that his chest hurt yesterday during a coughing spell. Upon physical examination, there was mild tenderness in the area of the right sixth through eighth ribs laterally that was more pronounced in the intercostal segments than over the ribs themselves. Pain also was reproduced with side-bending to the left. After negative plain radiographs, he was diagnosed with strained intercostal muscles, a common phenomenon after excessive muscular activity of the upper limbs and trunk. He was given a 2-wk course of nonsteroidal anti-inflammatory drugs, counseled to refrain from swinging for at least a week, and prescribed a course of physical therapy. Within 3 wk, he was back to full, pain-free activities. Key Point: Intercostal muscle strain symptoms are reproduced with forceful contraction, passive stretching, and palpation and improve with rest and conservative care. References 1. Gregory PL, Biswas AC, Batt ME. Musculoskeletal problems of the chest wall in athletes. Sports Med. 2002; 32:235Y50. 2. Saleeb SF, Li WY, Warren SZ, Lock JE. Effectiveness of screening for lifethreatening chest pain in children. Pediatrics. 2011; 128:1062Y8. 3. Sert A, Aypar E, Odabas D, Gokcen C. Clinical characteristics and causes of chest pain in 380 children referred to a paediatric cardiology unit. Cardiol. Young. 2013; 23:361Y7.

Syncope in Athletes of Cardiac Origin: 2B. From Personal History and Physical Examination Sections Francis G. O’Connor, MD, MPH, FACSM and Benjamin Levine, MD Personal History: Have You Ever Nearly Lost or Actualy Lost Consciousness? The History To determine the importance of a positive answer to this question, the following questions should be asked:

1. Did the syncopal event occur during or immediately after exercise; if the latter, was the patient standing still or moving around? 2. Prior to the syncopal event, were there any prodromal symptoms such as the following: chest pain, palpitations, visual changes, wheezing/shortness of breath, nausea, or itching? 3. After the syncopal event, what was the patient’s postevent clinical status? Did they wake quickly, or was there a prolonged period of unresponsiveness? Was there any observed seizure activity or loss of urine, stool, or tongue bite marks? Were there vital signs recorded on site, particularly the immediate postsyncope measurements? 4. What medications and supplements were being utilized prior to the event? 5. Is there a prior personal or family history of syncope or of sudden cardiac arrest/death? The evaluating physician’s first priority is to use the clinical history to distinguish between true syncope involving a loss of 254

Volume 14 & Number 3 & May/June 2015

consciousness with presumed hemodynamic compromise and exercise-associated collapse associated with exhaustive effort or postexercise hypotension. In true syncope from hemodynamic causes, the athlete typically recovers quickly with restoration of arterial pressure, unless resuscitation is required. After collapse associated with an exhaustive effort, however, athletes usually will have prolonged periods of ‘‘being out of it,’’ even in the supine position with normal heart rate and BP. This picture is in contrast to patients with syncope due to heat stress who are universally hypotensive and tachycardic. Athletes who are impaired, seeming ‘‘unconscious,’’ but able to assist in their own evacuation are unlikely to be in the throes of a life-threatening arrhythmia, although other metabolic or catastrophic abnormalities are possible (e.g., hyponatremia, exertional heat stroke). The postevent state provides important clues such as seizure activity, incontinence, and immediate vital signs (including body temperature). It must be emphasized however, that a seizure-like activity can be the result of reduced cerebral perfusion and therefore does not always imply epilepsy or neurologic problems. Reports from witnesses can be invaluable. Too often, syncope is assumed to be neurologic and the cardiac evaluation is not done, resulting in fatal outcomes. The second critical distinction is whether the event occurred during or immediately after exercise. Orthostatic hypotension occurring after exercise, usually associated with sudden cessation of activity, is much less ominous than the sudden loss of consciousness that occurs during exercise, which suggests cardiac arrhythmia with loss of blood flow to the brain. Syncope prompted by an abrupt loud noise such as a starting gun or immersion in cold water may provide a clinical clue to prolonged QT syndrome (LQTS). The third component of the history that provides clinical clues is a detailed assessment of events prior to the collapse. Prodromal symptoms such as palpitations (suggesting arrhythmia), chest pain (ischemia, aortic dissection), nausea (ischemia, high levels of vagal activity, or hyponatremia), wheezing, and pruritus (anaphylaxis) are significant, along with precipitating events like ‘‘only during exercise.’’ It is important to identify whether syncope occurs in the upright position (orthostatic hypotension) alone or also when sitting or supine (arrhythmia or nonhemodynamic cause). The fourth component of the evaluation requires assessment of the medication and supplement history. A comprehensive medication list, including over-the-counter medications and ergogenic aids is necessary; the practice of high-risk behaviors, such as recreational drug use should be carefully investigated. Finally, a personal and family history of sudden death is critical and, if present, may identify very high-risk subgroups with hypertrophic cardiomyopathy (HCM), LQTS, or right ventricular cardiomyopathy. Delineating a family tree will give a complete snapshot of the family history.

