Closed Head Injury 

Updated: May 04, 2022
Author: Leonardo Rangel-Castilla, MD; Chief Editor: Brian H Kopell, MD 

Overview

Practice Essentials

In the United States, closed head injury, or traumatic brain injury (TBI), has an annual incidence of approximately 500 in 100,000. Around 80% of all TBI cases are categorized as mild head injuries.[1]  Approximately 15% of these patients succumb to the injury upon arrival to the emergency department.[2]  In 2019, nearly 61,000 deaths were attributed to a TBI.[3]  Higher rates of morbidity and mortality resulting from TBI are seen in low-income and middle-income counties, making this a global health challenge.[4]  

Penetrating intracranial injuries have worse outcomes than closed head injuries. Data from the Healthcare Cost and Utilization Project (HCUP) National Inpatient Sample analyzed by the Centers for Disease Control and Prevention (CDC) show that during 2018, there were 223,050 nonfatal TBI-related hospitalizations. Unintentional falls were the most common mechanism of injury leading to nonfatal TBI-related hospitalization, followed by motor vehicle crashes. Proper and consistent use of recommended restraints (ie, seatbelts, car seats, and booster seats) and, particularly for persons aged ≥75 years, learning about individual fall risk from health care providers are steps the public can take to prevent the most common injuries leading to nonfatal TBI.[5]

Closed head injuries are classified as primary and secondary. A primary injury results from the initial anatomic and physiologic insult, which is usually direct trauma to the head, regardless of cause. A secondary injury results from hypotension, hypoxia, acidosis, edema, or other subsequent factors that can secondarily damage brain tissue. Free radicals are thought to contribute to these secondary insults, especially during ischemia.

(A computed tomography scan of left frontal acute epidural hematoma is shown below.)

CT scan of left frontal acute epidural hematoma (b CT scan of left frontal acute epidural hematoma (black arrow) with midline shift (white arrow). Note the left posterior falx subdural hematoma and left frontoparietal cortical contusion.

Head injury significantly contributes to death from trauma. Traumatic brain injury is increasingly viewed as a chronic condition, bringing long-term needs for patient and caregiver knowledge pertaining to symptom and problem management over time. The authors of a scoping review of TBI education for adult patients and families recommend further exploration of self-management training principles in long-term TBI care to assess the specific effects of education and other treatment elements.[6]

Those who survive are often left with severe neurologic deficits that may include a persistent vegetative state. A great financial burden is associated with head injuries because of lifelong disability. Injuries to the central nervous system tend to be most costly on a per-patient basis because they often result in debilitating physical, psychological, and psychosocial deficits that, in turn, require extensive long-term rehabilitation and care.

Pathophysiology

Primary injuries

Primary injuries are injuries that upon initial impact cause displacement of the brain due to direct impact, rapid acceleration-deceleration, or penetration.[7]  Primary closed head injury usually causes structural changes, such as epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, or cerebral contusion.

Concussion

Cerebral concussion is defined as an altered mental state that may or may not include loss of consciousness that occurs as a result of head trauma. Concussion is also known as mild traumatic brain injury (MTBI). The American Academy of Neurology Grading Scale is widely used to categorize the degree of concussion.

Table 1. American Academy of Neurology Concussion Grading Scale (Open Table in a new window)

Grade 1

Grade 2

Grade 3

Transient confusion

Transient confusion

...

No loss of consciousness

No loss of consciousness

Brief or prolonged loss of consciousness

Concussive symptoms or mental status change resolving within 15 minutes

Concussive symptoms or mental status change resolving after 15 minutes

 

...

Mild TBI or brain concussion usually results from closed brain injuries, such as when the head has been struck by an object like a bat or a fist during a fight, or when the head is affected by a nearby blast or explosion. Mild TBI causes a transient altered mental status, which can range from confusion to loss of consciousness. This cannot be diagnosed by routine computed tomography (CT) or magnetic resonance imaging (MRI). Special sequence MRI such as diffusion tensor imaging or functional MRI can lead to earlier diagnosis of concussion.[1]

Concussion is a common injury in childhood, with an estimated 1.4 million children sustaining a concussion annually in the United States.[8]

A systematic review of original research capturing people of all ages in a well-defined population area was conducted to estimate the incidence of sports-related TBI in the general population across injury severities, with the goal of informing injury prevention initiatives. Review authors reported that the incidence of sports-related TBI within hospital-based studies ranged between 3.5 and 31.5 per 100,000. One community-based study using multiple case ascertainment sources identified a higher incidence of 170 per 100,000. Sports-related TBI accounted for 1.2-30.3% of all TBI events.[9]

Sports-related concussions are frequent. The University of Michigan Health Neurosciences website reports that about 3.8 million concussions occur each year in the United States as the result of sports-related injuries. Many of these injuries go unreported and undiagnosed, resulting in mismanagement and premature return to activity, which can lead to prolonged symptoms and long-term consequences. Traumatic brain injury doubles risk of suicide and is the major determinant of acquired seizure disorders. Traumatic brain injury arising from closed head trauma significantly increases the risk of developing Alzheimer disease, Parkinson disease, and chronic traumatic encephalopathy (CTE), the last of which occurs particularly when football players and boxers are exposed to repetitive concussions.[10]  Repetitive concussions may result in chronic subclinical motor dysfunction linked to intracortical inhibitory system abnormalities.[11] Parkinsonian cognitive decline due to strionigral degeneration is now a well-known consequence of repetitive concussions; cumulative diffuse axonal injury effects in the midbrain are due to increased vulnerability to shear forces in that region. Increasing a player’s neck strength may be an effective way to minimize the risk of future concussions, as studies with Hybrid III dummies seem to indicate.[12]

Cerebral contusion

Cerebral contusions are commonly seen in the frontal and temporal lobes. They may accompany skull fracture—the so-called fracture contusion. The most worrisome trait of these contusions is their tendency to expand. This usually occurs from 24 hours to as long as 7-10 days after the initial injury. For this reason, cerebral contusions are often followed with a repeat head CT scan within 24 hours after injury.

Coup injuries (contusions), which are caused by direct transmission of impact energy through the skull into the underlying brain, occur directly below the site of injury. Contrecoup injuries are caused by rotational shear and other indirect forces that occur contralateral to the primary injury. Rotational force causes the basal frontal and temporal cortices to impact or sweep across rigid aspects of the skull, the sphenoid wing, and petrous ridges. Delayed enlargement of traumatic intraparenchymal contusions and hematomas is the most common cause of clinical deterioration and death. However, progression of contusion is highly variable, and although most contusions remain unchanged for days, a few enlarge—some quite rapidly.

