- Email: [email protected]
Commotio cordis: Are we aware?
Commotio cordis: Are we aware?
minor cutaneous bruise on the precordium. Retrospectively, it was thought to be a case of commotio cordis (CC). Commotio cordis is a condition which produces instantaneous death after a relatively minor hit on the precordium usually by a projectile such as hard balls played in different sports and games or by blows on the precordium which are otherwise appearing innocuous. The blows or hits are of sufficient intensity to induce ventricular fibrillation (VF) but not forceful enough to make visible injury to the myocardium or the thoracic cage.1 Although, the term and the condition was established a century before, it remained relatively obscure to the medical community.2 Earliest case reports can be traced to the 1870s from an Italian doctor Felice Meola and by a French surgeon Auguste Nelaton, but the most comprehensive studies in the past were done in the early 1930s by Georg Schlomka at Bonn University in Germany.3 In the seventies and eighties, there were several reports of such cases from North America4–6 that generated considerable interest in understanding, treating and preventing such an catastrophic event because of the tragedy involved and possibility of legal litigations.7 Much of the recent knowledge came from the report of Barry Maron and colleagues at the Minneapolis Heart Institute Foundation, MN, USA who described and analyzed 70 cases of CC.1 His subsequent works and contributions from MS Link and Mark Estes at Tufts-New England Medical Center at Boston, USA shed much light on different aspects of CC. The term CC means, in Latin, disturbance in the heart. Ferdinand Riedinger used the term CC to differentiate it from a more grievous injury that produces visible tissue damage to the thorax and the heart known as contusio cordis.3 Although, he used the term commotio thoracica, it became known to be as CC later. In 2001, Nesbitt et al defined CC as a mechanical stimulation of the heart by nonpenetrating, impulse-like impact to the precordium that, through intrinsic cardiac mechanisms, gives rise to disturbances of cardiac rhythm of varying type, duration, and severity, including sudden cardiac death, in the absence of structural damage that would explain any observed effects.3
Biswaranjan Mishra, MD DM*
ABSTRACT Instantaneous death after a relatively minor hit on the precordium is known as commotio cordis (CC). Mechanical stimulation of the heart by a nonpenetrating, impulse-like impact is sufficient to induce ventricular fibrillation (VF) in an otherwise normal heart, but not forceful enough to make structural damage to the myocardium or the thoracic cage. It is second to hypertrophic cardiomyopathy as a cause of sudden death in young individuals engaged in sport. When the blow on the chest coincide with the vulnerable period in the cardiac cycle produce a phenomenon similar to ‘R on T’ in premature ventricular complexes (PVC) resulting in VF. Two thirds of the events are sports related. Timing of the impact, hardness and speed of the projectile plays an important role in the pathophysiology of CC. Higher velocity projectiles may produce more severe injury resulting in tissue trauma but not CC. The site of impact on the chest is also crucial. It is the portion of the chest wall exactly overlying the left ventricle on the left of sternum which has to be struck to produce CC. Training persons involved in sports related activities in cardiopulmonary resuscitation and making defibrillators immediately available may prevent some deaths related to CC. Designing softer balls and protective devices may prevent although not eliminate CC. Keywords Cardiac arrest, commotio cordis, sudden cardiac death, sudden death in athletes, ventricular fibrillation
INTRODUCTION Recently, a teenaged school boy was brought to the hospital as he collapsed after a cricket ball hit him on the chest. The boy was fielding in a local cricket match. The ball hit his chest while he tried to take a catch from a straight hit by the batsman. He was declared brought dead in the hospital. A postmortem was ordered as a legal requirement. It was initially thought that probably the boy had some kind of undiagnosed congenital or primary myocardial disease as sudden death is not unusual during sport activities in young healthy individuals. Contrary to the presumption, the postmortem finding did not reveal any kind of cardiac disease, neither there was any injury to the heart nor was there any to the thorax except a
