Mild Traumatic Brain Injury: Initial Medical Evaluation and Management

Micelle J. Haydel

GENERAL PRINCIPLES

Definition

Mild traumatic brain injury (MTBI) describes patients with a transient alteration in consciousness, motor function or cognitive ability after a traumatic force to the head. These patients present with a normal or near-normal level of consciousness and have a low likelihood (less than 1%) of having a clinically significant intracranial injury (ICI), but do have a significant likelihood (up to 30%) of experiencing postconcussive symptoms [1,2].

Epidemiology

Almost 1.5 million people in the United States seek care for MTBI each year, while double that amount are thought to sustain sport- or recreation-related injury but do not seek care [3,4].

Classification

The Glasgow Coma Scale (GCS) is used extensively to classify traumatic brain injury (TBI) into levels of severity. Patients with a GCS of 13 to 15 are traditionally classified as having MTBI, although it is recognized that a patient with a GCS of 15 is generally managed differently than a patient with a GCS of 13. The American College of Surgeons Committee on Trauma and the CDC have recently changed their prehospital guidelines to recommend that patients with a GCS of 13 or lower be triaged to the highest level of care within a Trauma System [5].

Etiology

Leading causes of MTBI: [3,6]

• Falls—largely occurring in the very young and the very old

• Motor vehicle-related injury—primarily occurring in young adults

• Work, sports, and recreational injury

• Assault

Pathophysiology

MTBI is a complex pathophysiologic process caused by direct or indirect traumatic biomechanical forces to the head. Symptoms largely reflect a functional disturbance, rather than a structural injury that can be seen on standard computed tomography. The precise mechanisms responsible for the clinical features of mild TBI remain unclear, but using functional MRI, clinical symptoms can now be mapped to specific areas of the brain with axonal injury [7].

Mechanism of Injury

The primary injury is caused by the immediate mechanical force, whereas the secondary injury is caused by the evolving pathophysiological consequences that encompass complex neurobiological cascades, which are worsened by hypoxia, ischemia, and the release of excitatory amino acids, calcium, or other neurotoxins.

DIAGNOSIS

Risk Factors

Less than 10% of patients with MTBI have ICI visible on CT and less than 1% requires neurosurgical intervention. It is the clinician’s task to screen for the small subset of patients who harbor significant intracranial lesions, while minimizing excessive costs, radiation exposure, admissions, and unnecessary diagnostic procedures. Many of the risk factors for ICI in MTBI are history- and symptom-based, which makes it imperative that the clinician secure an accurate injury-related history.

Clinical Presentation

The majority of patients with MTBI have a straightforward clinical presentation and relatively rapid spontaneous resolution of symptoms. Some patients do have an unclear injury history with little or no physical evidence of trauma, making the diagnosis of MTBI more challenging.

• The mechanisms of injury associated with an increased risk of ICI include pedestrian struck by a motor vehicle, occupant ejected from a motor vehicle, or a fall over 3 ft. or 5 stairs [8].

• Anticoagulation: Preinjury anticoagulant or antiplatelet use, haemophilia, or platelet disorders are associated with increased risk of immediate and delayed ICI in patients with TBI [9,10].

• Past medical history: CNS surgery, past head trauma, or immediate posttraumatic seizures are associated with increased risk of ICI in patients with TBI [1].

• Age: Patients over the age of 65 have an increased risk of ICI due to MTBI [1], and older age has been shown to be an independent predictor of mortality in isolated MTBI [11–13]. Elderly patients with ICI often have fewer clinical clues or serious mechanisms of injury than younger patients [14].

• Reported loss of consciousness or posttraumatic amnesia marginally increase the risk of ICI, but their absence are useful as negative predictors only if the patient has no other associated symptoms or risk factors [1,15,16].

• Drug or alcohol use: chronic or concurrent intoxication are associated with increased risk of ICI in patients with MTBI [13,17].

• Sport-related injury: Several factors are thought to be predictive of poorer outcomes after MTBI: number of past concussions, severity and duration of symptoms, and time elapsed since last concussion [18].

