Glasgow Coma Scale and Glasgow Outcome Scale

A simple and reliable clinical assessment tool is needed for evaluating acute TBI. An accurate baseline assessment is crucial, and serial assessments are also needed, because neurological status may change with time, sometimes rapidly. TBI care is provided by a wide range of physicians, nurses, and allied health personnel. Many classification schemes have been developed; however, the Glasgow Coma Scale (GCS) (Table 103-1), introduced by Teasdale and Jennett in 1974, is the most widely used.² The GCS has proved to be accurate, capable of detecting clinically important changes in neurological status, and easy to use by a variety of health care professionals.

TABLE 103-1 The Glasgow Coma Scale

Total score ranges from 3 to 15.

Scores on the GCS range from 3 to 15. A GCS score of 3 to 8 is indicative of severe head injury, with a mortality rate of 35% to 40%. A GCS score of 9 to 12 is indicative of moderate head injury, with a mortality rate of 5% to 10%, and a score of 13 to 15 is indicative of mild head injury, with a mortality rate of less than 2%. Children older than 2 years and teenagers have a better prognosis than do adults. The postresuscitation GCS is one of the strongest predictors of ultimate outcome after TBI.

For example, a patient who opens eyes only in response to pain, has a best motor response of abnormal flexion to pain, and a best verbal response of incomprehensible sounds would receive 2 points for eye opening, 3 points for motor response, and 2 points for verbal response. The GCS score would therefore be 7, in the severe TBI category.

The GCS cannot be used reliably in patients younger than 2 years, because children in that age group are not able to carry out the normal motor and verbal responses required by the test. Various pediatric head injury scales have been proposed, but none has been widely adopted.

A reliable scale is also needed to assess the long-term outcomes of patients as they recover from TBI. The Glasgow Outcome Scale (Table 103-2) is a commonly used system that has been developed for this purpose. Serial testing indicates that more than two thirds of patients reach their final outcome category on the Glasgow Outcome Scale within 3 months of injury.

TABLE 103-2 The Glasgow Outcome Scale

Primary and Secondary Injury

Brain injury in TBI can be viewed as having two components: primary and secondary (Greenberg, 2001). The damage caused by the direct forces of the injury is known as the primary injury. Since the 1980s, there has been increasing recognition that further damage may occur after the traumatic event, as the result of brain ischemia or herniation. This phenomenon has come to be known as the secondary injury. Hypotension, hypoxia, raised intracranial pressure (ICP), and seizures are risk factors for the development of secondary injury and should be treated aggressively.

Diffuse and Focal Injury

TBI is also classified according to the distribution of injury, which may be diffuse, focal, or a combination of the two. Concussion is the classic example of a mild, diffuse injury, whereas diffuse axonal injury represents a more severe, diffuse injury. Cerebral contusion is the classic example of focal brain injury.

Concussion

The most common head injury is concussion, also known as mild traumatic brain injury. The hallmark of concussion is an alteration of consciousness as a result of nonpenetrating injury to the brain. There is often a period of amnesia for the event, and recovery is generally rapid. Aside from altered mental status, the neurological examination yields normal findings. Results of CT and MRI of the brain are normal.

No specific treatment for concussion is required. Prognosis is excellent, and a full recovery may be expected in most cases. Patients are allowed to return to their usual activities as their symptoms resolve.

Two complications of concussion warrant further discussion. First, it is now believed that the effects of repeated concussion are cumulative and can lead to the development of chronic dementia. The “punch drunk” syndrome that occurs in professional boxers exemplifies this phenomenon.

Another serious complication of seemingly mild head injury is the second-impact syndrome, a rare condition that has been described in athletes who sustain a second head injury while still symptomatic from an earlier injury. Although the individual appears to have only minimal impairment from the first injury, malignant cerebral edema, which is refractory to all interventions, occurs soon after the second injury. The mortality rate with second-impact syndrome is 50% to 100%. Recognition and increasing understanding of this syndrome have led to the development of guidelines that allow for a safe return to athletic competition while avoiding the devastating complications of second-impact syndrome. In addition to neurological examination and imaging studies, neuropsychological testing is now an important part of the decision-making process for allowing athletes to return to competition after TBI (Bailes, Day, 2001).⁴

Diffuse Axonal Injury

A more severe form of diffuse TBI is diffuse axonal injury. This type of injury is the result of shear and tensile forces within the brain. Clinical examination often reveals severe deficits, including coma and decerebrate posturing, in contrast to CT, which yields generally unremarkable findings. Diffuse axonal injury is often present in fatal head injury. Survivors may remain in a vegetative state or have other long-term deficits.