INCIDENCE Exact incidence of CC is unknown because of under reporting and low awareness of the condition. Early reports before 1970s are mostly from Europe and related to manual laborers and road traffic accidents in adults. As more cases started to be identified, it became known that it is much more common in children and adolescents and most often relates to sports, games and athletic activities.3 Sudden death in athletes is rare; it is estimated to be < 300 per year in > 10 million participants.8 Most of the deaths in athletes are due to underlying cardiac abnormality. In a US registry of sudden death in young competitive athletes, only 3% have normal heart.9 Seventy percent of reported cases are below the age of 16 years. Commotio cordis is second to hypertrophic
*Chief Consultant Cardiologist, Eko Imaging Institute, Cuttack, India. Correspondence: Dr. Biswaranjan Mishra, Chief Consultant Cardiologist, Eko Imaging Institute, Cuttack, India. E-mail: [email protected]
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of CC in soccer.11 The probable explanation is that hard core balls transmit energy to the chest directly after the impact, where as air filled balls collapse and itself absorb maximum of the energy without transmitting to the chest.11 Experimental models demonstrated that softer than normal baseballs reduced the chance of VF when compared to regular balls.18 Although, the speed of projectiles like hockey pucks can be very high up to 144 km/h (90 mph) but it takes only a modest speed to produce CC.1,16 Low-to-medium velocities in the range of 48–80 km/h (30–50 mph) is sufficient to induce VF but not enough to produce injury.19,20 Higher velocity projectiles may produce more severe injury resulting in tissue trauma but not CC which by definition does not have visible injury to the heart and thorax.15 When the velocity exceeds 80 km/h (50 mph), the probability of VF considerably decreases.21 The site of impact on the chest is also crucial. It is the portion of the chest wall exactly overlying the left ventricle on the left of sternum which has to be struck to produce CC.14 Part of the chest other than the portion lying over the heart did not produce VF in experimental models.19 When the hard projectile hits the precordium, the impact directly transmits the energy to the heart that abruptly raises the systolic pressure in the left ventricle and activates the mechanoreceptors present in the myocardial cell membrane which are stretch sensitive.22 Activation of mechanoreceptors in turn activates the K+ATP channels to open resulting in an inward current producing electrical inhomogenity. This phenomenon is known as mechanoelectric coupling. Data supports the susceptibility for VF due to inhomogeneous dispersion of repolarization occurring in the vulnerable period of the cardiac cycle at the time of impact.22 Mechanosensitivity of the K+ATP channels has been demonstrated in animal model.23 When critically timed, activation of these channels trigger VF leading to cardiac arrest.20 It is thought that more compliant chest wall in children with a short antero-posterior diameter is responsible for more direct transmission of energy to the heart which is responsible for the higher incidence of CC in children.11 Other mechanisms, proposed like coronary spasm or myocardial contusion consequent to sudden impact, are not established.13 In survivors, histological, serological, toxicological, and myocardial enzyme studies were consistently negative. Echocardiography revealed in some survivors a reversible wall motion abnormality. Coronary angiography did not reveal any spasm or thrombosis. Transient ST-segment elevations were noted in some survivors in anterior precordial leads, the mechanism of which is not understood.24 Echocardiographic analysis after the victim collapses irrespective of survival shows presence of other abnormalities like VT, idioventricular rhythm, complete heart block, and bradyarrhythmias in addition to VF.11
cardiomyopathy as a cause of sudden death in young individuals engaged in sport-related activities.10 To create a broader visibility, the United States Commotio Cordis Registry was initiated in 1996. It has acquired > 180 cases.11 In the registry, the mean age is 13.6 years, 95% are male out of which 87% are white. Only 16% survived the attack. Two-thirds of the events are sports related. Sixty-eight percent are from thrown projectiles such as baseball, hockey pucks, lacrosse ball, etc. or even by martial arts like karate. Most other cases are related to ordinary day-to-day and playful activities starting from parental discipline to friendly blows.11 There are reports of only two cases of cricket ball-induced CC in the US registry.11 Low incidence of cricket related CC may be because of the fact that cricket is less popular and played less often in United States. In India, the incidence of CC is unknown because of under reporting and under awareness of CC. The game of cricket has all the ingredients to cause CC. Therefore, the incidence may be quite high, particularly, in the present competitive form of cricket where players are more aggressive.