The Physical Examination Vital signs (including orthostatic measurements) should be included. Blood pressure (BP) should be measured in both arms and legs as well as after 5 min of moving to a standing position. Cardiovascular Preparticipation Evaluation

Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.

Special Tests/Referral The three tests that are core to the diagnostic evaluation of the athlete with syncope include the electrocardiogram (ECG), the echocardiogram, and the exercise stress test. Echocardiography should precede the exercise test, allowing the assessment of ventricular size and function, pulmonary pressures, and valve function/integrity. Rather than a standard Bruce protocol, a maximal symptom-limited exercise test should be used to reproduce the conditions that provoked the syncopal event. For example, a stuttering startstop test for a basketball or soccer player or a prolonged high-intensity race pace test for a runner. The exercise ECG also should be examined for appropriate shortening of the QT interval. Further testing should be ordered only as indicated and in consultation with the appropriate specialist. A complete review of all the advanced diagnostic tests is beyond the focus of this article. Tilt table testing should not be used in the syncope evaluation because of the high rate of false positive tests due to the steep Starling curve in athletes. The clinician is additionally reminded that not all syncope is cardiogenic. Athletes whose history suggests seizure activity may require an electroencephalogram and magnetic resonance imaging (MRI) of the brain to exclude a structural lesion, and seizures can be related to hyponatremia or heat stroke. Hematologic and metabolic abnormalities require testing as indicated, e.g., hypoglycemia in those with diabetes, athletes with eating disorders, or patients on beta-blockers. CASE EXAMPLES Case 1: Cross-Country Runner with Collapse at the Finish Line A 17-year-old female track star was competing in the district championships in the 5,000 m. She was having an excellent race and was part of the final pack that was in contention for a medal. Just after crossing the finish line (in 17 min 55 s), she collapsed to the ground and, according to bystanders, remained ‘‘unconscious’’ for about an hour. ECG, echocardiogram, and Holter monitor testing results were normal, although she did not faint during the period of recording. An athlete-specific exercise test was performed on a large treadmill at 10 mph; after 10 min, the patient started to cry and then slumped in the safety harness. At the moment of fainting, her rhythm was normal, pulse was 185 bpm, and BP was 140/70. The final impression was exercise-associated collapse, and the recommendation was better training and pacing to match demands of her sport. Key Point: History pointed away from life-threatening arrhythmia; athlete-specific exercise testing reproduced the problem during direct electrical and hemodynamic monitoring, allowing an accurate diagnosis. Case 2: Basketball Player with Collapse on the Free Throw Line A 21-year-old male college basketball star led a 12-point run, mostly by a series of impressive fast breaks, in the middle of the first half of an early round of the National Collegiate Athletic Association tournament. After the last www.acsm-csmr.org

