Subdural hematomas (SDH) are caused most commonly by head trauma from motor vehicle accidents, assaults, and falls (1). SDH form between the dura and the arachnoid membranes. Direct head trauma is the most frequent cause of SDH in sports, although a few cases of subacute SDH and chronic SDH without known direct head trauma have been reported from roller coaster rides and capoeira (Afro-Brazilian art form that combines elements of martial arts, music, and dance) (12,18,20).
Karate is a sport where head trauma can occur, although a retrospective study of karate injuries found that reported head injuries were predominately facial hematomas, and no cases of SDH were noted (4). This study also found that 83% of the injuries sustained during training occurred with free-style sparring activities, and high-level karate athletes (brown and black belts) had more injuries than lower-level karate athletes. This case report describes the first reported case of a noncontact, subacute SDH in a high-level karate instructor.
A 41-yr-old man, a double black belt karate instructor, presented to his primary care clinic complaining of a feeling of frontal heaviness in his head that had started 3 wk prior, after performing a high-velocity kick against a kick pad. He stated that he felt a popping sensation in his head upon contact of his foot with the kick pad. The heaviness sensation radiated to the upper eyelids and to the temporal area as he moved his head from side to side. His symptoms were constant and exacerbated by activity and standing up. His symptoms were relieved with rest. He initially sought care at an urgent care clinic in Mexico, and he was prescribed 100 mg of acetylsalicylic acid, which he had been taking daily since then to control his symptoms. The night before presenting at the primary care clinic, he experienced a burning sensation in his left shoulder with radiation to the ulnar aspect of the forearm and hand. He denied any history of head trauma, headaches, or similar symptoms in the past.
Past Medical History
Only was positive for allergic rhinitis and obstructive sleep apnea.
Patient denied tobacco and alcohol use. He works as a construction electrician and as a karate instructor. He is married and has a total of five children.
Positive for diabetes mellitus in maternal grandmother and adenocarcinoma of the stomach in paternal grandfather.
Review of Systems
Positive for nausea and palpitations. He denied visual abnormalities or change in motor function or balance. The rest of the review of systems was negative.
Vital signs were normal. Patient was in no distress and was alert and oriented to person, place, and time. Neck examination showed full range of motion with negative Spurling bilaterally. Cardiovascular and respiratory exams were normal. Neurologic examination (cranial nerves, strength, sensation, reflexes) was normal except for horizontal nystagmus. Romberg was slightly positive to the right, and he had an unsteady gait on tandem walking.
A brain magnetic resonance imaging (MRI) study was ordered and revealed a moderate to large subacute SDH in the right cerebral hemisphere, with a midline shift (MLS) of 6 to 7 mm (Figure).
Patient was admitted to the hospital under the care of Neurosurgery and underwent a successful burr-hole drainage procedure. The patient was discharged on the 2 d postoperative after an uneventful postoperative course in the hospital. The patient had regular follow-up over the next 3 months with his neurosurgeon. He experienced a small, spontaneous rebleed that resolved without any intervention. Otherwise, the patient had complete resolution of his symptoms.
At 3 months postoperative, the patient was allowed by Neurosurgery to return to karate but counseled to avoid any type of head movement and contact activities while practicing this sport.
Direct head trauma is the most common cause of SDH, where a static or dynamic mechanical load is delivered to the skull. In the case of noncontact head trauma, the brain injury can be explained by translation, rotation, or angular motion of the head, causing acceleration and deceleration of the brain. These motions can produce shearing forces on bridging veins, causing bleeding (7,18). This pathophysiology also was described in SDH cases attributed to roller coaster rides, capoeira, and head banging (12,18,20).
The clinical manifestations of SDH vary depending on the mechanism of injury and the time elapsed after onset. In acute SDH, there usually is some degree of head trauma involved, and the patient can present with a brief lucid interval between the head injury and loss of consciousness (19). Up to 80% of patients who experience an acute SDH have Glasgow Coma Scale (GCS) scores of 8 or lower (1). SDH in the posterior fossa are rare, and the patient can present clinically with headaches, vomiting, cranial nerve palsies, anisocoria, and ataxia (19).
In the case of subacute and chronic SDH, the mechanism of injury may be unclear, and the time elapsed since the injury can be several days to weeks. Patients with subacute and chronic SDH can present with fluctuating symptoms, such as headaches, apathy, unsteady gait, and alteration of consciousness (7,19).