Several prognostic factors are known to predict contusion enlargement. The strongest of these prognostic factors is the presence of traumatic subarachnoid hemorrhage. The size of the intraparenchymal hemorrhage means that large lesions are probably in an active phase of progression at the time of the initial CT scan. The concurrent presence of a subdural hematoma is also predictive. Clinical features, such as initial Glasgow Coma Scale score (GCS; see the Glasgow Coma Scale calculator) and intracranial pressure (ICP), are not predictive of progression. The ideal time for a re-scan is unclear, although most growth seems to occur within the first 24 hours of injury.[13]

Epidural hematoma

Epidural hematoma accounts for 1% of all head trauma admissions, as depicted in the image below.[14] Epidural hematomas most commonly (85%) result from bleeding in the middle meningeal artery but may occur in locations other than in the distribution of the middle meningeal artery. Such hematomas may develop as the result of bleeding from diploic vessels injured by overlying skull fractures.[15] Epidural hematomas are often associated with a "lucid interval"—a period of consciousness between states of unconsciousness. This lucent period is presumed to end when the hematoma expands to the point that the brainstem is compromised.

CT scan of left frontal acute epidural hematoma (b CT scan of left frontal acute epidural hematoma (black arrow) with midline shift (white arrow). Note the left posterior falx subdural hematoma and left frontoparietal cortical contusion.

Subdural hematoma

The most common surgical intracranial lesion is the subdural hematoma. This occurs in approximately 20-40% of patients with severe injuries, as depicted in the image below.[2, 16] A surface or bridging vessel (venous) can be torn when the brain parenchyma moves during violent head motion. The bleeding that results causes a hematoma to form in the potential space between the dura and the arachnoid. A lucid interval is less likely to develop with this type of injury than with an epidural hematoma. Subdural hematoma may result from an arterial rupture as well; these hematomas are found in the temporoparietal region and differ in form from those caused by the bridging vein rupture, which typically are seen in the frontoparietal parasagittal region. Hematoma thickness and midline shift of the brain are often analyzed; when midline shift exceeds hematoma thickness (positive displacement factor), the prognosis is poorer.[17]

CT scan of left frontoparietal acute subdural hema CT scan of left frontoparietal acute subdural hematoma (black arrow). Note the moderate amount of midline shift.

Intraventricular hemorrhage

Intraventricular hemorrhage is another intracerebral lesion that often accompanies other intracranial hemorrhages, as depicted in the image below. Intraventricular blood is an indicator of more severe head trauma. Intraventricular blood predisposes the patient to posttraumatic hydrocephalus and intracranial hypertension, which may warrant placement of an intraventricular catheter (if emergent drainage is needed) or a ventriculoperitoneal shunt for chronic hydrocephalus.

CT scan of bilateral acute intraventricular hemorr CT scan of bilateral acute intraventricular hemorrhages (black arrow). Note the comminuted skull fractures that involve bilateral frontal, temporal, and parietal bones (white arrow). Note the ischemic changes in both frontal lobes, subarachnoid hemorrhages in the intrahemispheric fissure and left frontal lobe, and multiple intraparenchymal hemorrhages in both frontal poles.

Traumatic subarachnoid hemorrhage

Subarachnoid hemorrhage is most commonly caused by trauma and results from tearing of small capillaries, with blood subsequently entering into the subarachnoid space. It commonly occurs over the convexity but may be seen in the basal cistern secondary to aneurysmal rupture.[1]

Diffuse axonal injury

One of the consistent pathologies associated with both clinical and experimental TBI is axonal injury, especially following mild TBI (or concussive injury).[18]  Despite the absence of any intracranial mass lesion or history of hypoxia, some patients remain unconscious after a TBI. Brain MRI studies have demonstrated a clear correlation between white matter lesions and impairment of consciousness after injury. The deeper the white matter lesion, the more profound and persistent the impairment of consciousness.[19]

The usual cause for persistent impairment of consciousness is the condition referred to as diffuse axonal injury (DAI), as depicted in the image below. Approximately 30-40% of individuals who die from TBI reveal postmortem evidence of DAI and ischemia.[20] This type of injury commonly results from traumatic rotation of the head, with mechanical forces that act on the long axons, leading to axonal structural failure. Diffuse axonal injury is caused by an acceleration injury—not by contact injury alone. The brain is relatively incompressible and does not tolerate tensile or shear strain well. Slow application of strain is better tolerated than rapid strain. The brain is most susceptible to lateral rotation and tolerates sagittal movements best.[21]

MRI of the brain that shows diffuse axonal injury MRI of the brain that shows diffuse axonal injury (DAI) and hyperintense signal in the corpus callosum (splenium), septum pellucidum, and right external capsule.

Studies suggest that the magnitude of rotational acceleration needed to produce DAI requires the head to strike an object or surface. These factors also increase the likelihood that DAI will be accompanied by other intracranial lesions.[21] Mechanical forces physically dissect the axons into proximal and distal segments. If a sufficient number of axons are involved, profound neurologic deficits and unconsciousness may ensue. Characterization of DAI using diffusion tensor magnetic resonance imaging (DTI) may provide a useful set of outcome measures for preclinical and clinical studies.[22]

One study found that DAI and younger age may contribute to increased risk of developing dysautonomia.[23]

These same forces may act on the cerebral circulation, causing disruption of vessels and various forms of micro–intracerebral hemorrhage and macro–intracerebral hemorrhage, including Duret hemorrhage, which is commonly lethal when it occurs in the brainstem. Duret hemorrhage of the midbrain and pons is a small punctate hemorrhage that is often caused by arteriole stretching during the primary injury, as depicted in the image below. Duret hemorrhage may also occur during transtentorial herniation as a secondary injury when arterial perforators are compressed or stretched.

MRI of the brain (sagittal view) that shows a Dure MRI of the brain (sagittal view) that shows a Duret hemorrhage in the splenium of the corpus callosum.

Secondary injuries

Secondary injuries consist of changes that occur after the initial insult.[7]  Secondary insult can take many forms.

  • Secondary intracranial insults to the brain include the following: hemorrhage, ischemia, edema, raised intracranial pressure (ICP), vasospasm, infection, epilepsy[24] , hydrocephalus.

  • Secondary systemic insults to the brain include the following: hypoxia, hypercapnia, hyperglycemia, hypotension, severe hypocapnia, fever, anemia, hyponatremia.

Management of acute closed head injury is intended to prevent secondary injuries while preserving neurologic functions that have not been damaged by the primary injury.

