Traumatic Brain Injury
Authors:
Catherine A. Marco, MD, FACEP, Professor, Department of Emergency Medicine, Program Director, Emergency Medicine Residency, University of Toledo Collge of Medicine, Toledo, OH.
Joanna L. Marco, BS, Ohio State University College of Medicine, Columbus.
Peer Reviewer:
Michael C. Bond, MD, FACEP, FAAEM, Assistant Professor, Residency Program Director, Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore.
Head trauma is a common presenting problem among emergency department (ED) patients. It has been estimated that 1-2 million Americans sustain traumatic brain injury (TBI) annually. Head trauma is a common cause of significant morbidity and mortality, and appropriate ED management can optimize the long-term effects of head trauma. Obtaining an injury-specific history can be important in elucidating the mechanism of injury and potential injuries to investigate. Specific attention to the physical examination is mandatory in the evaluation of head trauma, and should include an external examination, examination of head and facial bones, and neurologic examination. Careful attention should be paid to the trauma assessment to evaluate other coexisting injuries. Diagnostic tests including brain computed tomography are indicated in most cases of significant head trauma to exclude intracranial injury.
Following complete evaluation, minor head injury patients may be appropriately managed as outpatients with primary care or neurologic follow-up. Moderate or severe head trauma warrants hospital admission and emergent neurosurgical consultation. Prompt evaluation, treatment, and referral are indicated to reduce the incidence of long-term neurologic deficits.
— Ann M. Dietrich, MD, Editor
Epidemiology
The Centers for Disease Control and Prevention (CDC) estimates that there are at least 1.7 million cases of traumatic brain injury annually.1 ED visits for TBI among military members increased from 2008 to 2010.2 The majority of these cases are mild; 80% of TBI patients who present to an ED are discharged the same day.1 The morbidity and mortality of TBI is significant: Among severe TBI patients, mortality may range from 39-74% depending on age, and there are 50,000 deaths from TBI in the United States annually.3,4 Approximately 50% of mortality occurs within the first two hours of injury.5
Etiology
Falls are the leading cause of TBI in the United States, and are most likely to cause TBI-related hospitalization.1 Motor vehicle crashes are the second leading cause overall, and among young adults and children, are the most common cause of blunt head trauma.6 Death is most likely to occur in TBI patients whose injury resulted from a motor vehicle crash.1
TBI has a trimodal age distribution. ED visits for TBI are highest for ages 0-4, 15-24, and 75 and older. Among patients ages 0-4 and 75 and older, TBI is more likely to result from falls, and in the 15-24 age group, TBI is more likely to result from motor vehicle crashes. Deaths and hospitalizations due to TBI are highest for ages 75 and older.1
TBI rates are higher for males than females in every age group. Overall, there are 1.4 times more TBI in males than females.1 Among mild TBI (mTBI) patients who were seen in the ED, women were less likely to be injured while playing a sport and more likely to be injured in a motor vehicle crash.7 Women who presented to the ED with mTBI were also more likely to report post-concussive symptoms at three months post-injury.7
Additionally, TBI and post-concussion symptoms are common among soldiers recently returning from combat. Between 9-23% of these soldiers met criteria for concussion.8 Blasts are the most common mechanism of TBI among soldiers, although it is unknown whether this causes substantially different sequelae than are seen in common civilian injuries.9 An additional consideration is the high rate of post-traumatic stress disorder (PTSD) in this population: Concomitant PTSD is associated with a higher rate of post-concussive symptoms.10
Pathophysiology
An understanding of the pathophysiology of TBI is crucial to appropriate ED management. Head injuries can be divided into primary injuries, which result directly from the original mechanism of trauma and tend to involve direct physical damage, and secondary injuries, which occur more gradually and expand the original injury through dysfunctional cellular processes. Primary injuries include fractures, intracranial hemorrhage, contusions, tearing of the brain tissue, hematomas, diffuse axonal injury, cellular damage, loss of the blood-brain barrier, or neurochemical or electrochemical disruption. Secondary injuries result from subsequent metabolic derangement and include deleterious microcellular changes such as glutamate excitotoxicity, ion shifts, and free radical generation. The combination of primary and secondary injuries may cause permanent cell death and necrosis. The damage from primary and secondary injuries begins the inflammatory response. Unregulated inflammation inside the closed cranial vault may lead to increased intracranial pressure (ICP) and cerebral edema. Cerebral perfusion pressure (CPP) is calculated as mean arterial pressure (MAP) minus ICP. Increased ICP and brain swelling, in addition to causing direct damage to the brain tissue, also contribute to the compression of the brain vasculature, leading to decreased cerebral blood flow and tissue ischemia.11
A number of systemic factors are known to worsen TBI outcomes. These factors include hypotension, hyperpyrexia, hypoxia, and anemia.12 Hypotension reduces cerebral perfusion, worsens ischemia, and results in a doubling of mortality among TBI patients. Hypoxia and anemia similarly reduce the amount of oxygen available to cerebral tissue and also result in increased mortality in severe TBI.13 Because there is conflicting evidence about the significance of anemia as it relates to outcomes in TBI, judicious use of transfusions with minimal volumes is recommended.14-17 The mechanism for the deleterious effects of hyperpyrexia on TBI outcomes is less clear, although it may have to do with altered metabolism in injured areas of the brain.12
Following the initial head injury, of special concern to the emergency physician are diagnostic imaging, neurosurgical or neurologic consultation, ICP management, maintenance of adequate cerebral blood flow, and avoidance of systemic factors that may worsen outcomes (i.e., hypotension, hyperpyrexia, hypoxia, and anemia).
