Severe Anoxic Brain Injury From Blunt Chest Trauma: A Case Study Involving Commotio Cordis As an Etiology of Systemic Anoxia

By Lue, Aurora Bapineedu, Kuchipudi; Sori, Alan J; Fares, Louis II

To the Editor: I am writing about a case which involved a 14- yearold boy who was brought to our Trauma Center via ambulance unresponsive and intubated after he collapsed during a baseball game after being struck in the chest. He was the pitcher at the game and received a hard line drive to the chest. After a few seconds he collapsed and was assessed by a dentist in attendance as being cyanotic and pulseless. CPR was promptly initiated. An automated external defibrillator was reported to be on site but never implemented during the confusion. On arrival of the paramedics, the child was assessed and noted to have vomitus within the oropharynx, a lack of spontaneous breathing, and no pulse. He was subsequently intubated without any use of sedatives or paralytics. The electrocardiograph on the portable defibrillator revealed ventricular fibrillation. He then received an electric shock of 200 Joules and another 100 Joules for pulseless ventricular tachycardia that finally converted his arrhythmia to normal sinus. During the process he received both epinephrine and lidocaine intravenously. By this time, approximately 6 to 8 minutes had elapsed since he first collapsed.

In the trauma room, the child was connected to a ventilator and was found to be unresponsive but hemodynamically stable. Physical examination disclosed reactive pupils consistent with anisocoria with the left pupil (4 mm) being slightly larger than the right (3 mm), and a large erythematous discoloration was evident on his chest. The area of injury over the precordial area measured approximately 5 x 5 inches and was located to the left of his sternum (1 inch) and medial to his left nipple (1 inch). Cardiovascular rubs and murmurs were absent while pulmonary rales were detected. The Babinski reflex was also absent and upon insertion of a nasogastric tube no gag reflex was elicited. The child did not open his eyes and portrayed decorticate movements in response to pain. Apart from this, no other physical abnormalities were discovered. All initial laboratory tests, except the EKG recording of right bundle branch block in leads I, III, Vl and V2, were within normal limits. A FAST (Focused Assessment with Sonography for Trauma) exam confirmed the absence of a pericardial effusion and a preliminary echocardiogram lacked any structural abnormalities in either of the ventricles, chordae tendinae, or valves, only mild dyskinesia. CT scans were consistent with systemic anoxia and pulmonary aspiration. There was diffuse cerebral edema with small ventricles, massive pulmonary infiltrates and edema bilaterally, and ischemic viscera causing shock bowel and shock liver. An arterial blood gas confirmed metabolic acidosis.

The patient was admitted to the pediatric intensive care unit with a diagnosis of severe anoxic brain injury secondary to commotio cordis and a course of mannitol and fosphenytoin was initiated. On the second day of admission, the right bundle branch block resolved and T wave inversions developed in leads V3-V5. His cardiac enzymes increased dramatically from a TnI of 1.7 to 44.7, a creatinine kinase (CK) of 231 to 922 and a creatinine kinase MB (CKMB) of 13.5 to 75.7 and 6 days later normalized to 0.1, 598, and 1.1 respectively. A formal echocardiogram was performed and verified the absence of any mechanical or structural abnormalities. The patient’s neurological status improved slightly and he was placed on midazolam for increased agitation. A repeat CT scan on the third day of admission showed a decrease in cerebral swelling and more prominent sulci. Neurological assessment exhibited flexion and eye opening in response to pain and a positive gag reflex. In contrast, an MRA performed on the sixth day of admission was conclusive for hypoxia and ischemia with loss of the gray and white matter differentiation. Unfortunately the patient did not fully recover and the decision for a tracheostomy, feeding tube, and rehabilitation was facilitated. Eight months after the incident, his motor and verbal skills have improved although he is still unable to fully express himself and experiences spastic muscle movements.