Posttraumatic vasospasm can cause ischemic damage after severe TBI; parenchymal contusions and fever are risk factors. Diffuse mechanical injury and activation of inflammatory pathways may be secondary mechanisms for this vasospasm. Patients with parenchymal contusions and fever may benefit from additional screening.[25]

Brain herniation

Herniation of the brain occurs as the result of increased ICP. Types of herniation include the following:

  • Uncal transtentorial: compression of parasympathetic fibers running with the third cranial nerve; seen as ipsilateral fixed and dilated pupil with contralateral hemiparesis.
  • Central transtentorial: midline lesions such as lesions of the frontal or occipital lobes or vertex; seen as bilateral pinpoint pupils, bilateral Babinski signs, and increased muscle tone, followed by fixed midpoint pupils with prolonged hypertension and decorticate posturing.
  • Cerebellar tonsillar: compression on the lower brainstem and upper cervical spinal cord; seen as pinpoint pupils, flaccid paralysis, and sudden death.
  • Upward posterior fossa/cerebellar: displacement of the cerebellum in an upward direction through the tentorial opening; seen as conjugate downward gaze with absence of vertical eye movement and pinpoint pupils. [7]

Cerebral ischemia

Cerebral ischemia refers to inadequate oxygen perfusion to the brain resulting from hypoxia or hypoperfusion. The undamaged brain tolerates low levels of partial pressure of oxygen in arterial blood (PaO2) better than the severely injured brain. Traumatized brain tissues are very sensitive to even moderate hypoxia (90 mm Hg). Gordon and Ponten proposed 2 explanations for this phenomenon: (1) Respiratory alkalosis may shift the oxygen-hemoglobin curve to the left, thereby increasing the affinity of hemoglobin to oxygen and decreasing the ease of oxygen release; and (2) uneven cerebral blood flow (CBF) may result from focal vasospasm with loss of focal autoregulation in the area of injured brain tissue.[21] Approximately one third of patients with severe head injury experience ischemic levels of CBF.[26]

Cerebral blood flow is normally kept constant over a range (about 50-150 mm Hg) of cerebral perfusion pressure, as depicted in the image below. This is made possible by adjustments in vascular tone known as autoregulation (solid line). In patients with brain trauma, this autoregulation may malfunction and CBF may become dependent on cerebral perfusion pressure (CPP) (dashed lines). Autoregulation is absent, diminished, or delayed in 50% of patients with severe head injury.[26] The lowest CBF values occur within the first 6-12 hours after injury.[27, 28, 29, 30] The overall outcome of patients who experience ischemia is much worse than that of initially nonischemic patients.[26, 31, 32] The initial ischemia is thought to cause permanent irreversible damage, even if CBF is eventually optimized. Xenon CT scan is used to measure CBF as part of the armamentarium for diagnosis and treatment of abnormalities in CBF.

Cerebral blood flow/cerebral perfusion pressure ch Cerebral blood flow/cerebral perfusion pressure chart.

Brain edema

Brain edema is another form of secondary injury that may lead to elevated ICP, frequently resulting in increased mortality. Brain edema is categorized as vasogenic or cellular (or cytotoxic) edema.

Vasogenic edema occurs when a breach in the blood-brain barrier allows water and solutes to diffuse into the brain. Most of this fluid accumulates in the white matter and can be observed on head CT scan as hypodense white matter (on T1-weighted images) or on T2-weighted MRI as a bright signal area. The mechanism of cellular (cytotoxic) edema is less clear. Theories include increased uptake of extracellular potassium by injured brain cells or transport of bicarbonate (HCO3-) and hydrogen (H+) for chloride (Cl-) and sodium (Na+) by injured brain tissue as the mechanism of insult.[21]

Diffusion-weighted MRI has been used to evaluate the apparent diffusion coefficient (ADC). Higher ADC values are associated with vasogenic edema, and lower ADC values with a predominantly cellular form of edema. Regional measurements of ADC have been computed for patients with focal and diffuse injury. Researchers have concluded that the brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.[33]

Epidemiology

The male-to-female ratio for TBI is 2:1. The Centers for Disease Control and Prevention (CDC) has estimated that annually, about 1.5 million US individuals survive a TBI. Among these, approximately 230,000 are hospitalized. In the year 2000, 10,958 cases of TBI were diagnosed. By 2015, this number had jumped to 344,030. Mortality across all TBI severities is approximately 3%, and morbidity is more difficult to estimate.[1] Although only 10% of TBI cases occur in the elderly population, it accounts for up to 50% of TBI-related deaths.[7]

In the United States, closed head injury, or TBI, has an annual incidence of approximately 500 in 100,000. Around 80% of all TBI cases are categorized as mild head injuries.[1]  Approximately 15% of these patients succumb to the injury upon arrival to the emergency department.[2] In 2019, nearly 61,000 deaths were attributed to TBI.[3]  Higher rates of morbidity and mortality resulting from TBI are seen in low-income and middle-income counties, making this a global health challenge.[4]

Data from the Healthcare Cost and Utilization Project (HCUP) National Inpatient Sample analyzed by the CDC show that, during 2018, there were 223,050 nonfatal TBI-related hospitalizations; rates for persons aged 75 years or older were approximately 3 times higher than that for persons aged 65-74 years, and the age-adjusted rate for males was approximately double that for females. Unintentional falls were the most common mechanism of injury leading to nonfatal TBI-related hospitalization, followed by motor vehicle crashes. Proper and consistent use of recommended restraints (ie, seatbelts, car seats, and booster seats) and, particularly for persons aged 75 years or older, learning about individual fall risk from health care providers are steps the public can take to prevent the most common injuries leading to nonfatal TBI.[5]

The CDC estimates that 166 TBI-related deaths occur every day in the United States.[34]

Traumatic injuries remain the leading cause of death in children and in adults aged 45 years or younger. Traumatic brain injury resulting from military combat, sports, violence, falls, and vehicular accidents is a major cause of long-term physical, cognitive, and psychiatric dysfunction. Psychiatric disorders associated with TBI include depression, anxiety, and substance use disorder—all with significant implications for post-TBI recovery and rehabilitation.[35]

Head injury is an important cause of morbidity and mortality in children and young adults. Head injury, even closed head injury without visible violation of the globe or orbits, is associated with multiple sight-threatening complications. One such entity is traumatic optic neuropathy.[36]

Incidence varies by age, but children and young people experience closed head trauma more often than older populations. Older adults are more likely to die from a TBI than are those in other age groups. Although falls are the leading cause of nonfatal TBI, fall-related TBI deaths have increased, particularly in adults older than 75 years.[34]

In the United States, around 1.7 million people suffer TBI; older adolescents (aged 15-19 yr) and older adults (aged ≥65 yr) are most likely to sustain a TBI. Moderate to severe TBI is a primary cause of injury-induced death and disability.[1]

Prognosis

The prognosis for TBI is affected by many factors, including (1) type of injury (penetrating vs blunt), (2) severity of injury and accompanying neurologic deficit, (3) patient age, (4) comorbid conditions, and (5) secondary injuries.

