact-related premature ventricular depolarizations together with activation of the mechanosensitive K^+_ATP-channel probably provide the basis for ventricular fibrillation and sudden death following blunt thoracic trauma, as well as the ischemiclike ECG changes noted in those rare individuals who survive CC.

In a slightly different swine model of CC, ventricular fibrillation was reproduced by simulated baseball strikes of 30 mph. The force of chest trauma was shown to be inversely related to fatal outcome in CC. Conversely, the hardness of the object that strikes the chest was shown to be directly related to ventricular fibrillation. Perfectly timed strikes with regulation baseballs resulted in ventricular fibrillation in 35% of instances (compared to 90% when using the wooden object).

Softer-than-normal baseballs reduced the risk of ventricular fibrillation to 8% with very soft baseballs, 22% with moderately soft baseballs, and 29% with the least soft baseballs. The predilection for CC to affect individuals younger than 16 years in particular likely relates to chest configuration (ie, narrower anterior-posterior diameter) and increased chest compliance in young children, predisposing them to cardiac electrical disturbances that occur following only modest precordial trauma.

Frequency

United States

The actual prevalence of CC among children and adolescents in the United States is largely unknown. Although more than 128 cases have been reported to the US CC Registry, many instances likely go unreported.²

Mortality/Morbidity

According to the US CC Registry, approximately 15% of persons with CC have been resuscitated.¹

Race

According to data collected by the US CC Registry, 87% of cases of CC are in whites.¹

Sex

According to data collected by the US CC Registry, 95% of cases of CC occur in males.¹

Age

Although reported in a wide range of ages (3 mo to 50 y), CC occurs most frequently in male children aged 4-16 years, with a mean age of 14 years. Data from the US CC Registry show that 43% are younger than 12 years and that only 22% are aged 18 years or older.¹

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• In most reported cases of commotio cordis (CC), sudden death follows a seemingly inconsequential, nonpenetrating blow to the chest. Individuals who have witnessed the events universally believed that the chest trauma was of insufficient force to cause major injury and was out of proportion to the outcome. The person who is struck collapses immediately in approximately 50% of instances. In the remaining cases, the individual has a transient period of consciousness, during which he performs a brief purposeful activity, movement, or behavior (eg, picking up and throwing a ball, crying) before final collapse.
• According to data collected by the US CC Registry, at the time of the incident, 47% of persons struck were engaged in organized competitive sports.¹ The remainder were involved in normal daily activities or recreational sports.
• • Baseball, softball, and hockey are the sports activities most commonly involved. Other associated organized activities included karate, lacrosse, and football. Rare cases have also been associated with basketball, cricket, martial arts, boxing, street fights, and motor vehicle accidents.
  • In most instances (68%), the person was struck by a projectile, which was most commonly a pitched, thrown, or batted baseball or softball estimated to be traveling 30-50 mph at most.¹ Other projectiles have included hockey pucks and lacrosse balls. In 32%, chest trauma resulted from bodily contact with another person or a stationary object. Examples of this have included a player's helmet during a football tackle, the heel of a hockey stick, a karate kick, and a body collision.
• Survival after a CC event is unusual. Although efforts at resuscitation occur frequently, often involving trained bystanders or emergency medical technicians, the onset of cardiopulmonary resuscitation (CPR) is often delayed because observers underestimate the severity of the trauma or believe that the wind has been knocked out of the person. Survival has usually been associated with effective CPR efforts that are begun within 1-3 minutes of the collapse and are associated with chest thumps or electrical defibrillation. In events in which resuscitation is known to have been started in less than 3 minutes, the survival rate was 25%. The survival rate was only 3% in cases in which resuscitative efforts were delayed longer than 3 minutes. Although a number of individuals have been resuscitated with the restoration of a normal heart rhythm, many of these individuals experience irreversible ischemic encephalopathy and ultimately die as a result of the injury.

Physical

• Persons with CC are typically found to be unresponsive, apneic, pulseless, and without an audible heartbeat; many are cyanotic. Grand mal seizures have been evident in some persons with CC. Chest wall contusions and localized bruising that correspond to the site of chest impact are noted over the precordium in approximately one third of patients. Typically, the ribs or sternum is not structurally injured.

