Traumatic brain injury (TBI) results from biomechanical forces applied to the structures of the head and neck. Damage may be temporary or permanent and may arise from functional or structural alterations in the central nervous system. Severity is determined by clinical findings and imaging results. When indicated, noncontrast CT is the imaging modality of choice because it is more sensitive for bony injuries, less expensive, and more widely available than MRI. Mild TBI is associated with Glasgow Coma Scale (GCS) scores of 13 to 15 with no or only a brief initial loss of consciousness; results of head CT are typically normal. Moderate TBI is associated with GCS scores of 9 to 12 and/or an initial loss of consciousness of 30 minutes to 24 hours. Severe TBI is associated with GCS scores of 3 to 8 and/or an initial loss of consciousness of more than 24 hours (Table 11). In moderate and severe TBI, head CT may reveal a skull fracture, cerebral contusions and edema, and intracranial hemorrhage.
The terms mild TBI and concussion are often used interchangeably. Mild TBI is the most common presentation of TBI and frequently results from accidents, athletic activity, or military service activities. Guidelines for the use of head CT in mild TBI have been published by the Centers for Disease Activity and Prevention (Table 12). Although yet to be incorporated into management guidelines, serum measurements of brain-specific biomarkers released after mild TBI can help predict which patients may have intracranial lesions visible on CT scan. Elevated levels of ubiquitin carboxy-terminal hydrolase L1 and glial fibrillary acidic protein can be detected as early as 20 minutes after head injury. A recent study of patients within 12 hours of mild TBI (GCS scores of 9 to 15) showed that these elevated serum levels combined with certain clinical information had a sensitivity of 97.5% for predicting lesions visible on head CT scan; negative predictive value was 99.6%. Patients with mild TBI, a normal neurologic examination, and (when necessary) a normal head CT scan may be safely discharged from the emergency department.
Symptoms following a mild TBI may be divided into four domains: physical, cognitive, psychological, and sleep-associated (Table 13). Most symptoms resolve spontaneously within 7 to 10 days. Headache is consistently the most common symptom and is among the most disabling sequelae. Head trauma may cause new headache or worsen a preexisting headache condition. A previous history of migraine has been linked with increased incidence and severity of postconcussion symptoms. Posttraumatic headaches most commonly have the characteristics of migraine and tension-type headaches.
Treatment is matched to the headache phenotype. Acetaminophen, aspirin, NSAIDs, and triptans are effective acute therapies; opioids and butalbital products should be avoided. β-Blockers, antidepressants, and antiepileptic drugs may be useful for headache prevention in patients with persistent posttraumatic headache. Treatment of other postconcussion symptoms is largely symptomatic and based on little evidence. Visual, vestibular, and cognitive therapies may be helpful in certain settings. Stimulants, such as amantadine, are sometimes given to patients with cognitive symptoms. Regulated sleep, graded return to exercise, and temporary modification of school or work schedules are often recommended.
Severe TBI may present with an alteration in consciousness, seizures, repeated vomiting, or focal neurologic deficits. Bilateral periorbital or mastoid bruising and hemotympanum may be signs of basilar skull fracture.
The primary goal of initial management is prevention of hypotension and hypoxia. Normalization of blood oxygenation (arterial PO2 > 60 mm Hg [8.0 kPa]) and blood pressure (systolic > 90 mm Hg) has been shown to improve outcomes. Early management of elevated intracranial pressure with head elevation and mannitol may be required; continuous measurement of intracranial pressure also may be necessary. Head CT is the preferred imaging study, and serial scans may be necessary. Penetrating injuries, depressed skull fracture, and intracranial hemorrhage all may require urgent surgery.
Medical management includes mechanical thromboprophylaxis (with intermittent pneumatic compression) for deep venous thrombosis prevention, glycemic control, and treatment of infectious or gastrointestinal complications. Nutritional support with full caloric replacement by day 7 postinjury is recommended. Fever should be controlled aggressively, with some medical centers advocating induced hypothermia; acetaminophen is an appropriate initial treatment. Glucocorticoids worsen the prognosis of severe TBI and should be avoided.
Prophylactic antibiotics, such as ceftriaxone, are inappropriate for this patient. Fever is a common complication of severe head injury and should be managed aggressively with antipyretic agents.