Clinical Features
History. For patients presenting with head trauma, a detailed history is critical. Obtain details regarding the mechanism and severity of injury. Take the patient's past medical history and ask about all current medications, especially anticoagulants. Ask about recent drug or alcohol use and complaints prior to the trauma. Determine the patient's current level of consciousness and whether this is an altered baseline mental status. If there were witnesses to the injury, interview them to determine the patient's level of consciousness before and after the injury. Additionally, determine if there were witnessed seizures or apnea following the trauma. Medical causes of trauma should be considered, including stroke, seizure, arrhythmia, acute coronary syndrome, pulmonary embolus, anemia, or metabolic causes of weakness or altered mental status. Finally, inquire regarding pertinent symptoms occurring after the injury, such as headache, nausea, vomiting, visual or auditory symptoms, or memory impairment.
Physical Examination. It is important to establish the patient's mental status and Glasgow Coma Score (GCS) early. The GCS (see Table 1) is considered by some to be the "neurologic vital sign."6,18,19 TBI may be categorized by GCS score as mild (14-15), moderate (9-13), or severe (3-8). These categorizations correlate with patient outcomes and may be used to guide ED management.6 If GCS is difficult to obtain due to patient intoxication, sedation, intubation, or other reasons, the motor component of the GCS also correlates well with outcome.6 The Glasgow Coma Score improves more rapidly in intoxicated patients than their cohorts.20
Table 1. Glasgow Coma Score18
Best Eye Response |
Best Verbal Response |
Best Motor Response |
Opens eyes Opens eyes to Opens eyes in response to painful stimuli = 2 Does not open eyes = 1 |
Oriented, converses normally = 5 Disoriented, confused, converses = 4 Utters inappropriate words = 3 Incomprehensible = 2 No response = 1 |
Obeys commands = 6 Localizes painful stimuli = 5 Flexion or withdrawal to painful stimuli = 4 Abnormal flexion/decorticate rigidity = 3 Abnormal extension/ decerebrate rigidity = 2 No response = 1 |
Patients with mTBI require a more comprehensive evaluation of mental status than is provided by their GCS. Assess these patients for confusion, amnesia, and other signs of global impairment, and complete a full neurologic examination, including gait, if injuries do not preclude safe testing. Although a full cognitive function examination may be impractical in the ED, assessment of mental status and cognition is important to establish baseline functioning and determine the need for outpatient referral for neurocognitive testing and therapy.
Cervical spine immobilization should be maintained in all patients with head trauma until cervical spine trauma is excluded. Cervical spine trauma may be evaluated using the NEXUS criteria or Canadian C-spine Rule (CCR). NEXUS criteria suggest that patients who do not require cervical spine imaging include those who have normal mental status, are not intoxicated, have no focal neurologic deficit, have no distracting injuries, and have no midline cervical tenderness.21,22 The CCR may be used in alert patients in stable condition. This rule suggests that radiography is not indicated for alert patients younger than age 65, without a dangerous mechanism of injury, ambulatory at any time, absent cervical spine tenderness, and able to rotate the neck actively to 45 degrees to the left and right.23,24
Assess the patient's pupil size and responsiveness. In an unresponsive patient, this may indicate any of several underlying pathologies. A single fixed and dilated pupil may be a result of direct ocular trauma, or it may suggest an intracranial hematoma with uncal herniation potentially requiring emergency neurosurgery. Bilateral fixed and dilated pupils may indicate increased ICP, bilateral uncal herniation, drug intoxication, or severe hypoxia. Bilateral pinpoint pupils indicate either opiate intoxication or a pontine lesion. Examine the patient's head and neck for external indications of trauma. Scalp lacerations, contusions, or abrasions may indicate a depressed skull fracture. Signs of basilar skull fracture include hemotympanum, CSF rhinorrhea or otorrhea, Battle's sign, raccoon sign, and cranial nerve deficits.
Evaluate the patient's motor strength and symmetry and perform a cranial nerve exam, paying special attention to deficits indicating possible basilar skull fractures, including facial paralysis, decreased hearing function, dizziness, tinnitus, and nystagmus.
Before assessing brainstem function, check for concomitant cervical spine injury, which occurs in 7% of head injury patients.25 If there is cervical tenderness or the patient's obtundation prevents reliable examination, obtain computed tomography (CT) images of the cervical spine.26 Once cervical spine injury is excluded, brainstem function may be assessed with the oculocephalic (doll's eyes) and oculovestibular (calorics) maneuvers.