Each year in the United States, nearly 52,000 deaths occur as the result of TBI. Individuals who arrive for treatment with low Glasgow Coma Scale (GCS) scores have the worst outcomes. Even those who survive have prolonged recovery, and some are left with residual neurologic deficits. Complete recovery can take months or even years.[1]

It is interesting to note that many questions continue to demand answers. These include prognosis, permanency of symptoms, best short-term and long-term treatment strategies, and whether literature on sports-related TBI can be used as a guide. Imaging and therapeutic intervention research are under way in the hope of delivering better patient outcomes. The prognosis for patients with TBI depends on initial GCS score and neurologic deficits at presentation. Patients with a GCS less than 12 usually have a long recovery, and many continue to have residual neuropsychiatric deficits.[1]

The GCS has been reported to be most predictive of neurologic outcomes at 1 year after severe head injury, and 24-hour GCS score is the strongest predictor of cognitive recovery at 2 years after injury in patients with moderate to severe head injury.[37, 38]

In a study of mortality including 44 elderly patients (aged ≥75 yr) who underwent an operation for acute subdural hematoma, patients who were independent had 1-year mortality of 42% versus 69% for dependent patients (median follow-up, 4.2 yr; range, 2.5-6.4 yr). Patients taking antithrombotics had 56% mortality after the first postoperative year versus 30% for those not taking antithrombotics. All patients with an admission GCS score of 3-8 died within the first postoperative year if they had used antithrombotics or were dependent before the injury.[39]

Patients in the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) treated via craniotomy or craniectomy for subdural hemorrhage were studied for mortality, other adverse outcomes, and length of hospital stay. The most common individual adverse events were death (18% of patients died within 30 days of surgery) and intubation longer than 48 hours (19%). In total, 34% experienced a serious adverse event other than death, 8% returned to the operating room, and average hospital length of stay was 9.8±9.9 days. Increased mortality was associated with gangrene, ascites, American Society of Anesthesiologists (ASA) physical status class 4 or higher, coma, and bleeding disorders. Reduced mortality was associated with age younger than 60 years.[40]

A study of patients with chronic subdural hematoma found that neurologic status on admission was the best predictor of outcome. In addition, age, brain atrophy, thickness and density of hematoma, subdural accumulation of air, and antiplatelet and anticoagulant therapy were found to correlate significantly with prognosis.[41]

Pupillary function before and after resuscitation has some predictive value. In patients who initially have bilateral unreactive pupils (and whose pupils do not regain function), approximately 85% die or remain in a persistent vegetative state, as compared to 15% of those who regain pupillary function.[21]

Age also influences overall outcome. Infants and very young children tend to have a higher mortality rate. This is most likely due to the nature of their injuries and associated prolonged episodes of apnea. The mortality rate from closed head injury remains relatively constant until after the age of 35 years, at which time it begins to rise dramatically.[42]

The development and duration of fever is clearly associated with worse prognoses.[14]

Insulin deficiency due to diabetes mellitus (DM) has been found to impart increased risk for mortality in patients with moderate to severe TBI compared to patients without DM (14.4% vs 8.2% ).[43]

 

Presentation

Physical

A comprehensive evaluation should include utilization of the following tools:

  • Clinical history/presentation with thorough neurologic (Glasgow Coma Scale score) and psychiatric evaluation, including cognitive assessment
  • Laboratory studies
  • Imaging [1]

Neurologic and psychiatric evaluation

The Glasgow Coma Scale (GCS), first introduced by Teasdale and Jennett in 1974, has been the standard for objectively assessing individuals with traumatic head injuries (Table 2).[44] This scale comprises motor, verbal, and eye scores. The overall score generally refers to the best response/examination obtained within the first 6-8 hours after injury and following resuscitation and is considered to be a predictor of the patient's overall outcome.[2, 45, 46, 47, 48]

The GCS offers 2 main advantages in that it provides a reproducible, objective evaluation of neurological status, and it is a relatively simple way to monitor a patient's neurologic condition over time. The GCS has shortcomings because its reliability depends on the absence of confounding factors (eg, sedation, paralytics, hypothermia, hypotension, hypoxia). Additionally, it cannot compensate for lack of eye opening in patients with periorbital trauma or loss of verbal response in intubated patients, and it omits brainstem reflex assessment.[49, 50]

Most clinicians assign a verbal score of 1 and apply the modifier "T" to intubated individuals. This may not lead to an accurate assessment of the patient's true verbal score.[51] The motor component of the GCS score is most predictive of the severity of brain injury and correlates most strongly with overall outcome.[51]

The GCS is often used to categorize the severity of head injury as mild (15-13), moderate (12-9), or severe (≤8). In general, mild head injury does not usually involve significant primary brain injury, is not associated with neurologic deficits, and may or may not include loss of consciousness. Approximately 75% of head injuries are categorized as mild to moderate in nature.[52] Most authorities agree that a patient with severe head injury is one who is unconscious and unable to follow simple commands.

Table 2. Glasgow Coma Scale (Open Table in a new window)

Best Motor Response

Obeying commands

6

Localizing

5

Withdrawal (abnormal flexion)

4

Flexion (decorticate posturing)

3

Extension (decerebrate posturing)

2

No response

1

Verbal Response

Oriented

5

Confused

4

Using inappropriate words

3

Making incomprehensible sounds

2

No response

1

Eye Opening

Spontaneous

4

To command

3

To pain

2

No response

1

Total

 

3-15

Patients should also be evaluated for basic brainstem reflexes. This assessment should include evaluation of pupillary reflex, corneal reflex, gag/cough reflex, oculocephalic reflex, vestibulo-ocular reflex, and spontaneous breathing. Pupillary asymmetry or anisocoria greater than 1 mm (up to 1 mm may be physiologic) must be attributed to an intracranial lesion until proven otherwise.[51]

Careful attention must be given to evaluation of spontaneous breathing in the ventilated patient. A common pitfall is to mistakenly assess a patient as taking spontaneous breaths when sensitivity on the ventilator is set to a level that triggers a mechanical breath at the slightest effort by the patient.

Proper evaluation entails setting the ventilator sensitivity to zero, then reevaluating the patient after a few seconds, which does not allow time for hypoxia or hypercapnia to develop. The presence of any of the above reflexes confirms that the patient has at least basic brainstem reflexes. Complete absence of brainstem reflexes is an ominous sign.

 

Workup

Laboratory Studies

Lab studies include the following:

  • Serum levels of 2 biomarkers correlating with degree of brain injury, with GFAP more reliable up to 7 days after impact: glial fibrillary acid protein (GFAP), ubiquitin C-terminal hydrolase (UCH-L1)[1]

  • Complete blood count (CBC) including platelet count

  • Blood chemistries

  • Prothrombin time (PT) or international normalized ratio (INR)

  • Activated partial thromboplastin time (aPTT)

  • Anticonvulsant (eg, phenytoin) level: For patients who have been previously loaded or who were previously taking anticonvulsant medication, to ensure therapeutic levels

Serum sodium, urine specific gravity, urine osmolarity, and serum osmolarity tests should be ordered for individuals with urine output ≥250 mL/hr for 3 or more consecutive hours (pediatric patients, >3 mL/kg/hr) and for patients thought to have diabetes insipidus. Large doses of mannitol can mask diabetes insipidus by producing high urine output.

