A stroke, a disruption of blood supply to an area of the brain, can be classified as either hemorrhagic or ischemic.1 Hemorrhagic strokes occur less frequently and involve a rupture of a specific blood vessel. Ischemic strokes cause an occlusion of a blood vessel, thereby blocking blood flow to its supplied area of the brain. Furthermore, ischemic strokes can be sub-classified into varying types: large artery atherosclerosis, cardiogenic embolism, small vessel occlusive disease, stroke of determined cause, and stroke of undetermined cause. The first three types comprise approximately 60% of all diagnosed ischemic strokes.1 Both stroke classifications can result in profound long-term disability. Collectively, strokes are the third leading cause of death in the United States.1
The World Health Organization estimates that a stroke occurs every 5 seconds worldwide, with more than 5 million deaths and another 5 million permanent disabilities annually.2 In the United States specifically, a stroke occurs every 40 seconds, with approximately 87% being ischemic.1 Of these, approximately 5% to 10% occur in individuals younger than 45 years.3,4 Most cases can be avoided by controlling major modifiable risk factors. Among the most common and well-documented risk factors in this population are smoking, physical inactivity, hypertension, and dyslipidemia.3 Additional non-modifiable risk factors include race, ethnicity, sex, and family history. Although the majority of current literature focuses on stroke statistics for patients 45 years and older, one study investigating death from strokes in young adults in the United States ages 20 to 44 years found Blacks to be at a higher risk for strokes, as well as having a higher mortality rate.4 Additionally, men were found to be at a higher overall risk for mortality from stroke than women.4
We describe a case of acute ischemic stroke in a male collegiate football athlete. Despite being a young, healthy athlete with a low-risk lifestyle, the individual in our case review was both male and Black. He also fell into the small percentage of ischemic strokes of undetermined cause; thus, he did not have the advantage of controlling any modifiable risk factors.
A 22-year-old collegiate football player suffered a contact whiplash injury during a game in September 2018, resulting in a C4 and C5 central and right-sided disc herniation with transient bilateral paresthesia that restricted him from participation in contact sports. Personal previous history included three orthopedic surgeries, the most recent surgery in September 2017. Three weeks after sustaining the aforementioned neck injury, in October 2018, the athlete presented to the athletic training room at 6:45 AM to complete his approximately 1 hour of daily rehabilitation. After beginning team stretch at 8:15 AM, the head strength coach noticed this athlete began to fall behind the group and was not lifting his right arm during A-skips. An athletic trainer was called onto the field and immediately assisted the athlete into the athletic training room.
The athlete presented with steadily decreasing motor skills, particularly on the right side, evidenced by his inability to lift his right arm and his difficulty moving his right leg when being assisted to the examination table. The athlete also demonstrated left-sided facial twitch and right-sided facial droop. Although the athlete was initially able to place his left arm around the athletic trainer's shoulders to be assisted into the athletic training room, by the time he reached the table, he remained conscious but unresponsive to any additional verbal or painful stimuli, including deliberate motor function bilaterally and sternal rub. Eyes were inconsistently responsive to light but unfocused and unable to track. The athlete could not locate a voice when his name was spoken, nor could he follow any verbal commands given by his athletic trainers. Vital signs demonstrated a blood pressure of 117/82 mm Hg on the right arm, consistent and strong heart rate of 80 bpm, oxygen saturation at 98%, and normal respirations. During this 5-minute assessment, several differential diagnoses were considered, including hypoglycemic attack, reaction to improper use of prescription medication, propagation of disc herniation leading to decompensation of the neurological system, brain bleed, and stroke.
The emergency action plan was initiated by contacting Emergency Medical Services (EMS) at 8:31 AM, and an ambulance arrived by 8:35 AM. During the brief period of time before the ambulance arrived, the athlete's heart rate and respiratory rate remained steady and he remained conscious but unresponsive. A blood glucose reading taken by EMS at the scene was found to be normal at 98 mg/dL. The athlete was then transported by ambulance to a local hospital. Vital signs en route consisted of a blood pressure of 144/77 mm Hg on the right arm, heart rate of 74 bpm, respiratory rate of 12 breaths per minute, and oxygen saturation of 98%.
A computed tomography (CT) scan performed immediately on arrival was negative for a brain bleed. The athlete's condition remained steady, with no deterioration in symptoms or vital signs since arrival. The emergency department staff contacted a neurologist at a Level 1 trauma center for teleconsultation and a CT angiogram (CTA) was ordered. The CTA showed a 100% occluded middle cerebral artery, blocking a significant amount of blood flow to the brain (Figure 1). The athlete was administered 4 mg of a tissue plasminogen activator (tPA) at 10:13 AM and demonstrated signs of improvement within 10 minutes. He could now move his left extremities on command and track verbal stimuli with his eyes. He remained without right-sided motor function and unable to speak at this time.