Diagnostic Studies
Imaging. Noncontrast head CT is the initial diagnostic test to evaluate head trauma. Its routine use on patients with moderate or severe TBI is uncontroversial. Furthermore, CT should be considered for all patients with suspected injury and a GCS lower than 15, regardless of other symptoms, and on certain patients with a GCS of 15.27 Plain film radiographs are not sufficiently sensitive to exclude intracerebral hemorrhage, and there are no current evidence-based guidelines suggesting magnetic resonance imaging (MRI) over noncontrast CT.28
The aspect of clinical decision-making lies in determining which mTBI patients with a GCS of 15 require imaging. Since 1992, imaging for head injury has increased substantially.29 It has been suggested that Advanced Trauma Life Support imaging guidelines from the American College of Surgeons are not sufficiently evidence-based, and recommend a low bar for imaging, which may lead to excessive imaging in head trauma patients.30 In efforts to reduce treatment costs and radiation exposure, several imaging decision rules aimed at reducing unnecessary imaging have been developed. Of these decision rules, the most well-substantiated are the Canadian CT Head Rule and the New Orleans Criteria. (See Table 2.) Each of these rules aims to stratify patients with mild TBI into high and low risk for brain injury on CT. Each rule has been prospectively validated to be 100% sensitive in detecting patients requiring neurosurgical intervention.28,31-33 Each rule is limited by the entry requirement of loss of consciousness or amnesia, and neither rule applies to patients on anticoagulants or children (see section on pediatric head injuries).6,28
Table 2. Criteria for Determining if CT Is Indicated After Minor Head Injury, According to New Orleans Criteria and Canadian CT Head Rule36,37
Study |
Patient Population |
Indications for CT Scan |
Reported Validity, %* |
|
Sensitivity |
Specificity |
|||
Abbreviations: CCHR, Canadian CT Head Rule; CT, computed tomography; GCS, Glasgow Coma score; NOC, New Orleans Criteria |
||||
Haydel et al, 2000 (NOC) |
GCS of 15, loss of consciousness, no neurological deficit, age > 3 y |
Headache, vomiting, seizure, intoxication, short-term memory deficit, age > 60 y, or injury above clavicles |
100 |
24.5 |
Stiell et al, 2001 CCHR) |
GCS of 13-15, loss of consciousness, no neurological deficit, no seizure, no anticoagulation, age > 16 y |
High-risk patients: GCS score < 15 at 2 h postinjury, suspected skull fracture, any sign of basal skull fracture, vomiting (≥ 2 times), age ≥ 65 y+ Medium-risk patients: Retrograde amnesia > 30 minutes, dangerous mechanism (pedestrian vs. motor vehicle; ejected from motor vehicle; fall from height > 1 m or 5 stairs)# |
96.4 |
49.6 |
Head trauma patients with clinically suspected coagulopathy were twice as likely to have significant intracranial injury on CT as those without suspected coagulopathy; CT is recommended on all head injury patients with confirmed or suspected coagulopathy.34 Pay special attention to patients taking clopidogrel; their risk of intracranial hemorrhage after head trauma is 12%, more than double the risk of patients taking warfarin.35
Laboratory Tests. There are no routine laboratory tests for patients with isolated minor head trauma. A urine toxicology screen, blood alcohol level, electrolytes, and blood glucose may be useful in interpreting the patient's mental status. Coagulation studies should be considered when coagulopathy is suspected. Patients with significant head trauma and potential other injuries should have full trauma laboratory studies performed, including complete blood count, electrolytes, type and screen, urinalysis, toxicology screen, alcohol level, and pregnancy test (if indicated).
Although a number of serum biomarkers for clinically important TBI have been investigated, only one, S-100B, has showed any consistency in predicting injury severity to date. S-100B is an astrocyte-expressed protein that increases and decreases rapidly after head injury; it may be detected as early as 30 minutes after the injury and as late as four hours after the injury.27 Elevated S-100B has been shown to be 99% sensitive at detecting intracranial injury on CT, and it is currently being used as a standard of care in some European countries, although this test has not yet been approved by the Food and Drug Administration for clinical use in the United States.11,38 Patients with mTBI with a serum S-100B level less than 0.1 ng/L and without apparent extracranial injuries are likely to be at low risk for intracranial injury, and consideration may be given to not performing a CT.27
Management
Severe TBI. Patients with severe TBI have a GCS of 8 or less, or have intracranial contusion, hemorrhage, or brain laceration. Approximately 25% of adults with severe TBI require neurosurgical intervention, and the mortality rate of these patients is approximately 60%.13 Most adult survivors suffer from severe disability. Skull fractures are associated with increased mortality.39 For airway management, rapid sequence intubation should be performed.13 Some induction agents may cause hypotension, so it is important to maintain blood pressure during the procedure.6 Etomidate (0.3 mg/kg) causes less cardiovascular instability than other sedatives, and has a rapid onset and short duration of action.40 It may also help reduce ICP. Propofol (1-3 mg/kg IV) is another preferred induction agent due to its rapid onset and offset, its reliable reduction in ICP, and its antiseizure properties.40 However, caution must be used due to potential hypotension.
Treat hypotension, if present, as hypotension results in decreased ICP. Unless herniation is suspected, hypotension in the severe TBI patient is likely from another source of bleeding or hypovolemia. Use aggressive fluid resuscitation to raise the systolic blood pressure to at least 90 mm Hg; fluids and blood products do not increase ICP in hypotensive TBI patients.13,41 If fluid resuscitation is not effective, use vasopressors to maintain a MAP of at least 80 mm Hg in order to preserve CPP.6 Additionally, control any sources of bleeding and maintain the hematocrit at or above 30% to avoid anemia.6,14-17
Early post-traumatic seizures that occur in the first seven days after head trauma can cause further damage to the brain due to increased ICP, hypoxia, hypercarbia, and excess neurotransmitter release.42 Risk factors for post-traumatic seizures include GCS of less than 10, cortical contusion, depressed skull fracture, subdural hemorrhage, epidural hemorrhage, intracerebral hematoma, penetrating head wound, and seizure within 24 hours of injury.43 For patients with active seizures, benzodiazepines should be used as first-line anticonvulsants. Use lorazepam (0.05-0.15 mg/kg IV) or diazepam (0.1 mg/kg, up to 5 mg IV, every 5 minutes up to a total of 20 mg).13 Some neurosurgeons recommend prophylactic antiepileptic agents, and this decision should be made in conjunction with the neurosurgical consultant.