The exact pathophysiology of commotio cordis is unknown. Link et al.1 proposed a vascular model in 1998 and hypothesized that the transient nature of abnormalities such as cardiac enzymes, ST elevation, complete heart block, and left bundle branch block, was possibly secondary to coronary artery vasospasm. However, in 1999, they furthered their investigation and demonstrated that the underlying cause of the cardiac disturbance was instead due to the activation of cardiac ATP-dependent K+ channels.2 These channels are normally inactive and inhibited by ATP but become active in cases of hypoxia such as myocardial ischemia due to the reduction in the ATP/ ADP ratio. The study demonstrated a dramatic reduction in ventricular fibrillation secondary to commotio cordis when the channels were chemically blocked. Nevertheless the experiments were conducted using juvenile swines which raised questions regarding the differences in physiology and anatomy.

Analysis of the 128 cases reported in the United States Commotio Cordis Registry in 2001 revealed a broad spectrum of ages ranging from 3 months to 45 years.3 Although emphasis has been made on Little Leagues, these concerns are not unfounded with 44 per cent of cases being 12 years or younger versus 22 per cent who were 18 years or older.3 Investigation into the possibility of protective gear for those high-risk individuals such as athletes exposed to projectile objects (including physical contact) has lead to much resistance. Athletes cite the cumbersome and impractical nature of heavy pads and strict dress codes preventing them from using any unauthorized equipment. Although rare, occurrence of commotio cordis remains the second leading cause of death in young athletes (95% male),3 justifying a concerted effort to better protect athletes from preventable cardiopulmonary arrest. Survival rates drop significantly from 25 per cent to 3 per cent when CPR and defibrillation are delayed for over 3 minutes.4

In conclusion the minimum recommendation should be the presence of an automated external defibrillator at every sporting event with at least one ACLS/BCLS certified supervisor in attendance. Incidents involving commotio cordis often draw much attention and concern as children are the victims. This in turn has lead to an increase in public awareness about the dangers of commotio cordis. As of July 7, 2007, as a direct result of this case, within the state of New Jersey the use of all types of metal bats have been banned from baseball and softball games for children under the age of 18.5 Investigations showed that balls struck using aluminum bats had a much greater velocity when compared to wooden bats6 making it difficult for children who have slower reaction times, to avoid impact. However, though this restriction may have some positive results, it is too early at this time to be sure.


1. Link MS, Ginsburg SH, Wang PJ, et al. Cardiovascular manifestations of a rare survivor. Chest 1998;114:326-8.

2. Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the K+ATP channel as a mechanism by which sudden death is produced by low energy chest-wall impact (commotion cordis). Circulation 1999;100:413-8.

3. Maron BJ, Gohman TE, Kyle SB. Clinical profile and spectrum of commotio cordis. JAMA 2002;287:1142-6.

4. Salib EA, Cyran SE, Ciley RE, et al. Efficacy of bystander cardiopulmonary resuscitation and out-of-hosptial automated external defibrillation as life-saving therapy in commotion cordis. Journal of Pediatrics. 2005;147:863-6.

5. Assembly No. 3388. State of New Jersey, 212th Legislature. Introduced June 26, 2006. Available at: http://www.njleg.state

6. Greenwald RM, Penna LH, Crisco JJ. Differences in batted ball speed with wood and aluminum baseball bats: A batting cage study. Journal of Applied Biomechanics 2001;17:241-52.

Address correspondence and reprint requests to Aurora Lue, M.D., 361A South Huntington Avenue Unit 1, Jamaica Plain, MA 02130. E- mail: [email protected]

Aurora Lue, M.D.

Kuchipudi Bapineedu, M.D.

Alan J. Sori, M.D.

Louis Fares II, M.D.

Seton Hall University School of Graduate Medical Education

St. Joseph’s Regional Medical Center

Level Il Trauma Center, Paterson NJ

St. Francis Medical Center, Trenton NJ

Copyright Southeastern Surgical Congress Jul 2008

(c) 2008 American Surgeon, The. Provided by ProQuest LLC. All rights Reserved.

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