Imaging Studies

Computed tomography (CT) of the head and magnetic resonance imaging (MRI) are used to measure changes in anatomic or physiologic parameters of TBI. These include hemorrhage, edema, vascular injury, and intracranial pressure. However, for most cases of mild TBI, CT and MRI often show no abnormalities.[1]

Diffusion tensor imaging (DTI) is used to detect axonal injury for patients with mild to moderate TBI.[1]

Functional MRI (fMRI) is often used to differentiate patients with TBI from control groups and has been used to study activation patterns in patients with TBI.[1]

Perfusion single photon emission computed tomography (SPECT) is used to measure cerebral blood flow and activity patterns.[1]

Computed tomography scanning of the head is the criterion standard for patients with acute closed head injuries.[53] A head CT scan is warranted, except for patients with only minor head trauma who are neurologically intact and are not intoxicated with drugs or alcohol. Advantages and disadvantages of head CT scan are summarized in the following table.

Table 3. Advantages and Disadvantages of CT Scanning in Head Trauma Evaluation (Open Table in a new window)

Advantages

Disadvantages

Noninvasive and rapid

Traumatic vascular lesions may be missed.

Very sensitive for acute hemorrhage

DAI is likely to be missed.

Defines nature of ICH* (ie, SDH†, SAH‡)

Motion artifact may limit study.

Defines anatomic location of lesion

Posterior fossa lesions are poorly depicted.

Identifies fractures of the cranium

Depressed skull fractures at the vertex (or along the plane of an axial scan) are poorly depicted.

Sensitive to detecting intracranial air

The scanner has a weight limit, and a patient may be too heavy.

Sensitive in identifying foreign objects

A patient may decompensate while in the scanner.

*Intracranial hemorrhage.

†Subdural hemorrhage.

‡Subarachnoid hemorrhage.

Computed tomography scans are helpful in assessing the degree of intracranial injury, in predicting outcomes, and, if findings are normal, in avoiding unnecessary hospitalization[54, 55] ; are very sensitive to acute hemorrhage or skull fracture; and aid in evaluating (1) intracranial hemorrhage, (2) skull fracture, (3) mass effect and midline shift, (4) obliteration of basal cisterns, and (5) evidence of herniation (subfalcine, tonsillar, or uncal).

Computed tomography scans cannot diagnose a concussion (which is a clinical diagnosis) and are poor for diagnosing DAI. If DAI has occurred, CT scans may show small hemorrhages in the corpus callosum and cerebral peduncles. In this case, an MRI of the brain should be obtained on an elective basis when the patient is clinically stable because no effective treatment of DAI is currently available. Magnetic resonance imaging is more sensitive for detecting brainstem injuries, posterior fossa lesions, and brain edema. For advantages and disadvantages of CT scanning in patients with closed head injury, see Table 3, above.

As a general rule, a repeat head CT scan is recommended within 4-8 hours of the initial scan for patients with intracranial hemorrhage and/or coagulopathy.[56, 57, 58] A repeat head CT scan is recommended sooner for patients who are deteriorating neurologically.

Spinal cord injury should be considered in patients with closed head injury and is present in up to 10% of these patients.[51] Accordingly, the cervical spine should be evaluated (with 3 views) during the initial evaluation. C1-C2 should be evaluated with a thin-cut CT scan in intubated patients. If any abnormalities are noted on initial cervical plain radiographs, this area should be further evaluated with a CT scan. Magnetic resonance imaging may be necessary to image a spinal cord injury. A rigid cervical collar (Philly) should remain on at all times while the patient is being evaluated.

One study found that CT angiography (CTA) findings used in addition to other screening criteria may help identify injuries not captured when conventional screening guidelines are followed.[59]

In a systematic review of the clinical utility of single photon emission CT (SPECT) for TBI, SPECT was shown to offer some advantages over CT and MRI for detection of mild TBI and to have excellent negative predictive value. Review authors suggest that this may be an important second test in settings where CT or MRI is negative after a closed head injury with post-injury neurologic or psychiatric symptoms. Abnormal regions most commonly revealed by SPECT in cross-sectional studies were the frontal (94%) and temporal (77%) lobes. SPECT was found to outperform both CT and MRI in acute and chronic imaging of TBI, particularly mild TBI. It was found to have near 100% negative predictive value.[60]

The findings of one study strongly suggest that diffusion tensor imaging (DTI), but not "classic" MRI sequencing, is a precise and accurate measurement tool for assessing a degree of brain injury after blunt trauma. Diffusion tensor imaging is a valuable research tool for furthering our understanding of pathophysiologic mechanism(s) evoked by blast injury and may become a prognostic tool.[61]

Henninger and colleagues found that in 136 patients 50 years of age or older admitted to a neurologic/trauma intensive care unit (ICU), preexisting leukoaraiosis (white matter hyperintensities) was significantly associated with poor outcomes at 3 and 12 months. According to study findings, the independent association between leukoaraiosis and poor outcomes remained when analysis was restricted to patients who survived up to 3 months, had moderate to severe TBI [enrollment Glasgow Coma Scale [GCS] ≤12; P = 0.001], or had mild TBI (GCS 13-15; P = 0.002), respectively.[62]

Meningeal enhancement on contrast-enhanced fluid-attenuated inversion recovery (FLAIR) images can help detect traumatic brain lesions and other abnormalities that are not identified on routine unenhanced MRI in symptomatic patients with mild TBI. Contrast-enhanced FLAIR MRI is recommended when contrast MRI is indicated for patients with symptomatic prior closed mild head injury.

In a study of 25 patients, 3 additional cases of brain abnormality were detected on contrast-enhanced FLAIR images. Meningeal enhancement was identified on contrast-enhanced FLAIR images in 9 cases, and other routine image sequences showed no findings of TBI. Overall, additional contrast-enhanced FLAIR images revealed more extensive abnormalities than were evident on routine images in 37 cases.[63]

Patients who arrive for treatment with decreased GCS score and normal findings on head CT may have another condition that needs to be considered, such as one of the following:

  • Acute ischemic stroke (within 24 hours) that is not seen on head CT scan

  • Postictal state

  • Spinal cord injury

  • Intoxication or effects of illicit drug use

    • Substance use disorder has been associated with TBI and has significant implications for post-TBI recovery and rehabilitation.
    • Understanding the complex relationship between TBI and substance misuse enhances the clinical treatment of individuals with these 2 highly comorbid conditions. [35]
  • Prior medical conditions (speaking with family members may help in differentiating an acute from a chronic condition)

Procedures

Patients with severe brain injury (GCS score < 8), those who have labile blood pressure, those who require intensive care monitoring, and those who need surgical intervention are likely to require placement of an indwelling urinary catheter (Foley), placement of a central venous access catheter, and invasive blood pressure monitoring via an arterial line.