Management of Elevated ICP. Elevated ICP may compromise cerebral blood flow and oxygen delivery. If the ICP is high enough, life-threatening herniation may occur. Because ICP monitoring is not typically available in the ED, identification of elevated ICP must depend on history and physical exam findings. Signs and symptoms of elevated ICP include headache, nausea, vomiting, lethargy, hypertension, seizure, bradycardia, and agonal respirations.
Initial management of elevated ICP includes raising the head of the bed to 30 degrees to promote blood drainage, and hyperosmolar agents such as mannitol (0.25-1 g/kg) or hypertonic saline (HTS).11 The Brain Trauma Foundation recommends mannitol as the drug of choice, although HTS is used in many institutions.13,44 Mannitol is effective at reducing ICP and improving cerebral blood flow, CPP, and brain metabolism. However, its diuretic effect means that volume loss must be monitored to maintain adequate blood volume.
The use of HTS is controversial. Much of the current research on HTS has been weak due to the use of animal subjects, lack of randomization, or small sample size to give it a place in current treatment guidelines.45 A meta-analysis of HTS studies found that a majority of the studies suggested that HTS is at least as effective at reducing elevated ICP as mannitol.46 Additionally, HTS avoids the diuretic hypotension caused by mannitol.46
Hyperventilation may be used briefly to reduce ICP when other measures fail. Hyperventilation decreases blood PCO2, which causes cerebral vasoconstriction. The decreased blood volume in the brain may temporarily buffer the ICP from rising and delay impending herniation, but prolonged hyperventilation may dangerously reduce tissue perfusion, causing further brain injury. For this reason, prophylactic hyperventilation and prolonged hyperventilation are not recommended.
The use of recombinant activated factor VII (rFVIIa) in the treatment of intracranial hemorrhage is controversial. rFVIIa is a hemostatic agent. At more than $4,500 per dose, it may be prohibitively expensive for widespread use.13 Its use in the setting of TBI is not an FDA-approved indication of the drug. One study showed that patients with traumatic intracranial hemorrhage and pre-injury warfarin use who were given rFVIIa had decreased time to normal INR, which may be important in preventing ongoing hemorrhage, but it had no effect on mortality.48 The use of rFVIIa is not currently recommended; future research may elucidate its place in the standard of care.48
Intracerebral Hemorrhage. Epidural Hemorrhage. An epidural hemorrhage (EDH) is a hemorrhage between the dura mater and the cranial periosteum. EDH typically results predominantly from direct mechanical force causing a skull fracture. The source of bleeding is often the middle meningeal artery or dural sinus. The temporoparietal region is the most common site for EDH.
On noncontrast head CT, EDH appears as a biconvex or lens-shaped hyperdense region. (See Figure 1.) A large hemorrhage will produce midline shift or compression of the lateral ventricles, although the hemorrhage itself is limited from crossing suture lines by in-foldings of the dura.
The classic presentation of an EDH involves blunt head trauma with initial loss of consciousness, followed by a lucid period, and then rapid neurologic decline. However, it should be noted that this classic presentation occurs only in a minority of EDH cases. The development of signs and symptoms depends on how fast the EDH is developing. Bleeding from the middle meningeal artery may cause neurologic decline and herniation in a matter of hours, while bleeding from a dural sinus may result in a slower clinical presentation. After EDH is identified on noncontrast head CT, consult neurosurgery to determine if surgical intervention is necessary.
Subdural Hemorrhage. A subdural hemorrhage (SDH) forms between the dura and the arachnoid. An SDH frequently results from acceleration-deceleration injuries, such as those seen in motor vehicle crashes or falls. Acute SDH occurs in 11-21% of head trauma patients.47 Rupture of bridging veins in the subdural space is a common cause of SDH.13 Alcoholics and the elderly are especially susceptible to SDH because of weaker bridging veins and brain atrophy.
SDH may be acute (developing immediately after trauma), subacute (developing within 14 days of trauma), or chronic (developing after or lasting at least two weeks). On head CT, acute SDHs are hyperdense, sickle-shaped lesions that can cross suture lines. Subacute SDHs appear isodense and may be difficult to identify without IV contrast or MRI. (See Figure 2.) Layering of blood and cerebrospinal fluid (CSF) may be seen. Chronic SDH appears isodense or hypodense.
Patients with SDH may present in a variety of ways. Often, patients with acute SDH present with a decreased level of consciousness and a GCS of 8 or below. A minority of acute SDH patients may have a lucid period. Patients may also present with signs of elevated ICP. Patients with acute, subacute, or chronic SDH may have more subtle symptoms, such as headache, altered mental status, vomiting, seizures, or hemiparesis.
Traumatic Subarachnoid Hemorrhage. Traumatic subarachnoid hemorrhage occurs when the small subarachnoid vessels are torn. It is the most common CT abnormality in moderate and severe TBI patients, and is seen in the first CT scan in 33% of severe TBI patients.12 Patients with isolated traumatic subarachnoid hemorrhage present with headache, photophobia, and meningeal signs. On noncontrast head CT, traumatic subarachnoid hemorrhage appears as hyperdense blood collected in basilar cisterns, interhemispheric fissures, and sulci. (See Figure 3.)
Herniation. Cerebral herniation is a life-threatening condition in which increasing ICP or mass effect from an expanding hemorrhage displaces a part of the brain out of its normal anatomic location. Early identification of impending herniation and rapid treatment are crucial in managing this catastrophic condition.
The most common brain herniation is uncal herniation, in which the uncus of the temporal lobe is displaced downward through the edge of the tentorium. It is commonly caused by an expanding mass in the temporal lobe or lateral middle fossa. Uncal herniation compresses the parasympathetic fibers in the oculomotor nerve, causing ipsilateral fixed and dilated pupil. Uncal herniation may also compress the descending pyramidal tract, causing contralateral motor paralysis.
