Commotio Cordis Workup

  • Author: Steven M Yabek, MD, FAAP, FACC; Chief Editor: Stuart Berger, MD   more...
 
Updated: Mar 18, 2011
 

Laboratory Studies

  • In the past, findings from the workup of patients with commotio cordis (CC) have been limited mostly to postmortem studies on individuals who died as a result of the event. 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.
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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.
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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 cardiomyopathy have been found in any patients who survived commotio cordis.
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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 findings is uncertain.
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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.

Specialty Editor Board

Ira H Gessner, MD  Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

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.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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.

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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