Sudden death in sports is fortunately a rare occurrence. On November 22, 2002, I participated in the successful resuscitation of a young hockey player. Because the literature on management of blunt cardiac trauma in athletes is somewhat confusing, I felt that presenting our experience might assist others with clinical decision making.
The Canadian Hockey League (CHL) includes over 100 teams in Canada and the northern United States, with 25 players per team. They range in age from 16 to 20 years, but are serious athletes, playing a full 72-game schedule from September to May. It is estimated that 70% of National Hockey League players began their careers in Canadian Major Junior Hockey. Despite the number of hours spent in practice and games, I was unable to document a similar case in this league.
During the second period of a game with the Calgary Hitmen, one of our 17-year-old players was checked into the boards. The impact was not unusually forceful, but in this case the stick may have become trapped between his chest and the glass. His parents had come from Canada to watch their son play, and in retrospect his father thought that he seemed lethargic after the blow. He skated several more minutes, then came off the ice and complained of not feeling well. While sitting on the bench he had brief, generalized seizure activity, then fell backward. Our trainer threw a towel over the glass barrier, indicating an emergency, and I rapidly made my way down to assist. The player was found without pulse or respirations, so we quickly moved him into a hallway behind the stands and I began CPR with one of the resident physicians who accompany me to games. Our trainer ran to get the bag-mask ventilator and oxygen tank, but struck the valve on a doorway coming out of his office. For 10 minutes we simply alternated chest compressions with mouth-to-mouth ventilation, until a nurse from the first aid room brought our automated external defibrillator (AED). The player was found to be in ventricular fibrillation (Fig. 1), and a shock was delivered. It was unsuccessful, so we continued CPR. A total of four shocks were given, and at time mark 3:24 on the AED (roughly 14 minutes after the code began), the event in Figure 2 was recorded.
Paramedics arrived and established an intravenous line so medications could be given to stabilize his rhythm. He was breathing spontaneously and therefore not intubated. On arrival at the Emergency Department of a local hospital, he was awake and oriented with no recollection of the injury or subsequent events. His blood pressure was 127/78 mm Hg, with a pulse of 92 beats/min, and respirations of 22 breaths/min. Initial blood gas showed pH 7.25, pCO2 11 mm Hg, and pO2 495 mm Hg with a nonrebreather mask. Electrocardiography demonstrated inverted T waves in the anterolateral leads, suggestive of ischemia. The chest radiograph revealed bibasilar atelectasis, and computed tomography head scan was negative. All other laboratory tests were normal, except for a leukocyte count of 10,800 / mm3.
Initial cardiac enzymes included a creatine phosphokinase (CPK)-MB of 3.6 ng/mL, and troponin-I of 1.4 ng/mL. He was admitted to the hospital and underwent cardiac catheterization that demonstrated apical akinesis, with normal coronary arteries. Transthoracic echocardiogram (TTE) revealed an ejection fraction of 45%, with global hypokinesis, and dyskinesis of the distal apex. His CPK-MB peaked in 72 hours at 58.4 ng/mL (total CPK of 18,502 IU/L), and the maximum troponin-I was 10.4 ng/mL. TTE at that time showed an ejection fraction of 50% to 53% with normal global function, but hypokinesis of the apex.
After several cardiology consultations, it was decided to place a Guidant (Indianapolis, IN) automatic implanted cardioverter defibrillator (AICD) in a subpectoral pocket, to maximize the likelihood that he could play again. The wires were routed such that he could still do a bench press (important in hockey) and shoot, without kinking them. I subsequently consulted with Lon Castle of the Cleveland Clinic, and cardiology consultant to the National Football League. He felt that this was an isolated incident, and probably would not have placed the AICD, but also could not fault our conservative approach. A follow-up echocardiogram was normal, and he was transitioned back into training. His device did discharge once a few months later, but on interrogation he had simply exceeded the programmed maximal heart rate of 200 beats/min while skating aggressively. He has since retired from the sport, and apparently experiences vague chest pain with exercise.
There is a large body of literature concerning the catastrophic consequences of high-speed chest trauma from motor vehicle accidents, but those injuries are rarely seen in sports. The most significant sequelae of low-impact blunt thoracic trauma are commotio cordis (cardiac concussion), and contusio cordis (cardiac contusion). In the literature, these diagnoses are used almost interchangeably, which makes comparing and contrasting studies difficult . I believe part of the problem is that many of these patients don't come to the attention of clinicians unless they present with collapse, or sudden death.