PATHOPHYSIOLOGY Meola, who first described CC, attributed the mechanism to autonomic disturbance causing intense vagal stimulation resulting in cardiac arrest.3,12 Experimental model by Link et al in anesthetized juvenile swine has immensely helped to comprehend the pathophysiology of CC.13 Through their model which closely mimicked the actual event, several aspects of the pathophysiology leading to CC were established. The most important aspect is about the timing of the impact. The blow on the chest must coincide the vulnerable period in the cardiac cycle that is just before or 15–30 ms before the peak of the T wave in surface echocardiography (ECG) to produce a phenomenon similar to ‘R on T’ in premature ventricular complexes (PVC).14–16 The potential for inducing VF when a PVC falls on the vulnerable portion of the T wave is well known.17 In the model of Link et al as the impact of the projectile stimulates the heart in the vulnerable period, it gives rise to VF.13 When the impact is not critically timed to the vulnerable period, it consistently did not produce VF but transiently produced other ECG abnormalities like complete heart block, bundle branch block, nonsustained polymorphic ventricular tachycardia (VT) and ST-elevation. In these experimental animals, immediately after the impact, coronary angiography did not show stenosis or spasm, myocardial perfusion imaging with technetium 99 m sestamibi revealed nonsignificant defects, left ventricular angiograms, and echo after the impact revealed mild apical or distal septal hypokinesia in some which were away from the site of impact.13 Hardness and speed of the projectile also plays an important role. Harder the projectiles, more likely it is to produce CC. Hardcore balls are much more likely to produce CC than air filled balls. In the US registry, there is only one case report JICC Vol 2 Number 2
MANAGEMENT Survival in CC is uncommon usually because of the delay in initiating cardiopulmonary resuscitation (CPR). Frequently, 90
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Commotio cordis: Are we aware?
training in CPR, and on early access to AED. It recommended for use of sport-specific chest protectors, use of softer balls, and training of athletes in avoiding being hit on the chest. Of all, it is most vital to create awareness and to educate all persons involved in sports, games, athletics including the participants, coaches, the authorities, and also the public in general regarding the possibility of such a devastating condition occurring as a consequence of trivial or innocuous appearing chest blows which in some instances cannot be even remotely thought of to be fatal. All should be aware of the ways to prevent it, and at the same time, remain prepared to treat it. Of particular importance is knowledge and practice of CPR, and at the same time, immediate availability and acquaintance in use of an AED. Innovation in designing and continued research in making effective chest barriers that can successfully prevent CC is required.
bystanders fail to understand the gravity of the situation because of lack of knowledge regarding CC. Cardiopulmonary resuscitation is rarely successful. Like any other cardiac arrest airway, ventilation and chest compression are to be taken care of. Early electrical defibrillation by an automated external defibrillator (AED) may be lifesaving. Delay in electrical defibrillation decreases the chance of survival. When resuscitation starts within 3 minutes, the chance of survival is > 50%. Every 1 minute delay decreases the chance to 10%. After 3 minutes, the chance falls to < 3%.11 In experimental models, defibrillation in one minute of VF is completely successful. After 2 minutes, survival falls to 80%. Success rate of defibrillation further falls to 46% after 4 minutes and to 25% after 6 minutes.25 Until recently, AEDs were not approved for use in children younger than 8 years or who weigh < 55 lb (25 Kg). 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 in 2003 recommending AEDs in children aged 1–8 years.26 Chest thump is a class IIb indication for adult CPR in the absence of a defibrillator, but not recommended in children by ILCOR. In CC, chest thump is a reasonable option when a defibrillator is not immediately available so long as it does not delay an electrical defibrillation.27 Post resuscitation medications should follow AHA guidelines.28
Legal Implications Commotio cordis is an electrical phenomenon related to a critically timed event that results from a seemingly innocuous impact on the precordium. It is never intentional. Due to the unexpected nature and the tragedy involved, there are instances of criminal charges and even convictions.34
CONCLUSION PREVENTION