Intracranial pressure monitoring in patients with closed head injuries is a matter of controversy; however, most authors agree that invasive ICP monitoring is warranted for patients with a GCS score of 8 or less and an abnormal CT scan finding, for patients with suspected severe brain edema, and for those with ICP that is suspected to be significantly elevated.

Data from ICP monitoring can supplement a reliable neurologic examination, and this can be crucial for patients whose examination findings are affected by sedatives, paralytics, and other factors. Patients who have an abnormal head CT scan, a GCS score of 8 or less, or both, and who require emergent surgery on another organ system should be considered for some form of ICP monitoring before going to the operating room (or perhaps while in the operating room) because frequent neurologic examinations are not possible in this setting.

Intracranial pressure monitoring can be performed with an intraventricular catheter or with an intracranial fiberoptic monitor (Camino). Either procedure provides adequate ICP monitoring. The intraventricular catheter is preferred for closed head injuries when the ventricles are large enough to accommodate a catheter. The advantage of the catheter is its ability to drain CSF if ICP is elevated (>20 mm Hg), although ventricles compromised by mass effect make draining of much CSF difficult. An accurate pressure reading can be lost if the ventricle collapses around the catheter tip during drainage.

The advantage of the fiberoptic catheter is that ICP can be monitored for patients who have very small ventricles into which ventriculostomy catheters cannot be inserted. Pressure measurements are not prone to fluctuations in ventricular size.

 

Treatment

Medical Care

Intracranial hypertension is a common neurologic complication among patients who are critically ill. Intracranial hypertension is the common pathway in the presentation of traumatic head injury. The underlying pathophysiology of increased ICP is a topic of intense basic and clinical research; this has led to advances in our understanding of the physiology related to ICP. Few specific treatment options for intracranial hypertension have been subjected to randomized trials, however, and most management recommendations are based on clinical experience.

An anticonvulsant regimen should be started for patients with moderate or severe head injury. Administration should cease if no seizure activity occurs within the first 7 days after injury. For patients who have seizure activity during this time period, or who have undergone surgical procedures, one may opt to continue anticonvulsants for 6-12 months.

Consultations should be obtained as necessary for other accompanying injuries (eg, plastic surgeons for facial lacerations), with awareness that the patient's closed head injury takes precedence over all other non–life-threatening injuries.

Normal values of intracranial pressure

For healthy individuals with closed cranial fontanelles, central nervous systems contents, including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system. In the average adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF, and 110 mL of blood. The Monroe-Kellie hypothesis states that the sum of the intracranial volumes of blood, brain, CSF, and other components is constant, and that an increase in any one of these must be offset by an equal decrease in another.

The reference range of ICP varies with age. Values for children are not well established. Normal values are less than 10-15 mm Hg for adults and for older children, 3-7 mm Hg for young children, and 1.5-6 mm Hg for term infants. Intracranial pressure can be subatmospheric in newborns. Patients with ICP values greater than 20-25 mm Hg require treatment in most circumstances. Sustained ICP values greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension.

Cerebral dynamics overview

Cerebral perfusion pressure (CPP) depends on mean systemic arterial pressure (MAP) and ICP and is determined by the following relationship:

CPP = MAP – ICP, where MAP = (1/3 systolic BP) + (2/3 diastolic BP)

As a result, CPP can be reduced from an increase in ICP, a decrease in blood pressure, or a combination of both factors. Through the normal regulatory process, called pressure autoregulation, the brain maintains normal cerebral blood flow (CBF), with CPP ranging from 50 to 150 mm Hg. At CPP values less than 50 mm Hg, the brain may not be able to compensate adequately and CBF may fall passively with CPP.

After injury, the ability of the brain to autoregulate may be absent or impaired. When CPP is within the normal autoregulatory range (50-150 mm Hg), the ability of the brain to autoregulate pressure affects the response of ICP to a change in CPP. When pressure autoregulation is intact, decreasing CPP results in vasodilation, which allows the CBF to remain unchanged. This vasodilation can result in an increase in ICP. Likewise, an increase in CPP results in vasoconstriction of cerebral vessels and may reduce ICP. When pressure autoregulation is impaired or absent, ICP decreases and increases with changes in CPP.[64]

Treatment considerations

Elevate the head of the patient to 30° (this may be the least invasive method of lowering ICP). Some researchers have demonstrated improved ICP control with elevation (head of bed) to 45°, but evidence from use of multimodality monitoring has suggested 30° head elevation for maximum benefit.[21] Note that head elevation may reduce cerebral perfusion, even as it lowers ICP.

Provide hyperventilation. The goal is to maintain PaCO2 between 35 and 45 mm Hg. Judicious hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction.[7]  Note that aggressive hyperventilation may exacerbate cerebral ischemia to the point that secondary brain injury may occur. One study shows that patients who were hyperventilated to a PCO2 level of 25 mm Hg had worse outcomes than those kept at a nearly normal PCO2 level.[57] In addition, for most patients, hyperventilation is not necessary to control ICP.[29, 65, 66, 67] Hyperventilation reduces ICP only temporarily, progressively losing effectiveness after 16 hours of continuous use.[68]

Consider administering mannitol. This agent probably has several mechanisms of action. One obvious mechanism is through osmotic diuresis via drawing edema from the cerebral parenchyma. This usually takes 15-30 minutes, and the effect usually lasts 1.5-6 hours. Another mechanism is by immediate plasma expansion and decreased blood viscosity, thereby improving blood flow and eventually resulting in intracranial vasoconstriction in an attempt to maintain constant blood flow. This vasoconstriction ultimately leads to decreased intracranial volume (Monroe-Kelly hypothesis) and decreased ICP.[69, 70] Mannitol is also considered a free radical scavenger.[71] Administration of this drug to patients with severe TBI both with jugular bulb oxygen saturation[72] and with multimodal brain monitoring[73] suggests a potential change in the internal milieu that would improve cerebral oxygenation.

Check serial serum osmolarity levels to maintain osmolarity no greater than 315-320 mOsm/kg H2O to avoid acute renal failure. Some studies have raised concern that early use of mannitol can lead to hypotension, with an associated worse outcome.[74] For this reason, patients treated with mannitol must be kept euvolemic with isotonic fluid resuscitation as required.

Some evidence suggests that barbiturates may be effective in lowering refractory ICP; however, such administration often causes depressed myocardial function and CPP.[51] These drugs often have associated morbidity and do not significantly change outcomes.[75, 76]

  • Barbiturate-induced coma with electroencephalographic (EEG) burst suppression is often a "last ditch effort" to reduce ICP and should be reserved for patients with refractory ICP who are unresponsive to other measures. One may even consider decompressive craniectomy before using barbiturates. Barbiturate serum levels represent a poor estimation of therapeutic effect and should not be followed for treatment purposes. For this reason, all patients should have EEG monitoring for induced burst suppression. A loading dose of pentobarbital can be administered as a 10-mg/kg bolus (over 30 minutes), followed by 5 mg/kg/h for 3 doses, titrated to a low level of bursts per minute (2-5). Barbiturates are contraindicated in hypotensive patients.