Causes

• Clinical and experimental CC both result from sudden ventricular fibrillation. Precordial impacts probably result in activation of the normally inactive mechanosensitive K⁺_ATP channel, which leads to inhomogeneity of repolarization and ST segment elevation. Critically timed impacts also produce premature ventricular depolarizations, which sets the stage for ventricular fibrillation in the presence of ischemiclike conditions. 
• Impacts that occur only during a narrow, vulnerable period of repolarization result in ventricular fibrillation. Impacts during other portions of the cardiac cycle result in ST-segment elevation.
• Some observers believe that CC may include a component of coronary artery vasospasm, myocardial contusion, or both. They believe that this may help explain both the difficulty and the relatively rare success of resuscitative efforts. At present, whether these conditions have a pathophysiologic role in CC has not been determined.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• In the past, findings from the workup of patients with commotio cordis (CC) have been limited mostly to postmortem studies and tests on individuals who died as a result of the event. Additionally, the relatively few patients who survived the acute episode and who received the attention of trained medical personnel have provided little insight into the likely findings from laboratory and other studies in patients who survive CC. In general, patients who experience an episode of CC are surprisingly free of abnormal laboratory, imaging, or histologic findings, with the exception of the abnormalities revealed by ECG.
• Blood studies/toxicology: Results of postmortem toxicologic screening of blood and urine are universally negative. Results of serum toxicologic studies in patients who survive CC also are negative. Cardiac enzyme levels are usually within reference range and show no evidence of myocardial necrosis (ie, infarction). One survivor was reported to have a mildly elevated creatine kinase (CK) level, but the CK-MB fraction was within reference range.

Imaging Studies

• Echocardiography: Echocardiography in a patient who survives CC almost always shows an anatomically and functionally normal heart. No evidence is found for any of the underlying cardiac conditions (eg, hypertrophic or dilated cardiomyopathy, anomalous coronary artery origin, aortic root dilatation, congenital heart defects) that are sometimes associated with sudden cardiac death during athletics. The cardiac valves are normal, although an incidental finding of mitral valve prolapse was described in one survivor. Some survivors demonstrate mildly diminished global left ventricular systolic function or limited areas of hypokinesis. These abnormalities are of short duration, lasting only a few days.
• Angiography: A few patients have undergone cardiac catheterization and cineangiography upon arriving at a hospital following a CC episode. In general, cardiac and coronary artery anatomy were found to be normal. The patients did not demonstrate evidence of coronary artery spasm or thrombosis. Isolated incidences of areas of hypokinesis or akinesis have been documented within the left ventricle, similar to that reported based on findings of echocardiography.

Other Tests

• Electrocardiogram
• • The most common initial ECG findings in both nonsurvivors and survivors are ventricular fibrillation and asystole. Timing of the ECG following impact seems to be the major determinant in which rhythm is present. Patients undergoing resuscitation efforts during transport to an emergency department also have ventricular fibrillation if they have not been electrically defibrillated.
  • If an ECG is recorded relatively late during the resuscitative effort, asystole is the most common finding. In all likelihood, ventricular fibrillation was the initial rhythm following impact.
  • Patients who survive CC frequently demonstrate impressive ST-segment elevation, which is particularly evident in precordial leads V₁-V₃. The significance of this finding remains unclear because myocardial ischemia, the most common cause of ST-segment elevation, has not been shown to result from CC in humans or in animal models.
  • Complete heart block, left bundle-branch block, and, occasionally, idioventricular escape rhythms are also noted in persons who survive CC. These latter ECG findings, which last only 2-3 days, are remarkably similar to what was noted in the CC swine model when chest wall impacts were timed to occur outside the period of greatest vulnerability.
  • No permanent ECG findings have been described. No ECG evidence for congenital QTc prolongation, Brugada syndrome, or arrhythmogenic right ventricular dysplasia has been found in any patient who survived CC.

Histologic Findings

Data from many autopsy examinations of patients who died as a result of CC revealed virtually normal cardiac morphology in every instance. In many cases, the patient has small oval or circular abrasions or bruises over the precordium. Most are located directly over the left ventricle. Generally, no evidence is found of rib fractures, hemothorax, hemopericardium, or external myocardial contusion. The heart is found to be completely free of congenital or acquired structural entities known to predispose young people and athletes to sudden death. No evidence for aortic rupture or traumatic injury exists. Overall cardiac weight, wall thickness, and chamber dimensions are normal. Careful examination of the coronary arteries reveals no evidence of either damage or thrombosis.