Commotio cordis is a sudden unexpected death in young healthy persons which is devastating. The tragedy involved has wide social and legal ramification. It is being increasingly recognized particularly in North America. Most often it is related to games like baseball where the ball hits the victim on the precordium in the vulnerable period of the cardiac cycle but not with very high velocity. It is purely an electrical phenomenon as no appreciable injury occurs to the heart or thorax as confirmed from autopsy studies and experimental animal models. In India, description of CC is lacking as searched electronically. Cricket is one of the most popular games in India. Like baseball, cricket has all the substrate that can lead to CC. It uses a hard core ball and there is every possibility of a player being hit on the critical part of the chest in the critical time in the limit of speed that has every chance to produce CC. But, is it underreported due to lack of awareness or is it really uncommon? Other common games like hockey, kabadi, volley ball, different martial arts and athletic events all have the potential to cause CC. Besides, looking at the examples in US registry, where if trivial appearing harmless chest blows could produce CC, in India, where large number of people often live and travel in very crowded conditions, there is every possibility that such blows may be delivered quite frequently. Therefore, the potential for CC is very high. But is it underreported? We need to be more aware regarding the possibility of such a situation. Not only the medical fraternity but the public in general are to be educated in this regard. It is high time experimental models may be tested with conventional cricket balls for evaluating its potential to induce CC. ♦
Poor survival in CC underscores the importance of preventive measures. Training persons involved in sports related activities and also lay people in CPR and use of AED and making an AED immediately may prevent some deaths related to CC.29 Chest protection devices were developed to prevent structural chest injury and also to prevent CC but experimental models failed to show prevention of CC by these commercially available protection devices.30 In the US registry of CC, 40% deaths occurred despite use of protection devices.31 Therefore, it is imperative that new devices are to be designed particularly to prevent CC. As hardness of hitting projectiles is one of the important factors of the mechanism to produce CC, it is suggested that making regular balls softer may prevent CC. Experimental models have also shown that softer balls than normal as used in baseball is capable of preventing CC but not able to eliminate it.18 The 36th Bethesda conference made several recommendations for athletes regarding CC.32 It recommended for use of safety baseballs in children < 13 years. It also emphasized regarding immediate access to AED in sports venues. Recently, the National Athletic Trainers’ Association (NATA) of US made several recommendations for parents and coaches to take proactive steps to protect their athletes against CC. National Athletic Trainers’ Association’s Position Statement on Emergency Planning in Athletics is available in their website.33 It has emphasized on education of coaches, parents, officials, and players in the immediate recognition of CC, and also highlighted on JICC Vol 2 Number 2
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19. Maron BJ, Poliac L, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med 1995;333:337–42. 20. 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
REFERENCES 1. Maron BJ, Link MS, Wang PJ, Estes NAM III. Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol 1999; 10:114–20. 2. Kohl P. Commotio cordis: early observations. Heart 1999;82:397. 3. Nesbitt AD, Cooper PJ, Kohl P. Rediscovering commotio cordis. Lancet 2001;357:1195–7. 4. Dickman GL, Hassan A, Luckstead EF. Ventricular fibrillation following baseball injury. Phys Sportsmed 1978;6:85–6. 5. Green ED, Simson LR, Kellerman HH, Horowitz RN, Sturner WQ. Cardiac concussion following softball blow to the chest. Ann Emerg Med 1980;9:155–7. 6. Edlich RFJ, Mayer NE, Fariss BL, et al. Commotio cordis in a lacrosse goalie. J Emerg Med 1987;5:181–4. 7. Froede RC, Lindsey D, Steinbronn K. Sudden unexpected death from cardiac concussion (commotio cordis) with unusual legal complications. J Forensic Sci 1979;24:752–6. 8. Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes: clinical, demographic and pathological profiles. JAMA 1996;276:199–204. 9. Maron BJ, Doerer JJ, Haas TS, et al. Profile and frequency of sudden deaths in 1463 young competitive athlets; from a 25 year US national registry, 1980–2005. Circulation 2006;114(Suppl II):II830. 10. Priori SG, Aliot E, Blomstrom-Lundquist L, et al. Task force on sudden Cardiac Death of the European Society of Cardiology. Europace 2002;4:3–18. 11. Maron BJ, Gohman TE, Kyle SB, et al. Clinical profile and spectrum of commotio cordis. JAMA 2002;287:1142–6. 12. Zangwill SD, Strasburger JF. Commotio cordis. Pediatr Clin North Am 2004;51:1347–54. 13. 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 1998;338:1805–11. 14. 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 2001; 37:649–54. 15. Link MS, Maron BJ, VanderBrink BA, et al. Upper and lower energy limits of vulnerability to sudden death with chest wall impact (commotio cordis) [abstract]. J Am Coll Cardiol 2001;37(Suppl A):135A. 16. 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 1998;338:1805–11. 17. Naito M, Michelson E, Kaplinsky E, Dreifus L, David D, Blenko T. Role of early cycle ventricular extrasystoles in initiation of ventricular tachycardia and fibrillation: evaluation of the R on T phenomenon during acute ischemia in a canine model. Am J Cardiol 1982;49: 317–22. 18. Link MS, Maron BJ, Wang PJ, Pandian NG, VanderBrink BA, Estes NAM III. Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs. Pediatrics 2002;109:873–7.