Give special attention to preventing hypotension.[20, 31] Data from the Traumatic Coma Data Bank (TCDB) reveal that hypotension in patients with severe TBI increases mortality from 27% to 50%.[21] Traditional management has included fluid restriction to minimize cerebral edema, but this practice may be dangerous for patients who already have intravascular volume depletion.

  • Cerebral edema may occur regardless of the amount of intravenous fluid administered, and hypervolemia, per se, does not cause brain edema if serum sodium level and osmolarity are within normal limits. [21] However, treating patients with closed head injuries with liberal amounts of hypotonic intravascular fluid may cause intracerebral hemorrhages to blossom. Smaller amounts of hypertonic solutions may be equally effective without risk of fluid overload. [77, 78] The ultimate goal in treating patients with closed head injuries is to maintain a state of euvolemia. For a euvolemic patient who is hemodynamically stable, two-thirds maintenance of isotonic solution is recommended. Hypotonic fluids should be avoided because they may decrease serum osmolarity and increase brain swelling.

Patients with closed head injury are prone to acute coagulopathies. These coagulopathies are often the result of release of thromboplastin and tissue-activating protein from injured brain tissue. Release of these proteins leads to abnormal intravascular clotting, which consumes clotting factors, platelets, and fibrinogen and ultimately results in elevated prothrombin time (PT) and activated partial thromboplastin time (aPTT). For patients with acute intracranial hemorrhage, these coagulopathies must be addressed and corrected promptly.

  • Fresh frozen plasma (FFP) transfusions until coagulopathy is corrected is the preferred method. This is especially true for individuals who are taking anticoagulants (eg, warfarin) and are at high risk of continued bleeding. Winter and colleagues showed that prophylactic FFP administration in individuals with closed head injury confers no benefit. [79] Vitamin K plays an important role in correcting the coagulopathy; however, it usually takes 24-48 hours to be activated. During this interval, the patient's intracranial hemorrhage is likely to worsen.

Recombinant activated factor VII (rFVIIa) is a relatively new pharmaceutical agent developed for use in patients with hemophilia in whom inhibitors to clotting factors VIII or IX have developed.

  • Use rFVIIa to treat patients with coagulation disorders, those who have experienced trauma, and those with perioperative hemorrhage, intracerebral hemorrhage, or subarachnoid hemorrhage. rFVIIa is a safe and effective agent with the potential to revolutionize the treatment of neurosurgical patients with hemorrhage.
  • Cost is a major impediment to widespread use of rFVIIa, and evidence suggests that its use in the neurosurgical population may be subject to higher risk than in other populations studied thus far. Although further study is needed to better delineate the safety and efficacy of this drug, rFVIIa is clearly an agent with tremendous promise. [80] In placebo-controlled trials, off-label use of rFVIIa in high doses increased the risk of arterial events but not venous thromboembolic events, particularly among older patients. [81] Until more clinically significant data emerge, caution should be exercised when rFVIIa is used in off-label settings. [82]

Pyrexia commonly occurs in patients with head injuries, possibly because of posttraumatic inflammation, direct damage to the hypothalamus, or secondary infection. Fever should be avoided, as it increases cerebral metabolic demand and affects ICP.[7]  While the source of the infection is sought, maintain body temperature in a normothermic range with acetaminophen.

  • The most common cause is fever secondary to underlying infection. Less common is unexplained fever or "neurogenic" fever, which is estimated to occur in approximately 8% of patients who have head injuries with pyrexia. [83] Regardless of the cause of the elevated temperature, pyrexia alone increases metabolic expenditure, glutamate release, and neutrophil activity, while causing blood-brain barrier breakdown.
  • Pyrexia is also thought to exacerbate oxygen radical production and cytoskeletal proteolysis. [84, 85] These changes may further compromise the injured brain and may worsen neuronal damage. For this reason, the source of the fever must be identified and corrected.
  • Despite sound physiologic justification for treating fever in brain-injured patients, no evidence indicates that doing so improves outcome.

Hyperglycemia has been shown to have a detrimental effect on induced brain ischemia. Clinical trials support the correlation between hyperglycemia and poor overall outcome in patients with head injuries and recommend that euglycemia be maintained at all times.[86]

Some patients with severe head injuries may develop hypertension, either from an exacerbation of a chronic process or as a result of the head injury. Keep systolic blood pressure less than 180 mm Hg, particularly in patients who have an intracranial hemorrhage. This value requires adjustment for patients with a history of uncontrolled hypertension. If possible, avoid nitroprusside because it is a cerebral vasodilator and may actually increase ICP. A nicardipine grip is preferred for patients whose blood pressure is difficult to control. Corticosteroids have been used occasionally but have no proven benefit for patients with severe head injuries.[76]

  • Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased ICP. When ICP becomes elevated, ruling out new mass lesions that should be surgically evacuated is important. Medical management of increased ICP should include sedation and paralysis, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension that results from TBI. [64]

Surgical Care

As a general rule, indications for surgery include any intracranial mass lesion that causes significant or progressive neurologic compromise, particularly a decreased level of consciousness. The overall outcome of individuals with an intracranial lesion that causes significant mass effect is improved with rapid decompression; therefore, it is advisable to operate on these patients as soon as possible.

Before operating, one must always consider the patient's condition and must refrain from relying solely on radiographic evidence. For example, some patients with severe cerebral atrophy (eg, elderly patients) may accommodate a large intracranial hemorrhage, whereas most young individuals may experience neurologic deficits with relatively smaller intracranial hemorrhages. Note that some intracranial hemorrhages may be actively bleeding during the initial head CT scan; what may appear as relatively small on the initial scan may actually become quite significant in a short period of time. In this case, the patient's physical examination findings are more valuable than initial CT scan findings in evaluating his or her intracranial status.