jam, he was fouled and walked to the foul line. While standing waiting to shoot, he slumped to the ground. Witnesses observed generalized seizure activity. ECG showed LVH and unusual T waves in the right precordial leads, but his echocardiogram result was normal and short-term Holter monitoring did not identify any arrhythmias, although no symptoms occurred during the monitoring period. A stuttering exercise test was performed at high speed (15 mph) followed by sudden stops. After the fifth repeat, while standing quietly, there was a sudden drop in pulse to 45 bpm, BP was 60/40, and the patient fainted on the treadmill. The final diagnosis was postexercise hypotension (neurally mediated syncope). The recommendation was behavioral modification (avoid standing still if possible, learn leg crossing/butt clenching and toe bouncing maneuvers, stay well hydrated, and wear compression socks). Key Point: Standing still after intense exercise can lead to hypotension due to loss of the muscle pump and lead to neurally mediated syncope with bradycardia and hypotension. Athlete-specific exercise testing elicited the problem and led to simple, effective, nonpharmacologic therapy. Case 3: Football Player with Collapse while Running out for a Pass A 19-year-old male wide receiver for a junior college football team was running a crossing pattern during practice when witnesses observed him to weave, stumble, and fall to the ground. The trainer arrived at the scene to find him alert and oriented. His BP was 135/80; pulse was 110 bpm and regular. Physical examination result was normal; however, ECG results showed septal Q waves, LVH, and deep T wave inversions. Echocardiogram results showed a septal thickness of 1.8 cm, although without systolic anterior motion of the mitral valve. Holter monitoring revealed multiple runs of NSVT, and cardiac MRI showed multiple areas of delayed enhancement. The diagnosis was HCM; he was held from competition, and family members were screened for HCM. Key Point: Syncope during exercise is very concerning for an arrhythmia and underlying structural heart disease. Case 4: Lacrosse Player with Syncope during Exercise A lacrosse player had syncope while running wind sprints. Careful history examination documented that the syncope occurred during a sprint and not between sprints. ECG results showed nonspecific ECG changes, but the echocardiogram result was normal. The exercise test result was normal; cardiac MRI was performed and showed patchy areas of delayed enhancement indicating potential myocarditis. An electrophysiology (EP) study induced atrioventricular nodal reentrant tachycardia (AVNRT) but no ventricular arrhythmias. A 24-h Holter monitor showed no arrhythmias. The athlete had a major game coming up, and there was pressure to allow him to play. The patient had ablation of the AVNRT and was allowed to return to sports. He died in practice the following week. Key Point: The worrisome history plus noncoronary distribution of delayed enhancement on MRI are concerning for myocarditis. The conservative approach would have been Current Sports Medicine Reports

Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.

255

to treat with a beta-blocker and angiotensin-converting enzyme inhibitor, hold out of sports for at least 3 to 6 months, perhaps implant an implantable loop recorder so that a specific diagnosis could be made if another episode of syncope occurred, and then repeat the MRI looking for resolution of delayed enhancement. Pressure to play (athlete, coach, and parent) can influence medical decision making and steer the decision away from the athlete’s best interest. Case 5: A 23-year-old male second-year medical student completed a maximal-effort Wingate test as part of a research project; prior V˙O2max testing demonstrated a maximum of 55 mLIkgj1Iminj1. Immediately after the 30-s test, the student was extremely nauseous and rapidly exited the bike to move to a trash can to vomit; after two short wobbly steps, he collapsed to the ground. He was attended to immediately by the exercise staff in attendance; he had an estimated loss of consciousness for less than 30 s and had a first set of vital signs of heart rate of 140 bpm and BP of 110/60. There was no observed seizure activity and no prior complaint of chest pain. A subsequent evaluation in the sports medicine clinic demonstrated normal clinical examination results with no history of syncope; ECG results demonstrated early repolarization variation in the precordial leads. As the syncopal event occurred immediately after exercise, a treadmill stress test and echocardiogram were performed; the student completed 17 min of Bruce protocol and had a normal echocardiogram results. The diagnosis was postexertional syncope secondary to orthostatic hypotension. Key Point: Syncope during or immediately after exercise is always concerning and warrants conscientious examination to rule out structural cardiovascular disease. Intense anaerobic exercise, which can be seen in maximal efforts like the Wingate test or weightlifting, can precipitate syncope through orthostatic hypotension and a central effect of hypocapnia leading to, or aggravating, cerebral hypoperfusion. The history of the event provides not only insight into the diagnosis but also important opportunities for prudent recommendations for prevention.