Cardiac contusion implies a bruising of the heart muscle, and usually involves the right ventricle or septum. There is release of cardiac enzymes (CPK-MB, troponin-I), and electrical disturbance such as ST-segment elevation, sinus tachycardia, extra-systoles, right bundle branch block, or variable atrioventricular block. Transient ventricular tachycardia is occasionally seen, but ventricular fibrillation is uncommon. The athlete usually recovers rapidly without sequelae, and as such the actual incidence is unknown .
Commotio cordis (CC) is defined as a cardiac concussion, and like its cerebral counterpart, results in significant electrical disarray without any structural damage. It was probably first reported by Meola in 1879, who described a patient who collapsed after being struck in the chest with a stone . Since then, the US Commotio Cordis Registry (Minneapolis, MN) has documented 128 cases, and estimates that two to four occur each year. Baseball accounts for 57% of the total, followed by softball (10%), hockey (10%), football (4%) and soccer (4%). Data from the US Products Safety Commission reveal that blunt chest injury is the number one cause of traumatic death in baseball players between the ages of 5 and 14 years.
In the landmark work of Link et al. , wooden projectiles roughly the size and weight of baseballs were fired at the chest of pigs. With a velocity of 30 mph, impact over the precordium during the most vulnerable phase of ventricular repolarization (15–30 msec before peak T-wave) induced fibrillation in 90% of cases. Those that missed the precise location, or arrived at a different phase of the cardiac cycle, produced asystole or other arrhythmias. The refractory nature of treating such aberrant rhythms may account for a clinical impression that these patients are resistant to resuscitation. The pathophysiology is believed to involve activation of a normally dormant K+ ATP channel, which renders the myocardium unstable. The chest wall biomechanics of young athletes (95% of cases were male) are likely a contributing factor, with narrow anterior-posterior diameter, and greater compliance . In humans, the rate of survival is roughly 15%, but all of those regain normal cardiac activity. Some patients demonstrate transient left ventricular systolic dysfunction, or a limited area of hypokinesis that usually resolves in a few days .
Our case exhibits many features common to both of these conditions, and highlights the confusion in making a diagnosis. Was this cardiac contusion in an athlete who refused to stop skating, or did commotion cordis precipitate the ventricular tachycardia, and ultimately fibrillation? Hockey players usually don't complain about injuries, and the electrical events during his resuscitation erased any memory of antecedent symptoms. Fortunately, the principles of management remain the same. Athletes who collapse after a blow to the chest obviously require immediate CPR. Data from animal (swine) experiments reveals that survival with CPR initiated in less than 3 minutes is 25%, and drops to 3% if started later. Electricity is really the definitive treatment, and in pigs defibrillated within one minute, there was 100% survival. If defibrillation were delayed 2 to 4 minutes, survival decreased to 80%, and after 4 minutes none were saved. With CPR initiated immediately (as in our case), and then shocks delivered after 4 minutes, survival was 65%. Successful resuscitation in athletes is uncommon, but according to the CC registry, 74% of survivors had CPR initiated within 1 minute. Athletes struck in the chest that do not immediately collapse should be monitored for 24 hours, because fatal arrhythmias usually occur within that time period . They should have serum troponin-I (more sensitive than troponin-T) measured, and undergo a transesophageal echocardiogram (TEE) to evaluate cardiac function. Heart catheterization is rarely necessary .
The real key to survival is prevention, including adequate protective equipment, and softer baseballs for young athletes. In Link's studies with pigs, replacing the wooden disc with a regulation baseball reduced the likelihood of precipitating fibrillation from 90%, to just 35%. When the missile was a softer baseball, fatal arrhythmia could only be induced 8% of the time. Chest protection is essential, because one third of reported cases involve collision with another player or inanimate object, such as a stick. We were fortunate in our outcome, and this case helped raise awareness of blunt chest trauma across Canada, and the northern United States. Now every team in the CHL travels with an AED, and personnel are trained in its use. Parents and coaches of Little League baseball players must be aware of this rare, but often fatal condition, so that they might act appropriately in an emergency. They need to understand that CPR works in a young, healthy population, and include the use of an AED in their training.
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