Symptoms

Red Flag symptoms in patients with MTBI include:

• Neurologic signs shown to have a significantly high-positive likelihood ratio for ICI include persistent short-term memory deficits, seizures, deterioration in mental status, GCS less than 14, and focal neurological deficit [1,19].

• Repeated vomiting has a high-positive likelihood ratio for ICI in patients with MTBI [20].

• Headache (particularly if severe or persistent) has been associated with a small but significant increased risk of ICI in MTBI [1,19]. Headache can also be the presenting complaint in carotid dissection.

• Neck pain, though most commonly due to mechanical soft tissue injury, should trigger the clinician to consider cervical fractures, or carotid or vertebral artery dissection.

Physical Examination

Patients with MTBI must undergo a focused physical examination with attention to the neurological evaluation. All patients should have their cervical spine assessed promptly to determine need for c-spine immobilization or imaging. Physical findings suggestive of a depressed or basilar skull fracture are strongly correlated with ICI; otherwise, the most prognostic elements of the physical examination are the pupillary examination and the GCS [21]. The motor examination can identify subtle cranial nerve deficits [22], as well as balance and coordination deficits that may persist long after other symptoms of MTBI have resolved [18].

• Pupils: Pathological pupillary reflexes indicate both underlying pathology and severity of injury, and should be monitored serially. Pupillary abnormalities in patients with a GCS greater than 13 are most likely due to etiologies other than TBI [21].

• Motor: The cranial nerve examination should include attention to CN IV and VI, because subtle deficits may not be evident until the patient is taken through a careful extra-ocular exam [22]. Alterations in balance and gait have shown to be predictive of postconcussive symptoms [23]. Examination of gait and balance are useful, because they require the complex integration of motor, visual, cerebellar, vestibular, and proprioceptive functions. Coordination can be assessed using finger-to-nose and rapid alternating hand movements [18]. Gait (straight-line and tandem) is often used in the ED as a marker of balance.

• GCS: Scoring for each component of the GCS should be documented separately in order to provide complete information for subsequent measures (e.g., GCS 10 = E3 V4 M3) [24]. Motor deficits have the strongest correlation with poor outcome in patients with TBI [21], and a motor-only score has been shown to perform as well as the GCS [25,26].

• Cognitive Examination: While it has been shown that patients with a GCS of 13 or 14 are more likely to have ICI on head CT, focused cognitive testing has revealed that the correlation between CT findings and subtle cognitive deficits (found in up to 30% of patients with MTBI) are much less clear [27,28]. Cognitive deficits may be identified by testing short-term memory (e.g., 3-item recall, 5-number recall) and concentration (e.g., serial sevens, backwards months of the year, or “world” spelling).

Laboratory Studies

Routine laboratory and bedside studies have little value in the evaluation of patients with mild TBI. Certain groups of patients may benefit from routine laboratory and bedside studies:

• Patients with a GCS of 13 or 14 should undergo a bedside glucose, and may benefit from a blood count, electrolyte panel, and toxicology screen.

• Patients over the age of 65 and those with significant comorbid conditions or weakness should have an electrolyte panel, blood count, urinalysis, and electrocardiogram.

• Patients with known or suspected coagulation disorders, liver disease, or those taking anticoagulants benefit from coagulation studies.

Radiographic Assessment

Noncontrast CT is both highly sensitive and specific for the detection of fractures, contusions, epidural and subdural bleeds, and subarachnoid hemorrhages, and remains the diagnostic imaging technique of choice in patients with TBI [24]. Radiation exposure from head CT is relatively small, and risk of radiation-induced cancer is inversely related to age: a 40-year-old undergoing a single head CT has an added cancer risk of 1:8—10,000, but a 20-year-old has an added risk of 1:4—5,000 [29].

Immediate CT is indicated in TBI patients with:

• Evidence of basilar, depressed or open skull fracture

• Focal neurological deficits

• Altered mental status or GCS less than 13

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