Syncope in Athletes of Neurological Origin: 2B. From Personal History and Physical Examination Sections Chad A. Asplund, MD, MPH, FACSM and Jeffrey S. Kutcher, MD Personal History: Have You Ever Nearly Lost or Actually Lost Consciousness? The History (Regarding Neurologic Causes) To determine the importance of a positive answer to this question, the following questions should be asked for each episode of loss of consciousness:

1. Was consciousness completely lost? If so, for how long? 2. Was head trauma involved? 256

Volume 14 & Number 3 & May/June 2015

3. Was the episode witnessed? What did observers say happened? 4. Was a convulsion involved? If so, what was the duration of the convulsion and how long was the postictal period? 5. Was the episode preceded by fear, pain, prolonged standing, psychologic stress, or a medical procedure? 6. Was the episode preceded by a headache or visual symptoms? 7. Was the episode preceded by heart palpitations, lightheadedness, or tunnel vision? 8. Was the episode concurrent with the use of medications, performance enhancing substances, or illicit drugs? The first priority in the evaluation of a patient with history of loss of consciousness begins with thorough and directed history examination. It is imperative that the evaluator differentiate true syncope with transient loss of consciousness from presyncope, where consciousness is not lost. Presyncope is rarely caused by neurologic disease alone and may be a manifestation of cardiac disease, anxiety, or the side effect of a medication or supplement. If there is any concern for cardiac etiology, then at a minimum, an electrocardiogram should be performed before the neurologic evaluation continues. The second priority of the history examination is to focus on circumstances immediately before the event, the onset, the event itself, and the postevent period. Various aspects surrounding the event may help establish the diagnosis. A prodrome, postsyncopal fatigue, amnesia, or focal neurologic deficits will point the evaluator toward a neurogenic cause. Episodes of neurally mediated syncope are typically associated with postepisode fatigue and weakness, whereas the absence of a prodrome is more consistent with cardiac arrhythmia. Sensory auras, de´ja` vu or jamais vu, postictal confusion, or focal neurologic signs or symptoms all suggest a neurologic cause. Head trauma preceding loss of consciousness is highly suggestive of brain injury, such as concussion, cerebral contusion, or intracranial hemorrhage. Next, the observations of witnesses may be extremely helpful. Preevent behaviors, such as unresponsiveness or automatisms, are suggestive of seizure, as is tonic-clonic, convulsive activity. It is important to recognize that seizurelike activity that occurs prior to loss of consciousness or postural tone is more consistent with seizure while a convulsion that occurs after the patient has fallen to the ground may be the final common manifestation of cerebral hypoperfusion. Incontinence of bowel or bladder does not reliably differentiate neurologic from cardiac causes. Finally, medical history can be very helpful. History of psychologic or psychiatric disorders may point to a nonorganic cause of syncope such as a conversion disorder. History of migraine headaches should be considered as another possible cause for neurogenic syncope. In most patients, the cause of syncope can be determined with great accuracy from careful history and physical examination. However, the exact mechanism of syncope remains unexplained in approximately 35% of episodes and a neurologic cause for syncope is found in fewer than 10% of cases (1). Cardiovascular Preparticipation Evaluation

Copyright © 2015 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.

Syncope in athletes of cardiac origin: 2B. From personal history and physical examination sections.

Syncope in athletes of cardiac origin: 2B. From personal history and physical examination sections. - PDF Download Free
1MB Sizes 0 Downloads 15 Views