Central transtentorial herniation is less common. Its symptoms initially include bilateral pinpoint pupils, bilateral Babinski's signs, and increased muscle tone. Later, pupils are fixed at midpoint and decorticate posturing begins.
Cerebellotonsillar herniation involves the displacement of the cerebellar tonsils through the foramen magnum, causing pinpoint pupils, flaccid paralysis, and death.
Upward transtentorial herniation causes pinpoint pupils and conjugate downward gaze without vertical eye movements.
Cushing's reflex, which indicates increased ICP and imminent herniation, may occur during ED resuscitation of severe TBI. Its classic triad includes severe progressive hypertension, bradycardia, and diminished or irregular respiratory effort. However, the full triad may not be seen reliably in patients with increased ICP. If Cushing's reflex is identified, begin aggressive ICP management, including hyperventilation and hyperosmotic therapy.
Moderate TBI. Patients with a GCS of 9-13 are classified as having moderate TBI. They require close observation for changing mental status or neurologic findings, early imaging, and neurosurgical evaluation. If surgery is not needed, moderate TBI patients should still be admitted for observation.
One important presentation to recognize is the "talk-and-deteriorate" patient. This patient initially has a GCS of 9-13 and is able to speak, but deteriorates to a GCS of 8 or less within two days. Seventy-five percent of these patients have either an epidural or subdural hemorrhage, and are likely to have good outcomes if the hemorrhage is treated rapidly. To prevent such deteriorations, keep moderate TBI patients under close observation and use additional CT scans and neurosurgical consults as needed.
All moderate TBI patients should be admitted for observation, even if the initial CT scan appears normal.13
Mild TBI. Mild TBI (mTBI) is broadly defined as GCS of 14-15. The CDC has a more specific definition, which stipulates that at least one of the following conditions must occur after a head injury: confusion, disorientation, or impaired consciousness; amnesia surrounding the injury event; signs of neurologic dysfunction; or loss of consciousness lasting 30 minutes or less.49 Additionally, imaging abnormalities exclude patients from the classification of mTBI.
Intoxication, altered mental status, posttraumatic amnesia, or lack of reliable witnesses may make obtaining a history difficult. In the differential diagnosis, consider conditions with similar presentations, including seizure, syncope, intoxication, malingering, and psychiatric conditions.
Most patients with minor head trauma are usually asymptomatic by the time they present to the ED, although common complaints include headache, nausea, and vomiting. Perform a complete neurologic examination, exclude conditions with similar presentations, and use the New Orleans Criteria or Canadian CT Head Rule to determine whether the patient requires imaging. (See Table 2.)13
Low-risk mTBI patients who do not require CT imaging or who have a negative head CT scan may be safely discharged from the ED.13,28 If there is a reliable family member, patients may be discharged in the care of family members along with head injury instructions. If no reliable family is available, patients may be observed in the ED for 4-6 hours prior to discharge home. Patients on anticoagulants experiencing minor head trauma with a negative head CT scan should be observed for 24 hours and administered a repeat CT scan. If they do not decline after the observation period and the repeat scan is also negative, they may be discharged with low risk of delayed bleeding.50 Patients with an INR greater than 3 have significantly increased bleeding risk and should be admitted for observation.50
Higher-risk patients, including patients with bleeding disorders, patients with previous neurosurgical procedures, and patients with previous neurologic disease may be at additional risk for delayed complications, even after an initial negative CT scan. There is controversy in the literature regarding potential discharge of these patients from the ED.27
Before discharge, mTBI patients and families should be educated in plain language regarding "red flag" symptoms necessitating a return to the ED, as well as common post-concussive symptoms.11 (See Table 3.) Many mTBI patients are unable to fully remember discharge instructions, so it is important to involve family members and provide them with written instructions.51 The CDC has developed helpful resources about concussion for health care providers, patients, and coaches available to download and distribute to patients (www.cdc.gov/concussion).
Table 3. "Red Flag" Symptoms and Common Post-concussive Symptoms
"Red Flag" Symptoms |
Post-concussive Symptoms |
|
|
Post-concussive symptoms are worst in the acute phase after the injury and in the first month after the injury.52 Symptoms may include persistent headaches, memory impairment, depressive mood disorders, fatigue, insomnia, and disability.53 Post-concussive disorder can be predicted in the ED by testing immediate verbal recall and a quantitative recording of headache.54 At one-month follow-up, 63% of mTBI patients continue to have post-concussive symptoms, but most symptoms resolve in three months to one year.55 Physicians should be familiar with the fact that symptoms may persist for significant lengths of time. Additionally, early patient education about possible post-concussive symptoms and the likelihood of an overall positive outcome has been shown to speed recovery and decrease post-concussive symptoms.52
Patients should also be instructed to use acetaminophen in case of post-concussive headache. NSAIDs are also appropriate if imaging was negative. Narcotics should be avoided due to potential CNS side effects and dependence potential.11
Patients with mTBI should also be educated about appropriate return to activity. Patients with a high risk of re-injury in their normal activities should consider specific limitations on activity. Patients with sports-related concussions should wait at least one week to return to activity even if they are symptom-free. If they remain symptom-free at that point, their primary care physician may clear them to return to activity.13 Other recommendations for returning to activity according to injury severity are listed in Table 4. Newer guidelines recommend a gradual return to activities with careful monitoring of symptoms.56
Table 4. Return to Activity Recommendations by Concussion Severity28
Concussion Severity |
First Concussion |
Second Concussion |
Third Concussion |
PTA = post-traumatic amnesia; LOC = loss of consciousness |
|||
Grade 1 (mild): |
May return to play if asymptomatic |
May return in 2 weeks if asymptomatic at that time for 1 week |
Should terminate season and may return next year if asymptomatic |
Grade 2 (moderate) |
May return after being asymptomatic for 1 week |
Should wait at least 1 month, may return then if asymptomatic for 1 week, and should consider terminating season |
Should terminate season and may return next year if asymptomatic |
Grade 3 (severe) |
Should wait at least 1 month and may return then if asymptomatic for 1 week |
Should terminate season and may return next year if asymptomatic |
|
Additional Aspects
Alcohol Intoxication. Head injury severity is significantly higher in intoxicated patients. Additionally, intoxicated patients have higher mortality due to TBI and longer ICU lengths of stay.57 However, the actual yield of findings on CT scans of intoxicated patients is relatively low at 1.9%.58 Although alcohol intoxication is a risk factor for head injury, mortality among intoxicated patients with isolated severe TBI is not increased.59 Because of unreliable history and physical examination findings in intoxicated patients, a higher index of suspicion and obtaining CT scans is indicated.