Contusion

Cerebral contusion is the classic example of focal TBI. In the pre-CT era, cerebral contusion could be diagnosed only in the operating room during craniotomy or at the autopsy table. Thus, contusion was considered only in cases of severe TBI and was therefore thought to be pathognomonic for severe injury. Since the advent of CT, especially current high-resolution techniques, contusions have commonly been observed in patients with clinically mild and moderate TBI. It is now recognized that there is a wide range of severity associated with cerebral contusion. Tiny punctate contusions in patients with mild TBI have little or no clinical significance and carry the same prognosis as normal findings on CT.⁵ At the other end of the spectrum, large contusions with significant mass effect in patients with severe TBI can be life-threatening.

Contusions can be classified as coup or contrecoup injuries. Coup contusions occur at the location of impact, whereas contrecoup contusions occur on the opposite side or at a point distant from the impact. Contusions may be present in any part of the brain but are most common in the frontal and temporal lobes. Figure 103-1 shows a typical hemorrhagic contusion in the left inferior frontal region, just above the roof of the orbit.

Figure 103-1 Computed tomographic head scan shows a left frontal hemorrhagic contusion just above the orbital roof.

Contusions often enlarge during the first week after injury. Repeated CT should be considered if the patient exhibits clinical deterioration. Surgery may be necessary to resect areas of contused brain if there is significant mass effect with raised ICP. Temporal lobe contusions are particularly ominous because of their proximity to the brainstem and risk of herniation.

Intracerebral Hematoma

Intracerebral hemorrhage is bleeding within the brain parenchyma and generally occurs after severe head injury. As with contusion, the natural history of intracerebral hemorrhage is one of progressive enlargement during the first few days after injury. Intracerebral hemorrhage may develop on a delayed basis in areas of contusion. Individuals with coagulopathy from liver disease or anticoagulant medications are at increased risk for intracerebral hemorrhage. In these individuals, intracerebral hemorrhage may occur after low-impact injury. Small intracerebral hemorrhages can be observed, whereas larger intracerebral hemorrhages that cause significant mass effect should be resected.

Subdural Hematoma

Subdural hematoma is the result of bleeding over the surface of the brain, beneath the dura. Subdural hematoma may be acute or chronic. Acute subdural hematoma usually occurs after severe, high-impact injuries and is often associated with contusions of the adjacent areas of the brain. If the subdural hematoma is small (<5 mm in thickness) and the patient is stable clinically, a period of observation may be reasonable. If conservative management is elected, careful clinical observation and follow-up imaging are needed, because there is potential for the subdural hematoma to enlarge. Craniotomy to remove the hematoma is necessary if there is significant mass effect with raised ICP. At surgery, the hematoma is found to have a solid, jelly-like consistency.

Chronic subdural hematoma represents the gradual accumulation of liquefied hematoma in the subdural space, occurring over 2 or more weeks. Chronic subdural hematoma is usually present in elderly persons, who have more prominent subdural spaces as a result of cerebral atrophy. Chronic subdural hematoma, occurs most commonly after minor head injury. Sometimes the patient and family cannot even recall when the injury occurred. Over time, the hematoma gradually enlarges as a result of repeated episodes of minor bleeding and/or the drawing of fluid into the hematoma as a result of an osmotic effect. As in other forms of intracranial hemorrhage, risks of chronic subdural hematoma are elevated in individuals with coagulopathy caused by liver disease or anticoagulant medications. Surgery is often required and may involve either burr hole drainage or a craniotomy. At surgery, a chronic subdural hematoma is liquefied and is described as having a “crank case oil” appearance. The prognosis is guarded, and there is substantial risk of recurrent subdural hematoma that necessitates further surgery. Figure 103-2 shows bilateral chronic subdural hematomas.

Figure 103-2 Computed tomographic head scan shows bilateral chronic subdural hematomas.

Subdural hematoma may have both acute and chronic components if there is ongoing bleeding in the subdural space. The presence of a mixed acute and chronic subdural hematoma is readily identified on CT (Figure 103-3).

Figure 103-3 Computed tomographic head scan shows bilateral subdural hematomas with acute and chronic components.

Epidural Hematoma

Epidural hematoma represents acute bleeding into the epidural space. This bleeding may be either arterial or venous. The classic epidural hematoma is observed with a linear skull fracture of the temporal bone, which tears the middle meningeal artery, allowing blood to accumulate under pressure in the epidural space. However, sizable epidural hematoma of venous origin may also occur. Epidural hematoma is usually observed in children and young adults but is rare in elderly persons, because of the firm adherence of the dura to the inner table of the skull. A convexity epidural hematoma is usually readily identified on routine head CT; however, an epidural hematoma low in the middle cranial fossa may be missed on axial images as a result of artifact from the adjacent skull base. In such cases, coronal imaging may be helpful in demonstrating the hematoma. A right frontal epidural hematoma is shown in Figure 103-4.

Figure 103-4 Computed tomographic head scan shows a right frontal epidural hematoma.

(Courtesy of Daniel F. Broderick, MD.)

The typical clinical scenario of a patient developing an epidural hematoma is one in which the patient, often a child, sustains a blow to the head and is initially stunned but then rapidly regains awareness, only to deteriorate again over the next few minutes to hours. Typical clinical findings include dilation of a pupil, caused by a cranial nerve III palsy, ipsilateral to the injury, and progressive obtundation. Emergency craniotomy is usually required for an epidural hematoma. The lesion must be identified and evacuated as soon as possible in order to prevent brain herniation and to obtain a good outcome.

Traumatic Subarachnoid Hemorrhage

Subarachnoid hemorrhage may occur after head trauma. It may be an isolated finding, or it may occur in association with other findings, such as contusion and intracerebral hemorrhage. Whenever subarachnoid hemorrhage is present after a low-impact injury, or in cases in which the history of head trauma is vague or uncertain, the possibility of subarachnoid hemorrhage from an aneurysm must be considered. In these cases, magnetic resonance angiography, computed tomographic angiography, or conventional angiography should be performed. Vasospasm is much less common in traumatic subarachnoid hemorrhage than in aneurysmal subarachnoid hemorrhage. There is no specific treatment for traumatic subarachnoid hemorrhage. Patient management should be guided by the clinical examination and other findings on CT. There is a small risk of delayed hydrocephalus, so at least one follow-up computed tomographic scan is warranted.

Intraventricular hemorrhage may also occur after head trauma. Bleeding into the ventricular system is usually associated with severe TBI and poor long-term outcome. The presence of intraventricular hemorrhage is thought to be a marker, but not the cause, of poor clinical outcome. Late hydrocephalus may also occur after traumatic intraventricular hemorrhage. As with subarachnoid hemorrhage, whenever intraventricular hemorrhage is present after mild or questionable head trauma, the possibility of aneurysmal hemorrhage must be considered and appropriate screening performed.

Pneumocephalus

The finding of intracranial air, or pneumocephalus, indicates a skull fracture of either the convexity or cranial base. Air is readily identified on CT and may be in the extracerebral, intracerebral, or intraventricular space. Small quantities of intracranial air are of no pathological significance and resolve within a few days. In rare cases, large quantities of air enter the intracranial space and lead to mass effect on the brain. This condition is known as tension pneumocephalus and is the result of a persistent cerebrospinal fluid (CSF) fistula. Emergency surgery may be necessary to evacuate air and decompress the brain through the placement of drainage tubes. A diligent search for a CSF fistula must be undertaken. Surgery may be needed to obliterate CSF fistulae and prevent further entry of air into the brain.

Skull Fracture

A variety of skull fractures may be observed in TBI. Skull fractures are classified as simple or compound, linear or stellate, and depressed or nondepressed. The physician should perform a careful examination of any scalp lacerations to look for evidence of depressed bone fragments, CSF leakage, or exposed brain tissue in the wound. