Syncope Following Neck Trauma in a Football Player
John W. O'Kane, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 29 - NO.9 - SEPTEMBER 2001
In Brief: A college football player sustained a contusion to his anterior neck, over the carotid artery. Less than a minute later he fainted, then experienced episodes of postural dizziness with bradycardia and hypotension. He completely recovered within 3 hours from the time of injury. An unusual but possible cause of this patient's syncopal episode is posttraumatic carotid sinus syncope. This case illustrates the importance of checking vital signs in any athlete who experiences loss of consciousness, and that its occurrence in a collision sport is not always caused by a concussion.
Young, healthy athletes rarely experience syncopal episodes, so any loss of consciousness is worrisome for a team physician. This case report describes an episode of syncope following anterior cervical trauma, reviews the differential diagnosis, and suggests posttraumatic carotid sinus dysfunction as a possible cause for the syncopal episode.
A 19-year-old Division 1 football player sustained a right-sided anterior neck injury on a kick-off return. The injury occurred when he was on the ground and an opposing player stepped on his neck. He was able to walk from the field, but upon reaching the sideline he complained of dizziness. The player sat down on the bench and then lost consciousness, falling backward. He quickly regained consciousness, and the team physician was called to the scene. While supine, the player experienced moderate anterior neck pain.
During the initial exam, the player denied peripheral neurologic symptoms or posterior neck pain. He had no cervical spine tenderness and had full pain-free active range of motion in the neck. His football helmet was removed but when he tried to sit up, he quickly returned to supine, expressing light-headedness, dizziness, and a sense of impending loss of consciousness. The player said that he felt better lying down. He denied headache, visual changes, confusion, chest pain, shortness of breath, or palpitations.
The athlete had a normal respiratory rate but nonpalpable radial pulses. Carotid pulses were bilaterally equal at about 40/min. Bilateral carotid auscultation revealed no bruit. His systolic blood pressure was in the low 60s mm Hg. Heart auscultation revealed normal S1 and S2 without murmur, rub, or gallop, but he had persistent bradycardia of about 50/min.
His pupils were equal and reactive to light, his concentric ocular movements were intact, and his vision was normal to gross testing. His cranial nerves were intact.
His right anterior neck was swollen just anterior to the middle of the sternocleidomastoid muscle belly, and he had a superficial skin abrasion with induration. His upper thorax was nontender to anterior-posterior compression. His lungs were clear, and he had no abdominal tenderness or masses.
An ambulance crew arrived and found that his pulse oximetry without oxygen was 98%. Cardiac monitoring revealed sinus arrhythmia at 45 to 50/min, and blood pressure of 65/40 mm Hg.
The patient reported no history of cardiovascular problems, syncope, concussion, or seizure. He did not use regular medication or other substances, and had no known drug allergies. His family history was also unremarkable.
Diagnosis and Treatment
The initial differential diagnosis included posttraumatic carotid sinus or vasovagal syncope, seizure, and concussion. The athlete was transported to the locker room where 500 mL of normal saline was administered intravenously over 15 to 20 minutes. About 30 minutes after the injury, his pulse had recovered to 65/min, and his systolic blood pressure was 110 mm Hg.
He was transported to the emergency department to be monitored for an additional 30 minutes. A 12-lead electrocardiogram demonstrated sinus arrhythmia but was otherwise normal. His vital signs remained within the normal range, and he was able to stand and walk without any symptoms. His right anterior neck remained tender, but he had no additional swelling and continued to have a normal carotid pulse without bruit. The athlete was discharged from the emergency department, and he returned to play 3 days later without further symptoms.
Syncope or near-syncope is defined as transient loss of consciousness or dizziness with postural collapse accompanied by variable degrees of hypotension and bradycardia (1). It is most frequently caused by an acute decrease in cerebral blood flow.
In football, concussion is the most common cause of dizziness associated with loss of consciousness, but this athlete did not exhibit any characteristic postconcussive symptoms such as persistent dizziness, headache, confusion, amnesia, other mental status changes, or cranial nerve abnormalities (2). His clinical presentation and recovery were inconsistent with a seizure.
Syncope generally results from one of three mechanisms: neurocardiogenic (vasovagal), postural hypotension (orthostatic), or cardiogenic (1). Vasovagal and orthostatic syncope both involve a failure to increase arterial vascular resistance and heart rate in response to increased venous pooling and decreased arterial blood pressure. Insufficient cerebral circulation causes loss of consciousness. Vasovagal episodes often occur with emotional distress, and orthostatic episodes involve a change in position. In cardiogenic syncope, cerebral hypoperfusion is secondary to diminished cardiac output, most often secondary to a brady- or tachyarrhythmia.
A less common but well recognized form of syncope is carotid sinus syncope. The carotid sinuses, responsible for homeostasis of blood pressure, are located in the internal carotid artery just beyond the bifurcation from the common carotid artery (figure 1), and are richly innervated (3). In response to stretching from increasing blood pressure, receptors in the sinus reflexively lower heart rate and systemic vascular resistance. Abnormal sensitivity of these receptors is a well-documented (1) cause of bradycardia, hypotension, and syncope, particularly in the elderly. Carotid sinus massage works via this mechanism to lower heart rate or break tachyarrhythmias in susceptible individuals. One report in the literature (4) describes carotid sinus dysfunction as the cause of recurring syncope in a 17-year-old wrestler. His symptoms were preceded by his opponents' grabbing the side of his neck during a wrestling bout.
We believe that carotid sinus trauma may be the mechanism responsible for syncope in our patient. The athlete in this case report presented with a clear indication of an acute contusion over the carotid sinus with objective swelling. Direct impact to the carotid body and regional neuromuscular structures may have resulted in temporary dysfunction or regional swelling that may have temporarily increased local tissue pressure that stretched the receptors. Either scenario could have led to the inappropriate hypotension and bradycardia noted in this case. The player had no cognitive, other postconcussive, or postictal changes suggesting alternate causes for his symptoms. If dehydration was the cause, he should have had tachycardia. Although the athlete never complained of significant discomfort or emotional distress, a vasovagal reaction without carotid sinus dysfunction cannot be excluded as the cause of his syncope. The athlete's normal electrocardiogram, cardiac exam, and lack of any cardiac symptoms before or since this incident make a cardiogenic cause of his syncope very unlikely.
An Unusual Injury
In collision sports, many kinds of unplanned contact are possible, and sometimes unusual injuries occur. In this case, a syncopal episode was caused by contact, not concussion. To our knowledge, this is the first reported case of syncope in athletics following a contusion over the carotid sinus. Fortunately, no long-term consequences were evident, and the athlete returned to play uneventfully.
Dr O'Kane is an assistant professor of orthopedics and sports medicine and a team physician at the University of Washington in Seattle. Address correspondence to John O'Kane, MD, University of Washington Sports Medicine, Box 354060, Seattle, WA 98195-4060; e-mail to [email protected].