Head Injury in the Elderly. Among the elderly, 10% of falls requiring an ED visit cause TBI. Approximately 12% of elderly patients with a history of a fall without focal findings have an intracranial hemorrhage.60 Thus, a CT scan is indicated in elderly patients with trauma, even without focal findings or history of anticoagulation. When treating elderly patients who have fallen, maintain a high suspicion for intracranial hemorrhage until it is excluded by CT.
Pediatric Head Injuries. Pediatric head injuries occur commonly. Appropriate CT scanning is of particular importance in pediatrics to reduce the long-term risk of radiation exposure from unnecessary imaging.61-66 A recent study validated the PECARN prediction rule to predict which pediatric patients warrant imaging. The PECARN prediction rule recommends against imaging for patients, including: 1.) children younger than 2 years with normal mental status, no scalp hematoma except frontal, no loss of consciousness or loss of consciousness for less than 5 seconds, non-severe injury mechanism, no palpable skull fracture, and acting normally according to the parents; and 2.) children ages 2 years and older with normal mental status, no loss of consciousness, no vomiting, non-severe injury mechanism, no signs of basilar skull fracture, and no severe headache.66
Intimate Partner Violence. Women presenting to the ED with unwitnessed head, neck, or face injuries are more likely to be victims of intimate partner violence.67 In cases of intimate partner violence, head, neck, and face injuries occur commonly, often in association with other injuries. Suspicion should be further raised by reports of causes of injury that cannot be verified and by multiple injuries occurring with the head, neck, or face injury.67 Women with head, neck, or face injuries should be screened for possible intimate partner violence. The Partner Violence Screen or the Woman Abuse Screening Tool are both appropriate screening tools that increase the specificity of using head, neck, and face injuries as a potential marker for intimate partner violence in the ED.68
Disposition
Consultation. Conditions that require emergent neurosurgical consultation include herniation signs, intracranial imaging abnormalities, and declining mental status. Additionally, neurosurgical consultation may be considered for patients with focal neurologic deficits or who meet any of the "high-risk" criteria under the Canadian CT Head Rule: GCS score < 15 at 2 hours after injury, suspected open or depressed skull fracture, any sign of basilar skull fracture, or age greater than 64 years.69
Admission Criteria. Following complete evaluation, minor head injury patients may be appropriately managed as outpatients with primary care or neurologic follow-up and appropriate medical management. Moderate or severe head trauma warrants hospital admission and emergent neurosurgical consultation.
Summary
Head trauma is a common cause of significant morbidity and mortality, and appropriate ED management can optimize the long-term effects of head trauma. Careful attention should be paid to the trauma assessment to assess other coexisting injuries. Diagnostic tests including head computed tomography are indicated in most cases of significant head trauma to exclude intracranial injury. Following complete evaluation, minor head injury patients may be appropriately managed as outpatients with primary care or neurologic follow-up and appropriate medical management. Moderate or severe head trauma warrants hospital admission and emergent neurosurgical consultation. Prompt evaluation, treatment, and referral are indicated to reduce the incidence of long-term neurologic deficits.
References
- Langlois JA, Rutland-Brown W, Thomas KE. Traumatic brain injury in the United States: Emergency department visits, hospitalizations, and deaths. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2006.
- Armed Forces Health Surveillance Center (AFHSC). Surveillance snapshot: Emergency department visits for traumatic brain injury. MSMR 2011;18(5):15.
- Andriessen TM, Horn J, Franschman G, et al. Epidemiology, severity classification, and outcome of moderate and severe traumatic brain injury: A prospective multicenter study. J Neurotrauma 2011;28(10):2019-2031.
- Hukkelhoven CWPM, Steyerberg EW, Rampen AJJ, et al. Patient age and outcome following severe traumatic brain injury: An analysis of 5600 patients. J Neurosurgery 2003;99(4):666-673.
- Dewall J. The ABCs of TBI. Evidence-based guidelines for adult traumatic brain injury care. JEMS 2010;35(4):54-61; quiz 63.
- Wright DW, Merck LH. Chapter 254: Head trauma in adults and children. In: Tintinalli JE, Stapczynski JS, Cline DM, et al, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011.
- Bazarian JJ, Blyth BJ, Mookerjee S, et al. Sex differences in outcome after mild traumatic brain injury. J Neurotrauma 2010;27:527-539.