Histologic examination results are almost always normal and reveal no evidence of acute or chronic myocardial infarction, infection, or inflammation. Evidence of active or healed myocarditis or arrhythmogenic right ventricular dysplasia has never been found in this setting. Rarely, hemorrhage has been reported in the anterior left ventricular wall and in the arteriovenous (AV) node and specialized conduction system. The significance of these uncommon histologic findings is uncertain.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The treatment of commotio cordis (CC) is no different from any other cardiopulmonary emergency associated with asystole. Prompt attention to airway maintenance, ventilation, and chest compressions is key. Patients should receive electrical defibrillation as quickly as possible, as indicated by ECG monitoring. The relatively low rate of survival is primarily caused by the delay in instituting effective CPR measures. Bystanders frequently fail to appreciate the severity of the event and delay appropriate evaluation and resuscitation because they lack knowledge of CC or mistakenly believe that the trauma was insignificant. Many observers have commented that they believed that the wind was knocked out of the person. Experience suggests that survival is associated with resuscitation efforts begun within 1-3 minutes of collapse.

• Electrical defibrillation
• • The hallmark of effective resuscitation is rapid direct current defibrillation after the recognition of ventricular fibrillation. Time to defibrillation is probably the single most important determinant of survival in cardiac arrest. The likelihood of successful defibrillation decreases rapidly over time, in part because ventricular fibrillation generally evolves to asystole within a few minutes.
  • Experimental data gathered using the CC swine model suggest that defibrillation within 1 minute of ventricular fibrillation onset results in a 100% survival rate and that defibrillation after 2 minutes results in an 80% survival rate. In animals in which ventricular fibrillation was present for more than 4 minutes, the survival rate was 0% unless CPR was instituted after defibrillation (in which case, the likelihood of survival increased to 65%).
  • Clinically, out-of-hospital defibrillation within 3 minutes of a witnessed adult arrest produces survival rates of greater than 50%. Generally, every 1-minute delay in defibrillation beyond the first 3 minutes decreases the likelihood of survival by approximately 10%.
  • Because emergency paramedical technicians cannot be expected to arrive at the scene of a cardiac arrest in less than 5 minutes, the expanded use of automated external defibrillators (AEDs) may save the lives of countless young people who go into arrest due to blunt trauma to the precordium. AEDs, even when used by persons with minimal training, can recognize and automatically terminate fatal arrhythmias.
  • Until recently, these devices were not approved for use in children younger than 8 years or who weigh less than 55 lb (25 kg). In July 2003, the Pediatric Advanced Life Support (PALS) Task Force of the International Liaison Committee on Resuscitation (ILCOR), with the support of the American Heart Association (AHA), issued new recommendations stating that AEDs may be used in children aged 1-8 years with no signs of circulation. Ideally, if available, the device should be outfitted with a special pediatric pad and cable set, which attenuates the charge to deliver a more appropriate pediatric dose. Studies have shown that current AED algorithms provide highly specific and reasonably sensitive rhythm analysis in children.


• Precordial thump
• • Use of the precordial thump during CPR is controversial. Although precordial thump remains a class IIb action (acceptable, possibly helpful) in adult CPR during a witnessed arrest with no pulse and no defibrillator immediately available, it is not mentioned as an option in pediatric CPR or PALS.
  • A forceful precordial thump can convert ventricular fibrillation into sinus rhythm in some instances. Alternatively, it may cause deterioration of a regular rhythm, such as ventricular tachycardia, to ventricular fibrillation, asystole, or electromechanical dissociation.
  • In the past, the AHA has cautioned against the use of the precordial thump in children. Because a single thump can be delivered quickly, its use as emergency therapy for pediatric CC, in which the child is pulseless and no defibrillator or cardiac monitor is immediately available, should be reinvestigated. If used in this setting, it should never be allowed to delay electrical defibrillation and should always be followed by standard CPR modalities.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medications may be required to treat arrhythmia following basic CPR, electrical defibrillation, or both. Follow current AHA guidelines.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Deterrence/Prevention

• The recently published 36th Bethesda Conference on Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities had a number of recommendations regarding commotio cordis (CC).³
• • Children and adolescents aged 13 years and younger should use age-appropriate safety baseballs.
  • Although chest wall protectors may prevent traumatic injury in some sports, the evidence to promote their widespread use to prevent CC is insufficient. In a more recent study, 38% of competitive athletes who experienced CC were wearing commercial chest protectors at the time of the event. In 22% of these patients, projectiles directly struck the chest protector. In 78% of these patients, the chest protector failed to adequately cover the precordial area at the time of impact.
  • All sports venues should have immediate access (within 5 min) to an AED.
  • Survivors of CC should undergo a thorough cardiac evaluation, including a 12-lead ECG, ambulatory Holter monitoring, and a complete echocardiogram.
  • Eligibility for returning to competitive sports following a CC episode is, at present, a decision left to individual clinical judgment.
• Because risk is proportional to the hardness of the object that strikes the precordium, consideration may be given to the use of specially designed, softer-than-normal safety baseballs in recreational and Little League baseball.