Computed tomography angiography of the brain (arrow points to the area of the brain deprived of blood flow due to the clot in the middle cerebral artery).
At this point, the athlete was transferred via LIFE STAR ground transport at 10:25 AM to the Level 1 trauma center. On arrival, a CTA was repeated and the athlete was immediately taken for angiographic intervention to remove the clot. Research has shown endovascular intervention can result in a “substantially lower degree of patient disability”; therefore, a surgical thrombectomy was performed to allow for optimal patient outcomes.5 The clot was completely removed by 12:30 PM and the athlete was placed in the intensive care unit.
Approximately 2 hours following surgery, in the intensive care unit, the athlete was awake and alert. He had complete return of motor function, with full strength testing for upper and lower quarter screens. Fine motor skills were moderately impaired; however, the athlete was able to write legibly. Although he still had slightly diminished sensation in portions of his right arm, particularly the C6-C7 dermatomes, all other sensation tested normal. He was able to speak a few reflexive responses, while also processing verbal commands. The athlete was transferred to a step-down unit 1 week after surgery and a regular hospital room in the subsequent 2 days.
During this time, he underwent daily physical and speech therapy and several diagnostic tests to determine the cause of the ischemic stroke. Magnetic resonance imaging of the brain was completed, documenting significant damage to a portion of brain tissue (Figure 2). A full hematological work-up was negative for any genetic disorders or clotting factors. An echocardiogram with bubble study was negative for a patent foramen ovale. Constant cardiac monitoring presented negative results for any fibrillations or abnormalities. Results of an electrocardiogram were also negative. Testicular ultrasound to rule out testicular cancer presenting via stroke had a negative result.
Magnetic resonance imaging of the brain (arrow points to the damaged area of the brain affected by the ischemic stroke) immediately following angiographic intervention.
The athlete was discharged to an acute care facility 10 days following surgery. At this time, the athlete completed a 3-mile run and had improved to speaking in full sentences, with moderate verbal paraphasia and malapropisms. One week later, he was discharged to outpatient treatment and care of his sister-in-law, a speech pathologist. The athlete withdrew from classes for the fall semester and continued his follow-up care at home, seeing several specialists. The cardiologist repeated a cardiac ultrasound, finding normal results, and inserted an implantable loop recorder to monitor cardiac activity. No abnormalities were detected via the implantable loop recorder over the next several months. The neurologist repeated a full hematological work-up, which was negative again, and he recommended repeating this work-up annually. The athlete was prescribed the use of daily aspirin indefinitely. The primary care physician began a course of atomoxetine 25 mg for attention deficit disorder, of which the athlete had complaints prior to the neck injury and stroke, and also to assist with his speech therapy progression. Finally, the speech pathologist cleared the athlete for a limited return to academics for the spring semester and the athlete enrolled in two classes.
On returning to the university and resuming care with the sports medicine staff, the athlete followed up with several of his initial health care providers. He was cleared from his cervical neck injury by the neurosurgeon, after a normal CT myelogram. However, the initial case neurologist, while noting remarkable improvements, also noted minor residual speech and processing difficulties, which indicated his brain had not yet fully healed from the stroke. It was recommended that the athlete not return to competitive football because the impact of hits on a still healing brain could have significant unknown risks, particularly due to the idiopathic etiology of this individual case. In July 2019, a joint decision among the head team physician, sports medicine staff, neurosurgeon, neurologist, and university academics was made that a return to contact football was not recommended, and the athlete was medically disqualified.
This particular case is categorized as an ischemic stroke of undetermined cause. This case is unique in several ways, one of which is the incredibly positive outcomes. He has resumed complete weightlifting and conditioning activities, with full strength and sensation, and more than 95% of normal speech. Despite a trend toward increasing mortality rates from ischemic strokes among young adults, this athlete completed his collegiate degree the following year.4 He has continued with a remarkable recovery, considering the 5-year mortality rate of ischemic strokes of uncertain cause is 48.6%.1
Additionally, this case is unique due to the unknown etiology, because this individual is a healthy young athlete with no history of cardiovascular issues. Numerous specialists were unable to determine a cause for the stroke after extensive and repeated testing. However, it was discovered that this athlete had a significant family history, because all of his mother's siblings sustained a stroke. All were due to specific causes, such as patent foramen ovale, chronic high blood pressure, or cancer, and all occurred later in age. Familial history of stroke is associated with a 1.4- to 3.3-fold increased risk for stroke.1 Finally, the athlete's previous history of recent injury, a whiplash cervical disc herniation, leads to an interesting question. It is suspected this shearing injury could have caused a microtear in the vascular structures of the brain, leading to the formation of an arterial clot over the next 3 weeks leading up to his stroke. This hypothesis is not able to be supported via diagnostic testing. It does, however, lend to the distinctiveness of the case.