An epidural hematoma arises when an arterial structure is breached and blood collects between the dura mater and skull in a “lentiform” fashion (Figure 2). Most epidural hematomas involve a laceration of the middle meningeal artery from a temporal bone fracture. Lateral extension is limited by dural attachments at the skull sutures, and expansion occurs inward toward the brain parenchyma. Many patients with an epidural hematoma have a “lucid interval” followed by rapid neurologic compromise. Headache, vomiting, and declining mental status may occur early. Stupor or coma with ipsilateral oculomotor nerve (cranial nerve III) palsy and contralateral hemiparesis may signal transtentorial (uncal) herniation. Urgent surgical evacuation is recommended for those with a GCS score less than 9, anisocoria, or a hematoma greater than 30 mL in volume.
A subdural hematoma (Figure 3) is a collection of blood between the brain and dura mater. Rupture of bridging veins within this space is typically responsible. This may occur spontaneously, as a complication of anticoagulation, or after trauma. Because of cerebral atrophy and subsequent tension on the subdural bridging veins, older persons and those with alcoholism are particularly susceptible. Presentations may be acute, subacute, or chronic. Whereas acute subdural hematoma typically presents with coma or neurologic compromise, chronic hematoma may be associated with nonspecific symptoms, including altered mental status or somnolence, in addition to focal neurologic findings. In patients with acute subdural hematomas, a hematoma thickness greater than 10 mm, a score less than 9 on the GCS, and the presence of pupillary asymmetry or fixation are all indications for immediate surgical treatment. In patients with chronic hematomas, a hematoma thickness greater than 10 mm, a midline shift greater than 5 mm, and significant neurologic compromise are all indications for drainage.
Any athlete suspected of sustaining a mild TBI should be immediately removed from play and assessed by a licensed health care provider trained in the evaluation and management of concussion. Guidelines recommend initial screening with a symptom checklist and neurologic examination involving specific cognitive evaluation and balance testing. Neuropsychological testing provides an objective and more sensitive measure of cognitive function; it should be employed as part of a comprehensive TBI management program for patients with persistent symptoms. Rest, both cognitive and physical, is required for the first days to weeks. Return to play requires the resolution of symptoms and normalization of cognition. The patient should progress through gradual step-wise increases in physical activity without the return of postconcussive symptoms before returning to play. There are no available guidelines for permanent disqualification from contact sports for athletes with mild TBI.
Chronic traumatic encephalopathy is being recognized with increasing frequency in athletes who play contact sports. The result of multiple concussions and head trauma, chronic traumatic encephalopathy may manifest as progressive neuropsychiatric symptoms, including depression and dementia, years after the inciting events. See Cognitive Impairment for more information.
TBI is a common consequence of service in the armed forces, particularly among those deployed to a combat theater. Mild TBI, which often lacks abnormalities on neurologic examination or imaging, is highly prevalent and accounts for 80% of TBI diagnoses. Guidelines recommend that military personnel undergo screening for TBI when exposed to trauma involving a direct blow to the head, a vehicular accident, or an explosive blast and when they are instructed to by a superior officer. The Military Acute Concussion Evaluation and a requisite 24-hour rest period are mandated, with return to duty requiring complete recovery. Headache is the most common symptom after TBI and the best prognostic indicator in returning service members. A posttraumatic headache still present at 1 year postinjury is likely to be permanent. Other sequelae of mild TBI in this population include posttraumatic stress disorder (PTSD), depression, anxiety, insomnia, and disorders of cognition and balance. The prevalence of PTSD is higher in military personnel with mild TBI than in civilians with mild TBI, and thus screening for PTSD in the former group is mandatory. Returning service members with any TBI are best managed through a multidisciplinary approach. Treatments are largely symptomatic and supportive.
Adults older than 75 years are at particular risk for hospitalization and death from TBI. Falls, motor vehicle accidents, and accidental blows to the head are the leading mechanisms of injury in this population. Prevention of these events is an essential aspect of geriatric medicine. See MKSAP 18 General Internal Medicine for more information.
Anticoagulation is associated with an increased risk of intracranial hemorrhage after trauma. Intracranial hemorrhage in patients treated with warfarin has significant morbidity and a mortality as high as 50%; immediate correction of the INR limits hematoma expansion. Reversal of direct-acting anticoagulant agents with specific reversal agents, if available, also should be performed. The reinitiation of anticoagulation after intracranial hemorrhage is clinically challenging and is supported by scant empirical evidence. Hemorrhagic complications in this population appear to be greatest within the first 24 hours of injury, and the risk of thromboembolism is highest between days 3 through 5 after injury. For patients with lower risk of hematoma expansion (such as younger patients or those whose hemorrhage is small in size) and higher risk of thromboembolism (such as those with a mechanical heart valve), the optimal time to resume anticoagulation may be 72 hours after trauma.