Some authors have suggested a decompressive craniotomy/craniectomy (ie, removal of a bone flap with or without dural opening) to provide more space for the brain to expand, for treatment of uncontrollable ICPs before irreversible ischemic brain damage has occurred. The role of decompressive craniotomy/craniectomy in the absence of compressive pathology (such as subdural hematoma) for patients with closed head injuries has not been well documented. However, most authors agree that children benefit more from decompressive craniotomy/craniectomy than adults, and some authors are advocates of very early decompressive craniotomy/craniectomy for uncontrollable ICP in children.[87] It seems clear that older individuals, particularly those older than 50 years, do less well with elective decompressive craniotomy/craniectomy.[88, 89]

One study investigated complications associated with use of a dural substitute, the Neuro-Patch, during decompressive craniectomy. Results suggest that it has not been found to increase the incidence of neurosurgical site infection and hydrodynamic complications, including subdural hygroma and CSF leakage, following decompressive craniectomy or cranioplasty for severe TBI. However, patients with the Neuro-Patch more often encounter extra-axial hematoma at the site of craniectomy, which forms a compressive lesion on the adjacent brain.[90]

Despite inclusion of a relatively small number of patients, a meta-analysis of 2 randomized, controlled trials convincingly and strongly suggests that early induction of hypothermia to and below 35°C for 48 hours before or soon after craniotomy improves outcomes for patients with intracranial hematoma after severe TBI. This study is trendsetting rather than definitive, and confirmation by a prospective clinical trial is required.[91]

Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, one study suggests that good recovery may be possible if an aggressive surgical approach is taken, particularly for those with extradural hematoma. Of 82 patients who underwent surgery for extradural or subdural hematoma, among those with extradural hematoma the mortality rate was 29.7%, with a favorable outcome seen in 54.3%. For patients with acute subdural hematoma, the mortality rate was 66.4%, with a favorable outcome in 6.6%.[92]

Diet

Historically, physicians believed that patients with closed head trauma should be on NPO status. However, this thinking has changed, and the current goal for patients with TBI is to provide nutrition as soon as possible after injury. The consequences of hypermetabolism, hypercatabolism, and altered immune function are part of the response to traumatic head injury. Once a person with acute TBI develops this hyperdynamic state, excessive protein breakdown ensues. This can lead to malnutrition. Lack of nutrient supplementation in these patients is associated with increased morbidity and mortality. Enteral nutrition is the preferred mode of feeding but often is not tolerated by the patient with head injury. Parenteral nutritional support can be given to these patients without worsening of cerebral edema.[93]

 

Guidelines

Guidelines Summary

Brain Trauma Foundation

Brain Trauma Foundation (BTF) Guidelines for Management of Severe Head Injury were the first clinical practice guidelines published by any surgical specialty. These guidelines have earned a reputation for rigor and have been widely adopted around the world. Implementation of these guidelines has been associated with a 50% reduction in mortality and reduced costs of patient care. Over their 25-year history, these traumatic brain injury (TBI) guidelines have been expanded, refined, and made increasingly more rigorous in conjunction with new clinical evidence and evolving methodologic standards. Perhaps the greatest limitation of TBI guidelines now is the lack of high-quality clinical research, as well as novel diagnostics and treatments with which to generate substantially new recommendations.[94]

Brain Trauma Foundation guidelines have been provided for treatment of severe TBI in infants, children, and adolescents.[95]  

Monitoring guidelines include the following:

  • Intracranial pressure (ICP) monitoring is recommended.
  • Advanced neuromonitoring (brain oxygenation) should be reserved for patients with no contraindications to invasive neuromonitoring and for patients who are not brain dead.

Threshold guidelines include the following:

  • Targeting a threshold of under 20 mm Hg in ICP treatment is recommended.
  • Maintaining a minimum cerebral perfusion pressure (CPP) of 40 mm Hg is recommended.

Treatment guidelines include the following:

  • Bolus hyperosmolar therapy (HTS) of 3% saline is recommended for patients with ICP; recommended effective doses range from 2 to 5 mL/kg over 10-20 minutes.
  • For refractory ICP, a bolus of 23.4% HTS is recommended.
  • Avoiding bolus administration of midazolam and/or fentanyl during ICP crises is recommended due to risks of cerebral hypoperfusion.
  • Draining cerebrospinal fluid (CSF) through an external ventricular drain (EVD) is recommended for managing increased ICP.
  • Prophylactic treatment is recommended for reducing the occurrence of early (within 7 days) posttraumatic seizures (PTSs).
  • Moderate (32-33°C) hypothermia is recommended for controlling ICP but is not recommended over normothermia for improving overall outcomes.
  • For hemodynamically stable patients with refractory ICP, high-dose barbiturate therapy is recommended.
  • Decompressive craniectomy (DC) is recommended for treating neurologic deterioration, herniation, or intracranial hypertension refractory to medical management.
  • Initiating early enteral nutritional support (within 72 hours from injury) is recommended for decreasing mortality and improving outcomes.
  • Corticosteroids are not recommended for ICP.
 

Medication

Medication Summary

Neurosurgeons have commonly given prophylactic anticonvulsants to individuals with intracranial hemorrhage. The appropriate duration of treatment is not well established. Individuals who have experienced seizure activity can reasonably be treated with anticonvulsants for 6-12 months, after which reevaluation is necessary. Temkin and colleagues suggest that treatment for longer than 8 days after injury does not reduce the frequency of long-term seizure disorders. Anticonvulsants may be used to treat early (< 7 days) posttraumatic seizures. According to Greenberg, prophylactic anticonvulsants do not reduce the frequency of late (≥7 days) posttraumatic seizures.[96]

The anticonvulsant medication recommended for adults is phenytoin or fos-phenytoin (18 mg/kg of loading dose), ensuring therapeutic levels of 10-20 mg/dL. Note that a "therapeutic level" does not necessarily have a direct bearing on adequate control of seizures. A relatively common adverse effect of long-term phenytoin use is gingival hyperplasia and hirsutism, which precludes long-term use in children. Phenobarbital is an acceptable alternative for children who require long-term anticonvulsive therapy (10-20 mg/kg loading dose, then 3-5 mg/kg/day divided bid/tid) to achieve a therapeutic level of 10-40 mg/dL.

The antiepileptic drug levetiracetam is used in the setting of acute brain injury for seizure treatment or prophylaxis; it is a desirable alternative to phenytoin and is associated with fewer complications when used as monotherapy. Checking for therapeutic levels is not needed. The dose is 500 mg bid IV or PO and is advanced to 1000 mg bid.[97]  A review of management approaches to TBI conducted to promote best clinical practice found that for seizure management, levetiracetam appears to be as effective as phenytoin, but the optimal dose remains unclear. Review authors state that there has been a lack of clear outcome benefit for any individual osmotherapy agent, with no difference in mortality or neurologic recovery. They recommend that further research is needed to determine the optimal package of care and interventions for patients with TBI. Future studies should focus on patient-centered outcome measures such as long-term neurologic recovery and improved quality of life.[98]

Anticonvulsants

Class Summary

These agents are indicated for short-term (1 week) or long-term (6- to 12-month) posttraumatic seizure control for patients who have experienced posttraumatic seizure activity. Phenobarbital may be considered as long-term anticonvulsive therapy for children.

Phenytoin (Dilantin)

Used as acute seizure prophylaxis for individuals with closed head injuries.

Phenobarbital (Barbita, Luminal, Solfoton)

Used as acute seizure prophylaxis for children with closed head injuries.