Implications for Clinical Practice
Several important points can be drawn from this complex case. The first is the importance of early recognition of crucial signs and symptoms, despite the fact that this medical condition is not common in the collegiate population.6 The American Heart Association Guidelines for Early Management of Acute Ischemic Stroke notes seeking timely care rely strongly on early symptom recognition for patients with stroke.6 These recommendations also emphasize the importance of quick transportation to the closest hospital capable of administering a tPA when a stroke case is suspected.
This lends to a second and more broadly applicable emphasis, the importance of familiarity with the emergency action plan. In choosing between the two hospitals we typically use in emergency situations, recognizing that the closer hospital was the ideal choice for this particular emergency versus the farther away, Level 1 trauma center, was a crucial part of successful implementation of the emergency action plan. This choice allowed the tPA to be administered in a timelier fashion, another key element in effective stroke management.6 In this case, quick activation of EMS and coordination with emergency personnel and this local hospital played a substantial role in the successful outcome of this case (Table 1). Athletic trainers should be sure to practice and review the emergency action plan regularly to ensure communication plans and individual roles are well established and seamless.
Timeline of Stroke Presentation and Emergency Care
Additionally, a critical portion of the emergency action plan is immediate access to the necessary equipment. As a staff, we have a plan that incorporates an “emergency cabinet” within the athletic training room, containing equipment such as a blood pressure cuff, pulse oximetry monitor, and vacuum splints. Because the emergency trauma bag itself is often out on the field during athletic activities, this portion of the plan provided solid redundancy to ensure we had quick access to the equipment needed to evaluate this athlete in the athletic training room and continuously monitor vitals signs until EMS arrived.
Finally, this athlete had a significant family history that may have influenced his condition. Athletic trainers should ensure a comprehensive family history is thoroughly reviewed during each athlete's pre-participation physical examination to establish accurate information for the treatment of potential injuries or illnesses.
Despite low occurrence in the collegiate population, rare emergent conditions such as this case can present themselves. Athletic trainers are often on the front lines of these incidents and familiarizing ourselves with emergency medicine and action plans is a crucial part of providing the best possible health care to our student-athletes.
- Grysiewicz RA, Thomas K, Pandey DK. Epidemiology of ischemic and hemorrhagic stroke: incidence, prevalence, mortality, and risk factors. Neurol Clin. 2008;26(4):871–895, vii. doi:10.1016/j.ncl.2008.07.003 [CrossRef]
- World Health Organization. Global Burden of Stroke. Available at: https://www.who.int/cardiovascular_diseases/en/cvd_atlas_15_burden_stroke.pdf
- Von Sarnowski B, Putaala J, Grittner U, et al. Lifestyle risk factors for ischemic stroke and transient ischemic attack in young adults in the stroke in young Fabry patients study. Stroke. 2013;44(1):119–125 doi:10.1161/strokeaha.112665190 [CrossRef]
- Poisson SN, Glidden D, Johnston SC, Fullerton HJ. Deaths from stroke in US young adults, 1989–2009. Neurology. 2014;83(23):2110–2115. doi:10.1212/WNL.0000000000001042 [CrossRef]
- Saver JL, Goyal M, van der Lugt A, et al. HERMES Collaborators. Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis. JAMA. 2016;316(12):1279–1288. doi:10.1001/jama.2016.13647 [CrossRef]
- Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019;50(12):e344–e418. doi:10.1161/STR.0000000000000211 [CrossRef]
Timeline of Stroke Presentation and Emergency Care
|6:45 AM||Athlete presented normally for routine rehabilitation session|
|7:45 AM||Athlete ate breakfast with the team|
|8:15 AM||Athlete began team stretch|
|8:25 AM||Athlete began developing lack of motor control|
|8:31 AM||EMS activated|
|8:35 AM||EMS arrived and began transport of athlete to local hospital|
|10:13 AM||tPA administered|
|10:25 AM||Transported to a Level 1 trauma center|
|11:30 AM||Angiographic intervention to remove clot|
|12:30 PM||Athlete admitted to the ICU|