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Commotio Cordis
Commotio cordis, a condition in which blunt force
trauma to the chest causes sudden cardiac arrest
without evidence of myocardial disease or injury, is
the third most common cause of cardiovascular death
in young athletes. This can be distinguished from a
cardiac contusion by the absence of structural damage
to the heart or its overlying structures. It has a wide
spectrum of clinical manifestations, and until approximately 15 years ago, it was unrecognized in the general population and medical community. Since then,
the National Commotio Cordis Registry in Minneapolis has recorded 224 cases with only 9 per cent of
those afflicted being older than 25.1 Here, we present
the case of a 16-year-old male who passed away as a
result of commotio cordis.
A healthy 16-year-old male arrived, via emergency
medical services, to the emergency room (ER) in full
cardiac arrest secondary to chest blunt force trauma.
The young man had been hit with a baseball after
a missed catch during practice. At the time, he was
wearing catchers gear including a chest protector.
After being hit, the young man complained of shortness
of breath and fell to the ground. Emergency medical
services were called and determined the young man was
unresponsive, pale, and devoid of any respiratory effort.
The patient was intubated at the scene and basic life
support was initiated. While in transport, the patient had
gone into ventricular fibrillation and was given four
shocks from an automated external defibrillator device.
On arrival to the ER, the patient was still in asystole,
despite resuscitation efforts. His Glasgow Coma Scale
score was determined to be a 3T, and no blood pressure
or pulse could be obtained. Advanced life support measures were continued in the ER including chest compressions, amiodarone, epinephrine, sodium bicarbonate,
atropine, and calcium chloride. During resuscitation efforts, cardiac monitoring showed intervals of ventricular
Address correspondence and reprint requests to Sahil Parikh, D.O.,
Department of Surgery, St. Josephs Regional Medical Center, 703
Main Street, Paterson, NJ 07053. E-mail: tobeyslame@gmail.com.

fibrillation along with agonal respirations. A defibrillator

was placed; however, it was not used due to the transient
nature of the arrhythmia. A focused assessment by sonography of the heart was done, which showed no cardiac muscle activity, no effective flow, and no evidence
of tamponade or effusion. Laboratory results drawn
after cardiopulmonary resuscitation and defibrillation returned with a Troponin of 0.354 ng/mL, and
a creatine kinase-MB fraction of 7.4 ng/mL. Approximately 75 minutes after arrival to the ER, the patient
was pronounced dead.
Due to its high mortality, commotio cordis is a rare but
serious complication of blunt force trauma in the pediatric
population. Survival after cardiopulmonary resuscitation
has only been reported in 25 per cent of cases in the national registry.1 Although several factors may contribute
to commotio cordis, the two main determinants are location and timing. In order for this phenomenon to occur,
the blow must be confined to an area directly over the
heart during the upstroke of the T-wave. This impact to
the heart leads to an increase in left ventricular pressure,
causing stretching of the myocardial cell membranes.
This, in turn, activates the stretch-sensitive ion channels
of the heart, resulting in an increase in dispersion of repolarization. In this state, the heart is more susceptible to
ventricular fibrillation.2 The results have been reproduced in a swine model and are reportedly due to the
potassium, adenosine triphosphate channels.3 The nature
of the injury leaves children more susceptible to commotio cordis. With a nonfully developed chest cage,
children incur the blunt of trauma without protection to
the internal organs. In addition to this, the increased incidence of blows to the chest in children result in higher
rates of commotio cordis in the pediatric population.
Due to the serious nature of commotio cordis, efforts
are underway to determine how to avoid the lethal effects of blunt force trauma. Primary prevention should
be aimed at the public awareness of such an entity,
thereby, limiting the number of direct blows to the chest
wall. Unfortunately, protective equipment has not been
shown to be effective in eradicating commotio cordis.1
Therefore, secondary prevention, such as the increased

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THE AMERICAN SURGEON

availability of automated external defibrillators, is of

the utmost importance. The devices are paramount to
recovery from shockable arrhythmias and can be used
by the layperson. Primary and secondary prevention
of commotio cordis will help turn a uniformly deadly
process into a more avoidable and less-refractory
condition.
Sahil Parikh, D.O.
Jennifer To, D.O.
Tameka Scott, D.O.
Carl P. Valenziano, M.D.

February 2012

Vol. 78

St. Josephs Regional Medical Center

Paterson, New Jersey
REFERENCES

1. Maron BJ, Estes M. Commotio cordis. N Engl J Med 2010;

362:91727.
2. Walker J, Calkins H, Nazarian S. Evaluation of cardiac arrhythmia among athletes. Am J Med 2010;123:107581.
3. 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 1999;100:4138.

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