Prognosis

• Survival from a CC event is the exception. Although efforts at resuscitation occur frequently, often involving trained bystanders or emergency medical technicians, the onset of CPR is often delayed. Survival has usually been associated with effective CPR efforts that are begun within 1 minute of the collapse and that are associated with chest thumps or electrical defibrillation. Although a number of individuals have been resuscitated with the restoration of a normal heart rhythm, these individuals may experience irreversible ischemic encephalopathy and ultimately die as a result of the injury.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Although mortality in commotio cordis (CC) is seemingly a chance event and clearly accidental in almost every instance, criminal charges have been pursued in some cases. As many as 5% of cases reported to the US CC Registry (occurring on and off the athletic field) have resulted in murder or manslaughter convictions. This may be primarily related to the lack of understanding of how blunt chest impact can result in an unintended electrophysiologic cardiovascular catastrophe.
• In 1998, a man from Washington, DC, was sentenced to a prison term of up to 18 years following the sudden death of his 11-year-old son immediately following 2 seemingly innocuous, but punitive, chest blows. The Cook County Chicago Office of the Medical Examiner recently reported deaths involving 2 boys, aged 3 years and 14 months. In both instances, deliberate fatal blows were delivered to the anterior chest with a closed fist. Both children collapsed immediately, were found to be in ventricular fibrillation by paramedics, and could not be resuscitated.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Maron BJ. Sudden death in young athletes. N Engl J Med. Sep 11 2003;349(11):1064-75. [Medline].
2. Doerer JD, Haas TS, Estes NAM, Link MS, Maron BJ. Evaluation of chest barriers for protection against sudden death due to commotio cordis. Am J Cardiol. March 15 2007;99(6):857-9. [Medline].
3. Maron BJ, Estes NAM, Link MS. 36th Bethesda Conference: Eligibility recommendations for competitive athletes with cardiovascular abnormalities. Task Force 11: Commotio Cordis. J Am Coll Cardiol. Apr 19 2005;45(8):1371-3. [Medline].
4. Abrunzo TJ. Commotio cordis. The single, most common cause of traumatic death in youth baseball. Am J Dis Child. Nov 1991;145(11):1279-82. [Medline].
5. Futterman LG, Lemberg L. Commotio cordis: sudden cardiac death in athletes. Am J Crit Care. Jul 1999;8(4):270-2. [Medline].
6. Link MS, Estes NA 3rd. Mechanically induced ventricular fibrillation (commotio cordis). Heart Rhythm. Apr 2007;4(4):529-32. [Medline].
7. Link MS, Ginsburg SH, Wang PJ, et al. Commotio cordis: cardiovascular manifestations of a rare survivor. Chest. Jul 1998;114(1):326-8. [Medline].
8. Link MS, Maron BJ, VanderBrink BA, et al. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. J Am Coll Cardiol. Feb 2001;37(2):649-54. [Medline].
9. Link MS, Maron BJ, Wang PJ, et al. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol. Jan 1 2003;41(1):99-104. [Medline].
10. 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. Jun 18 1998;338(25):1805-11. [Medline].
11. Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis). Circulation. Jul 27 1999;100(4):413-8. [Medline].
12. Maron BJ, Gohman TE, Kyle SB. Clinical profile and spectrum of commotio cordis. JAMA. Mar 6 2002;287(9):1142-6. [Medline].
13. Maron BJ, Link MS, Wang PJ, Estes NA 3rd. Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol. Jan 1999;10(1):114-20. [Medline].
14. 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. Mar 15 1997;79(6):840-1. [Medline].
15. Vincent GM, McPeak H. Commotio cordis: a deadly consequence of chest trauma. Phys Sportsmed. Nov 2000;28(11):31-9. [Full Text].

Article Last Updated: Jul 17, 2007