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22.
23. 24.
25.
26.
27. 28.
29.
30.
31.
32.
33. 34.
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low-energy chestwall impact (Commotio cordis). Circulation 1999; 100:413–8. Link MS, Maron BJ, Wang PJ, VanderBrink BA, Zhu W, Estes NA 3rd ed. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol 2003; 41:99–104. Bode F, Franz M, Wilke I, Bonnemeier H, Schunkert H, Wiegand U. Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis. J Cardiovasc Electrophysiol 2006;17:1011–7. Van Wagoner D. Mechanosensitive gating of atrial ATP-sensitive potassium channels. Circ Res 1993;72:973–83. Abrunzo TJ. Commotio cordis: the single, most common cause of traumatic death in youth baseball. Am J Dis Child 1991;145: 1279–82. Link MS, Maron BJ, Stickney RE, et al. Automated external defibrillator arrhythmia detection in a model of cardiac arrest due to commotio cordis. J Cardiovasc Electrophysiol 2003;14:83–7. Samson RA, Berg RA, Bingham R. Use of Automated External Defibrillators for Children: an Update An Advisory Statement From the Pediatric Advanced Life Support Task Force, International Liaison Committee on Resuscitation. Circulation 2003;107:3250–5. Maron BJ, Estes NAM III, Link MS. Emergency treatment for commotio cordis. JAMA 2002;287:3080. ACC/AHA/ESC 2006 Guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. Online version at http://circ. ahajournals.org. Link MS, Maron BJ, Stickney RE, et al. AED utility in commotio cordis: a pediatric model of sudden death [abstract]. PACE 2001; 24:614. Weinstock J, Maron BJ, Song C, Mane PP, Estes NAM III, Link MS. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics 2006;117:1404–5. Doerer JJ, Haas TS, Mark NA, Estes NAM III, Link MS, Maron BJ. Evaluation of chest barriers for protection against sudden death due to commotio cordis. Am J Cardiol 2007;99:857–9. 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 2005;45:1371–3. http://www.nata.org/publicinformation/files/emergencyplanning. pdf Maron BJ, Mitten MJ, Greene Burnett C. Criminal consequences of commotio cordis. Am J Cardiol 2002;89:210–3.
© 2012 ICC
minor cutaneous bruise on the precordium. Retrospectively, it was thought to be a case of commotio cordis (CC). Commotio cordis is a condition which produces instantaneous death after a relatively minor hit on the precordium usually by a projectile such as hard balls played in different sports and games or by blows on the precordium which are otherwise appearing innocuous. The blows or hits are of sufficient intensity to induce ventricular fibrillation (VF) but not forceful enough to make visible injury to the myocardium or the thoracic cage.1 Although, the term and the condition was established a century before, it remained relatively obscure to the medical community.2 Earliest case reports can be traced to the 1870s from an Italian doctor Felice Meola and by a French surgeon Auguste Nelaton, but the most comprehensive studies in the past were done in the early 1930s by Georg Schlomka at Bonn University in Germany.3 In the seventies and eighties, there were several reports of such cases from North America4–6 that generated considerable interest in understanding, treating and preventing such an catastrophic event because of the tragedy involved and possibility of legal litigations.7 Much of the recent knowledge came from the report of Barry Maron and colleagues at the Minneapolis Heart Institute Foundation, MN, USA who described and analyzed 70 cases of CC.1 His subsequent works and contributions from MS Link and Mark Estes at Tufts-New England Medical Center at Boston, USA shed much light on different aspects of CC. The term CC means, in Latin, disturbance in the heart. Ferdinand Riedinger used the term CC to differentiate it from a more grievous injury that produces visible tissue damage to the thorax and the heart known as contusio cordis.3 Although, he used the term commotio thoracica, it became known to be as CC later. In 2001, Nesbitt et al defined CC as a mechanical stimulation of the heart by nonpenetrating, impulse-like impact to the precordium that, through intrinsic cardiac mechanisms, gives rise to disturbances of cardiac rhythm of varying type, duration, and severity, including sudden cardiac death, in the absence of structural damage that would explain any observed effects.3
Biswaranjan Mishra, MD DM*