- Laker SR. Epidemiology of concussion and mild traumatic brain injury. American Academy of Physical Medicine and Rehabilitation 2011;3:S354-S358.
- Summers CR, Ivins B, Schwab KA. Traumatic brain injury in the United States: An epidemiologic overview. Mount Sinai Journal of Medicine 2009;76:105-110.
- Brenner LA, Ivins BJ, Schwab K, et al. Traumatic brain injury, posttraumatic stress disorder, and postconcussive symptom reporting among troops returning from Iraq. J Head Ttrauma Rehabil 2010;25:307-312.
- Blyth BJ, Bazarian JJ. Traumatic alterations in consciousness: Traumatic brain injury. Emerg Med Clin North Am 2010;28:571-594.
- Biros MH, Heegaard WG. Head injury. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice, 7th ed. Philadelphia, PA: Mosby/Elsevier; 2010:295-322.
- Heegaard W, Biros M. Traumatic brain injury. Emerg Med Clin North Am 2007;25:655-678.
- Kramer AH, Le Roux P. Red blood cell transfusion and transfusion alternatives in traumatic brain injury. Curr Treat Options Neurol 2012 Feb 8. [Epub ahead of print].
- Yang CJ, Hsiao KY, Su IC, Chen IC. The association between anemia and the mortality of severe traumatic brain injury in emergency department. J Trauma 2011;71(6):E132-E135.
- Warner MA, O'Keeffe T, Bhavsar P, et al. Transfusions and long-term functional outcomes in traumatic brain injury. J Neurosurg 2010;113(3):539-546.
- Utter GH, Shahlaie K, Zwienenberg-Lee M, et al. Anemia in the setting of traumatic brain injury: The arguments for and against liberal transfusion. J Neurotrauma 2011;28:155-165. Epub 2010 Dec 2.
- Teasdale G, Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 1974;2:81–84.
- King JT Jr, Carlier PM, Marion DW. Early Glasgow Outcome Scale scores predict long-term functional outcome in patients with severe traumatic brain injury. J Neurotrauma 2005;22(9):947-954.
- Shahin H, Gopinath SP, Robertson CS. Influence of alcohol on early Glasgow Coma Scale in head-injured patients. J Trauma 2010;69(5):1176-81; discussion 1181.
- Hoffman JR, Schriger DL, Mower W, et al. Low-risk criteria for cervical-spine radiography in blunt trauma: A prospective study. Ann Emerg Med 1992;21:1454-1460.
- Dickinson G, Stiell IG, Schull M, et al. Retrospective application of the NEXUS low-risk criteria for cervical spine radiography in Canadian emergency departments. Ann Emerg Med 2004;43(4):507-514.
- Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 2003;349(26):2510-2518.
- Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA 2001;286(15):1841-1848.
- Mulligan RP, Friedman JA, Mahabir RC. A nationwide review of the associations among cervical spine injuries, head injuries, and facial fractures. J Trauma 2010;68(3):587-592.
- Demetriades D, Charalambides K, Chahwan S, et al. Nonskeletal cervical spine injuries: Epidemiology and diagnostic pitfalls. J Trauma 2000;48:724.
- Jagoda AS, Bazarian JJ, Bruns JJ Jr, et al. Clinical policy: Neuroimaging and decision making in adult mild traumatic brain injury in the acute setting. Ann Emerg Med 2008;52(6):714–748.
- Bruns JJ Jr, Jagoda AS. Mild traumatic brain injury. Mount Sinai Journal of Medicine 2009;76:129-137.
- Smith-Bindman R, McCulloch CE, Ding A, et al. Diagnostic imaging rates for head injury in the ED and states' medical malpractice tort reforms. AJEM 2010;29:656-664.
- Mendelow AD, Timothy J, Steers JW, et al. Management of patients with head injury. Lancet 2008;372:685-687.
- Smits M, Dippel DW, de Haan GG, et al. External validation of the Canadian CT Head Rule and the New Orleans Criteria for CT scanning in patients with minor head injury. JAMA 2005;294(12):1519-1525.
- Papa L, Stiell IG, Clement CM, et al. Performance of the Canadian CT Head Rule and the New Orleans Criteria for predicting any traumatic intracranial injury on computed tomography in a United States Level I trauma center. Acad Emerg Med 2012;19(1):2-10.
- Harnan SE, Pickering A, Pandor A, et al. Clinical decision rules for adults with minor head injury: A systematic review. J Trauma 2011;71(1):245-251.
- Medzon R, Bracken M, Rathlev NK, et al. Clinically suspected coagulopathy in blunt head trauma. J Emerg Med 2010;39(4):399-405.
- Nishijima DK, Offerman SR, Ballard DW, et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury warfarin or clopidogrel use. Ann Emerg Med 2012;59(6):460-468.
- Haydel MJ, Preston CA, Mills TJ, et al. Indications for computed tomography in patients with minor head injury. N Engl J Med 2000;343(2):100-105.
- Stiell IG, Lesiuk H, Wells GA, et al; Canadian CT Head and C-Spine Study Group. Canadian CT head rule study for patients with minor head injury: Methodology for phase II (validation and economic analysis). Ann Emerg Med 2001;38(3):317-322.
- Topolovec-Vranic J, Pollmann-Mudryj MA, Ouchterlony D, et al. The value of serum biomarkers in prediction models of outcome after mild traumatic brain injury. J Trauma 2011;71(5 Suppl 1):S478-S486.