Anticoagulation therapy with warfarin or aspirin can contribute to the development of spontaneous SDH and chronic SDH, especially in the elderly (11). This patient was prescribed aspirin for his headaches, and this likely exacerbated his subdural bleed. It is important to consider the diagnosis of SDH as a possible complication of anticoagulation therapy (aspirin, warfarin).
The diagnostic approach will depend on the severity of the patient's presentation. For patients with minor head injury (GCS of 13 to 15), close clinical observation can be sufficient (6). Clinical guidelines such as the New Orleans Criteria and the Canadian CT Head Rule can reduce unnecessary head imaging, as well as detect injuries that require surgery (9,16,17). In moderate (GCS of 8 to 12) and severe (GCS lower than 8) head injury cases, neuroimaging plays a critical role in initial evaluation and management.
Computed tomography (CT) plays a key role in the assessment of patients with head trauma due to its widespread availability and rapidity of scanning, as well as the high sensitivity for demonstrating mass effect and intracranial bleeding. This imaging method helps to determine whether observation or immediate neurosurgical intervention is needed (3).
The role of MRI in the evaluation of acute head injuries is growing given its high sensitivity for detecting small, subacute, and chronic hemorrhages (3). Moreover, because of its soft-tissue detail, it is more effective at detecting brain contusions and secondary effects of trauma, such as edema and hypoxic-ischemic encephalopathy (5,6).
The use of cerebral angiography for the assessment of head injury has declined dramatically since the development of helical CT. Although it still is the gold standard for the diagnosis of carotid and vertebral dissection, less invasive techniques like CT angiography and magnetic resonance angiography are preferred (3).
When SDH is diagnosed, the choice between observation and operative management needs to be determined and will depend on CT parameters, GCS score, age, pupillary exam, comorbidities, and (in delayed decisions) neurological deterioration and intracranial pressure (ICP) (1).
The Surgical Management of Traumatic Brain Injury Author Group found that a hematoma thickness greater than 10 mm and a MLS greater than 5 mm were critical parameters for surgical management despite the GCS score (1).
Servadei et al. used these parameters in addition to clinical stability and ICP equal or less than 20 mm Hg to select comatose patients for nonoperative treatment. A good outcome was reported in 67% of the patients in the nonsurgical group versus 23% in the surgical group. They also recommended a repeat CT scan within 6 h of injury in all nonsurgically managed patients because of the risk of missing the evolution or overestimating the volume of the hematoma in the initial CT scan (15).
Age is an important factor in the outcome of SDH. Howard et al. found that age greater than 65 yr was associated with the following: simple falls as mechanism of injury, a lucid interval followed by neurological deterioration, larger bleeding volumes, and excessive delay to hematoma evacuation. These factors are thought to contribute to a poor outcome (10).
The time between clinical deterioration and surgery is key in the management of SDH and is related directly to the outcome. One study reported that periods greater than 2 h were associated with a mortality rate of 80% compared with 47% when surgical intervention occurred in less than 2 h (8). In another study, it was found that a delay in surgery of more than 4 h was associated with a mortality rate of 90% compared with 30% if performed in less than 4 h (14).
Different surgical techniques for the treatment of SDH, such as burr-hole and drill trephination, craniotomy, and decompressive craniectomy, are used routinely, and the choice of technique will depend on the surgeon's expertise and training and other individual patient factors (1).
The use of subdural drains after burr-hole drainage in chronic SDH has been found to be superior, as evidenced by a recurrence rate of 9.3% when a drain was placed compared with 24% when it was not (13).
Determining return-to-play criteria after an athlete experiences an intracranial bleed can be challenging given the limited information found in the scientific literature on this topic. According to Cantu (2), such injuries almost always preclude return to collision sports, except under specific circumstances and after at least 1 yr following the injury. An important point noted in Cantu's recommendations is that if an athlete requires surgery to treat an intracranial bleed, return to collision sports is contraindicated. If complete neurologic recovery is achieved following surgical intervention, return to noncontact sports may be allowed. Because of the surgical procedure performed in this athlete, he should not return to any collision sport, including karate.
After being discharged by Neurosurgery, attempts to reach him for primary care follow-up were not successful.
This case illustrates the importance of maintaining a high index of clinical suspicion for SDH, even in a primary care setting, along with emphasizing the point that significant intracranial bleeds can occur without direct head trauma. Finally, note the fairly benign clinical presentation (symptoms and physical examination), despite the large SDH and significant MLS.
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