ABSTRACT Instantaneous death after a relatively minor hit on the precordium is known as commotio cordis (CC). Mechanical stimulation of the heart by a nonpenetrating, impulse-like impact is sufficient to induce ventricular fibrillation (VF) in an otherwise normal heart, but not forceful enough to make structural damage to the myocardium or the thoracic cage. It is second to hypertrophic cardiomyopathy as a cause of sudden death in young individuals engaged in sport. When the blow on the chest coincide with the vulnerable period in the cardiac cycle produce a phenomenon similar to ‘R on T’ in premature ventricular complexes (PVC) resulting in VF. Two thirds of the events are sports related. Timing of the impact, hardness and speed of the projectile plays an important role in the pathophysiology of CC. Higher velocity projectiles may produce more severe injury resulting in tissue trauma but not CC. The site of impact on the chest is also crucial. It is the portion of the chest wall exactly overlying the left ventricle on the left of sternum which has to be struck to produce CC. Training persons involved in sports related activities in cardiopulmonary resuscitation and making defibrillators immediately available may prevent some deaths related to CC. Designing softer balls and protective devices may prevent although not eliminate CC. Keywords Cardiac arrest, commotio cordis, sudden cardiac death, sudden death in athletes, ventricular fibrillation
INTRODUCTION Recently, a teenaged school boy was brought to the hospital as he collapsed after a cricket ball hit him on the chest. The boy was fielding in a local cricket match. The ball hit his chest while he tried to take a catch from a straight hit by the batsman. He was declared brought dead in the hospital. A postmortem was ordered as a legal requirement. It was initially thought that probably the boy had some kind of undiagnosed congenital or primary myocardial disease as sudden death is not unusual during sport activities in young healthy individuals. Contrary to the presumption, the postmortem finding did not reveal any kind of cardiac disease, neither there was any injury to the heart nor was there any to the thorax except a
INCIDENCE Exact incidence of CC is unknown because of under reporting and low awareness of the condition. Early reports before 1970s are mostly from Europe and related to manual laborers and road traffic accidents in adults. As more cases started to be identified, it became known that it is much more common in children and adolescents and most often relates to sports, games and athletic activities.3 Sudden death in athletes is rare; it is estimated to be < 300 per year in > 10 million participants.8 Most of the deaths in athletes are due to underlying cardiac abnormality. In a US registry of sudden death in young competitive athletes, only 3% have normal heart.9 Seventy percent of reported cases are below the age of 16 years. Commotio cordis is second to hypertrophic
*Chief Consultant Cardiologist, Eko Imaging Institute, Cuttack, India. Correspondence: Dr. Biswaranjan Mishra, Chief Consultant Cardiologist, Eko Imaging Institute, Cuttack, India. E-mail: [email protected]
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of CC in soccer.11 The probable explanation is that hard core balls transmit energy to the chest directly after the impact, where as air filled balls collapse and itself absorb maximum of the energy without transmitting to the chest.11 Experimental models demonstrated that softer than normal baseballs reduced the chance of VF when compared to regular balls.18 Although, the speed of projectiles like hockey pucks can be very high up to 144 km/h (90 mph) but it takes only a modest speed to produce CC.1,16 Low-to-medium velocities in the range of 48–80 km/h (30–50 mph) is sufficient to induce VF but not enough to produce injury.19,20 Higher velocity projectiles may produce more severe injury resulting in tissue trauma but not CC which by definition does not have visible injury to the heart and thorax.15 When the velocity exceeds 80 km/h (50 mph), the probability of VF considerably decreases.21 The site of impact on the chest is also crucial. It is the portion of the chest wall exactly overlying the left ventricle on the left of sternum which has to be struck to produce CC.14 Part of the chest other than the portion lying over the heart did not produce VF in experimental models.19 When the hard projectile hits the precordium, the impact directly transmits the energy to the heart that abruptly raises the systolic pressure in the left ventricle and activates the mechanoreceptors present in the myocardial cell membrane which are stretch sensitive.22 Activation of mechanoreceptors in turn activates the K+ATP channels to open resulting in an inward current producing electrical inhomogenity. This phenomenon is known as mechanoelectric coupling. Data supports the susceptibility for VF due to inhomogeneous dispersion of repolarization occurring in the vulnerable period of the cardiac cycle at the time of impact.22 Mechanosensitivity of the K+ATP channels has been demonstrated in animal model.23 When critically timed, activation of these channels trigger VF leading to cardiac arrest.20 It is thought that more compliant chest wall in children with a short antero-posterior diameter is responsible for more direct transmission of energy to the heart which is responsible for the higher incidence of CC in children.11 Other mechanisms, proposed like coronary spasm or myocardial contusion consequent to sudden impact, are not established.13 In survivors, histological, serological, toxicological, and myocardial enzyme studies were consistently negative. Echocardiography revealed in some survivors a reversible wall motion abnormality. Coronary angiography did not reveal any spasm or thrombosis. Transient ST-segment elevations were noted in some survivors in anterior precordial leads, the mechanism of which is not understood.24 Echocardiographic analysis after the victim collapses irrespective of survival shows presence of other abnormalities like VT, idioventricular rhythm, complete heart block, and bradyarrhythmias in addition to VF.11
cardiomyopathy as a cause of sudden death in young individuals engaged in sport-related activities.10 To create a broader visibility, the United States Commotio Cordis Registry was initiated in 1996. It has acquired > 180 cases.11 In the registry, the mean age is 13.6 years, 95% are male out of which 87% are white. Only 16% survived the attack. Two-thirds of the events are sports related. Sixty-eight percent are from thrown projectiles such as baseball, hockey pucks, lacrosse ball, etc. or even by martial arts like karate. Most other cases are related to ordinary day-to-day and playful activities starting from parental discipline to friendly blows.11 There are reports of only two cases of cricket ball-induced CC in the US registry.11 Low incidence of cricket related CC may be because of the fact that cricket is less popular and played less often in United States. In India, the incidence of CC is unknown because of under reporting and under awareness of CC. The game of cricket has all the ingredients to cause CC. Therefore, the incidence may be quite high, particularly, in the present competitive form of cricket where players are more aggressive.
PATHOPHYSIOLOGY Meola, who first described CC, attributed the mechanism to autonomic disturbance causing intense vagal stimulation resulting in cardiac arrest.3,12 Experimental model by Link et al in anesthetized juvenile swine has immensely helped to comprehend the pathophysiology of CC.13 Through their model which closely mimicked the actual event, several aspects of the pathophysiology leading to CC were established. The most important aspect is about the timing of the impact. The blow on the chest must coincide the vulnerable period in the cardiac cycle that is just before or 15–30 ms before the peak of the T wave in surface echocardiography (ECG) to produce a phenomenon similar to ‘R on T’ in premature ventricular complexes (PVC).14–16 The potential for inducing VF when a PVC falls on the vulnerable portion of the T wave is well known.17 In the model of Link et al as the impact of the projectile stimulates the heart in the vulnerable period, it gives rise to VF.13 When the impact is not critically timed to the vulnerable period, it consistently did not produce VF but transiently produced other ECG abnormalities like complete heart block, bundle branch block, nonsustained polymorphic ventricular tachycardia (VT) and ST-elevation. In these experimental animals, immediately after the impact, coronary angiography did not show stenosis or spasm, myocardial perfusion imaging with technetium 99 m sestamibi revealed nonsignificant defects, left ventricular angiograms, and echo after the impact revealed mild apical or distal septal hypokinesia in some which were away from the site of impact.13 Hardness and speed of the projectile also plays an important role. Harder the projectiles, more likely it is to produce CC. Hardcore balls are much more likely to produce CC than air filled balls. In the US registry, there is only one case report JICC Vol 2 Number 2
MANAGEMENT Survival in CC is uncommon usually because of the delay in initiating cardiopulmonary resuscitation (CPR). Frequently, 90
© 2012 ICC
Commotio cordis: Are we aware?
training in CPR, and on early access to AED. It recommended for use of sport-specific chest protectors, use of softer balls, and training of athletes in avoiding being hit on the chest. Of all, it is most vital to create awareness and to educate all persons involved in sports, games, athletics including the participants, coaches, the authorities, and also the public in general regarding the possibility of such a devastating condition occurring as a consequence of trivial or innocuous appearing chest blows which in some instances cannot be even remotely thought of to be fatal. All should be aware of the ways to prevent it, and at the same time, remain prepared to treat it. Of particular importance is knowledge and practice of CPR, and at the same time, immediate availability and acquaintance in use of an AED. Innovation in designing and continued research in making effective chest barriers that can successfully prevent CC is required.
bystanders fail to understand the gravity of the situation because of lack of knowledge regarding CC. Cardiopulmonary resuscitation is rarely successful. Like any other cardiac arrest airway, ventilation and chest compression are to be taken care of. Early electrical defibrillation by an automated external defibrillator (AED) may be lifesaving. Delay in electrical defibrillation decreases the chance of survival. When resuscitation starts within 3 minutes, the chance of survival is > 50%. Every 1 minute delay decreases the chance to 10%. After 3 minutes, the chance falls to < 3%.11 In experimental models, defibrillation in one minute of VF is completely successful. After 2 minutes, survival falls to 80%. Success rate of defibrillation further falls to 46% after 4 minutes and to 25% after 6 minutes.25 Until recently, AEDs were not approved for use in children younger than 8 years or who weigh < 55 lb (25 Kg). 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 in 2003 recommending AEDs in children aged 1–8 years.26 Chest thump is a class IIb indication for adult CPR in the absence of a defibrillator, but not recommended in children by ILCOR. In CC, chest thump is a reasonable option when a defibrillator is not immediately available so long as it does not delay an electrical defibrillation.27 Post resuscitation medications should follow AHA guidelines.28
Legal Implications Commotio cordis is an electrical phenomenon related to a critically timed event that results from a seemingly innocuous impact on the precordium. It is never intentional. Due to the unexpected nature and the tragedy involved, there are instances of criminal charges and even convictions.34
CONCLUSION PREVENTION
Commotio cordis is a sudden unexpected death in young healthy persons which is devastating. The tragedy involved has wide social and legal ramification. It is being increasingly recognized particularly in North America. Most often it is related to games like baseball where the ball hits the victim on the precordium in the vulnerable period of the cardiac cycle but not with very high velocity. It is purely an electrical phenomenon as no appreciable injury occurs to the heart or thorax as confirmed from autopsy studies and experimental animal models. In India, description of CC is lacking as searched electronically. Cricket is one of the most popular games in India. Like baseball, cricket has all the substrate that can lead to CC. It uses a hard core ball and there is every possibility of a player being hit on the critical part of the chest in the critical time in the limit of speed that has every chance to produce CC. But, is it underreported due to lack of awareness or is it really uncommon? Other common games like hockey, kabadi, volley ball, different martial arts and athletic events all have the potential to cause CC. Besides, looking at the examples in US registry, where if trivial appearing harmless chest blows could produce CC, in India, where large number of people often live and travel in very crowded conditions, there is every possibility that such blows may be delivered quite frequently. Therefore, the potential for CC is very high. But is it underreported? We need to be more aware regarding the possibility of such a situation. Not only the medical fraternity but the public in general are to be educated in this regard. It is high time experimental models may be tested with conventional cricket balls for evaluating its potential to induce CC. ♦
Poor survival in CC underscores the importance of preventive measures. Training persons involved in sports related activities and also lay people in CPR and use of AED and making an AED immediately may prevent some deaths related to CC.29 Chest protection devices were developed to prevent structural chest injury and also to prevent CC but experimental models failed to show prevention of CC by these commercially available protection devices.30 In the US registry of CC, 40% deaths occurred despite use of protection devices.31 Therefore, it is imperative that new devices are to be designed particularly to prevent CC. As hardness of hitting projectiles is one of the important factors of the mechanism to produce CC, it is suggested that making regular balls softer may prevent CC. Experimental models have also shown that softer balls than normal as used in baseball is capable of preventing CC but not able to eliminate it.18 The 36th Bethesda conference made several recommendations for athletes regarding CC.32 It recommended for use of safety baseballs in children < 13 years. It also emphasized regarding immediate access to AED in sports venues. Recently, the National Athletic Trainers’ Association (NATA) of US made several recommendations for parents and coaches to take proactive steps to protect their athletes against CC. National Athletic Trainers’ Association’s Position Statement on Emergency Planning in Athletics is available in their website.33 It has emphasized on education of coaches, parents, officials, and players in the immediate recognition of CC, and also highlighted on JICC Vol 2 Number 2
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19. Maron BJ, Poliac L, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med 1995;333:337–42. 20. 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
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