eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Commotio Cordis: Differential Diagnoses & Workup

Author: Steven M Yabek, MD, FAAP, FACC, Pediatrix Cardiology Associates of New Mexico (a Division of Mednax Medical Group), Presbyterian Hospital Medical Center
Contributor Information and Disclosures

Updated: Sep 4, 2009

Differential Diagnoses

Anomalous Left Coronary Artery From the Pulmonary Artery
Cardiomyopathy, Hypertrophic
Long QT Syndrome
Myocardial Infarction in Childhood
Myocarditis, Viral
Ventricular Fibrillation

Workup

Laboratory 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 commotio cordis. In general, patients who experience an episode of commotio cordis 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 commotio cordis are also 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 commotio cordis almost always shows an anatomically and functionally normal heart. No evidence is found for any of the underlying cardiac conditions (eg, hypertrophic cardiomyopathy, anomalous origin of a coronary artery from the wrong sinus, aortic root disruption) 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 commotio cordis 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

  • 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 commotio cordis 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 commotio cordis 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 commotio cordis. These latter ECG findings, which last only 2-3 days, are remarkably similar to what was noted in the commotio cordis 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 commotio cordis.

Histologic Findings

  • Data from many autopsy examinations of patients who died as a result of commotio cordis 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 cardiomyopathy has not been reported. 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.

More on Commotio Cordis

Overview: Commotio Cordis
Differential Diagnoses & Workup: Commotio Cordis
Treatment & Medication: Commotio Cordis
Follow-up: Commotio Cordis
Multimedia: Commotio Cordis
References
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References

  1. Maron BJ. Sudden death in young athletes. N Engl J Med. Sep 11 2003;349(11):1064-75. [Medline].

  2. 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].

  3. Maron, BJ: Clinical Features of Commotio Cordis. Presentation of Registry Data at Heart Rhythm Society Scientific Sessions [database online]. Boston, Massachusetts: May 15, 2009.

  4. Animal Model of Commotio Cordis: Presentation at Heart Rhythm Society Annual Scientific Sessions [database online]. Boston, Masachusetts: Link MS; May 15, 2009.

  5. 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].

  6. Amir O, Schliamser JE, Nemer S, Arie M. Ineffectiveness of precordial thump for cardioversion of malignant ventricular tachyarrhythmias. Pacing Clin Electrophysiol. Feb 2007;30(2):153-6. [Medline].

  7. 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].

  8. Drezner JA, Chun JS, Harmon KG, Derminer L. Survival trends in the United States following exercise-related sudden cardiac arrest in the youth: 2000-2006. Heart Rhythm. Jun 2008;5(6):794-9. [Medline].

  9. [Guideline] Drezner JA, Rogers KJ. Sudden cardiac arrest in intercollegiate athletes: detailed analysis and outcomes of resuscitation in nine cases. Heart Rhythm. Jul 2006;3(7):755-9. [Medline].

  10. Osoria J, Dosdall DJ, Robichaux Jr RP, Tabereaux PB, Ideker RE. In a Swine Model, Chest Compressions Cause Ventricular Capture and, By Means of a Long-Short Sequence, Ventricualar Fibrillation. Circ Arrhythmia Electrophysiol. 2008/10;1:282 - 9.

  11. 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].

  12. Futterman LG, Lemberg L. Commotio cordis: sudden cardiac death in athletes. Am J Crit Care. Jul 1999;8(4):270-2. [Medline].

  13. Link MS, Bir C, Dau N, Madias C, Estes NA 3rd, Maron BJ. Protecting our children from the consequences of chest blows on the playing field: a time for science over marketing. Pediatrics. Aug 2008;122(2):437-9. [Medline].

  14. Link MS, Estes NA 3rd. Mechanically induced ventricular fibrillation (commotio cordis). Heart Rhythm. Apr 2007;4(4):529-32. [Medline].

  15. Link MS, Ginsburg SH, Wang PJ, et al. Commotio cordis: cardiovascular manifestations of a rare survivor. Chest. Jul 1998;114(1):326-8. [Medline].

  16. 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].

  17. 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].

  18. Maron BJ, Gohman TE, Kyle SB. Clinical profile and spectrum of commotio cordis. JAMA. Mar 6 2002;287(9):1142-6. [Medline].

  19. 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].

  20. 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].

  21. Vincent GM, McPeak H. Commotio cordis: a deadly consequence of chest trauma. Phys Sportsmed. Nov 2000;28(11):31-9. [Full Text].

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Further Reading

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Keywords

commotio cordis, CC, low-impact chest trauma, cardiac concussion, ventricular fibrillation, cardiac arrest, sudden cardiac death, myocardial infarction, heart attack, anomalous origin of a coronary artery, hypertrophic cardiomyopathy, congenital prolongation of the QTc interval, asystole, automated external defibrillators, AED, blunt chest impact, precordium, arrhythmogenic right ventricular cardiomyopathy, primary electrical disorders, catecholaminergic ventricular tachycardia, primary electrical phenomenon, coronary artery vasospasm, myocardial contusion, precordial trauma, trauma to the precordium, precordial thump, precordial blunt trauma, treatment, diagnosis

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Contributor Information and Disclosures

Author

Steven M Yabek, MD, FAAP, FACC, Pediatrix Cardiology Associates of New Mexico (a Division of Mednax Medical Group), Presbyterian Hospital Medical Center
Steven M Yabek, MD, FAAP, FACC is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, New Mexico Pediatric Society, Society for Pediatric Research, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Ira H Gessner, MD, Professor Emeritus, Pediatric Cardiology
Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Hugh D Allen, MD, Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine
Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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