- Tseng WC, Shih HM, Su YC, et al. The association between skull bone fractures and outcomes in patients with severe traumatic brain injury. J Trauma 2011;71(6):1611-4; discussion 1614.
- Urwin SC, Menon DK. Comparative tolerability of sedative agents in head-injured adults. Drug Safety 2004;27(2):107-133.
- Van Aken HK, Kampmeier TG, Ertmer C, et al. Fluid resuscitation in patients with traumatic brain injury: What is a SAFE approach? Curr Opin Anaesthesiol 2012 Jul 20. [Epub ahead of print]
- Tang ME, Lobel DA. Severe traumatic brain injury: Maximizing outcomes. Mount Sinai Journal of Medicine 2009;76:119-128.
- The Brain Trauma Foundation. Role of antiseizure prophylaxis following head injury. J Neurotrauma 2000;17:549-553.
- Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. II. Hyperosmolar therapy. J Neurotrauma 2007;24 Suppl 1:S14-20.
- Härtl R, Froelich M. Mannitol and hypertonic saline: Going head to head. Crit Care Med 2008;36(3):1005-1006.
- Mortazavi MM, Romeo AK, Deep A, et al. Hypertonic saline for treating raised intracranial pressure: Literature review with meta-analysis. J Neurosurgery 2012;116(1):210-221.
- Frontera JA, Egorova N, Moskowitz AJ. National trend in prevalence, cost, and discharge disposition after subdural hematoma from 1998-2007. Crit Care Med 2011;39(7):1619-1625.
- Nishijima DK, Dager WE, Schrot RJ, et al. The efficacy of Factor VIIa in emergency department patients with warfarin use and traumatic intracranial hemorrhage. Acad Emerg Med 2010;17(3):244-251.
- Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Report to Congress on Mild Traumatic Brain Injury in the United States: Steps to Prevent a Serious Public Health Problem Atlanta, GA: Centers for Disease Control and Prevention; 2003:1-47.
- Menditto VG, Lucci Moira, Polonara S, et al. Management of minor head injury in patients receiving oral anticoagulant therapy: A prospective study of a 24-hour observation protocol. Ann Emerg Med 2012;59(6):451-455.
- Jagoda AS. Mild traumatic brain injury: Key decisions in acute management. Psychiatric Clin North Am 2010;33(4):797-806.
- Carroll LJ, Cassidy JD, Peloso PM, et al. Prognosis for mild traumatic brain injury: Results of the WHO collaborating centre task force on mild traumatic brain injury. J Rehabil Med 2004;(43 Suppl):84-105.
- Zumstein MA, Moser M, Mottini M, et al. Long-term outcome in patients with mild traumatic brain injury: A prospective observational study. J Trauma 2011;71(1):120-127.
- Faux S, Sheedy J, Delaney R, et al. Emergency department prediction of post-concussive syndrome following mild traumatic brain injury — an international cross-validation study. Brain Inj 2011;25(1):14-22.
- Cunningham J, Brison RJ, Pickett W. Concussive symptoms in emergency department patients diagnosed with minor head injury. J Emerg Med 2011;40(3):262-266.
- McCrory P. Consensus Statement on Concussion in Sport: The Third International Conference on Concussion in Sport, held in Zurich, Nov. 2008. Br J Sports Med 2008;43:176-184.
- Choi Y, Jung K, Eo E, et al. The relationship between alcohol consumption and injury in ED trauma patients. AJEM 2009;27:956-960.
- Godbout BJ, Lee J, Newman DH, et al. Yield of head CT in the alcohol-intoxicated patient in the emergency department. Emerg Radiol 2011;18:381-384.
- Talving P, Plurad D, Barmparas G, et al. Isolated severe traumatic brain injuries: Association of blood alcohol levels with the severity of injuries and outcomes. J Trauma 2010;68(2):357-362.
- Gangavati AS, Kiely DK, Kulchycki LK, et al. Prevalence and characteristics of traumatic intracranial hemorrhage in elderly fallers presenting to the emergency department without focal findings. JAGS 2009;57:1470-1474.
- Raja AS, Andruchow J, Zane R, et al. Use of neuroimaging in US emergency departments. Arch Intern Med 2011;171:260-262.
- Kocher KE, Meurer WJ, Fazel R, et al. National trends in use of computed tomography in the emergency department. Ann Emerg Med 2011; Aug 11 (Epub ahead of print)
- Dorfman AL, Fazel R, Einstein AJ, et al. Use of medical imaging procedures with ionizing radiation in children: A population-based study. Arch Pediatr Adolesc Med 2011;165(5):458-464.
- Cohen MD. Pediatric CT radiation dose: how low can you go? Am J Roentgenol 2009;192:1292-1303.
- Furlow B. Radiation dose in computed tomography. Radiol Technol 2010;81:437-450.
- Kuppermann N, Holmes J, Dayan, PS et al; for the Pediatric Emergency Care Applied Research Network (PECARN). Identification of children at very low risk of clinically-important brain injuries after head trauma: A prospective cohort study. Lancet 2009;374:1160-1170.
- Wu V, Huff H, Bhandari M. Pattern of physical injury associated with intimate partner violence in women presenting to the emergency department: A systematic review and meta-analysis. Trauma Violence, & Abuse 2010;11(2):71-82.
- Perciaccante VJ, Carey JW, Susarla SM, et al. Markers for intimate partner violence in the emergency department setting. J Oral Maxillofac Surg 2010;68:1219-1224.
- Van Essen TA, Heeringa JJ, Muizelaar J-P. (In)appropriate neurosurgical consultation. Clin Neurol Neurosurg 2010;112(9):775-780.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content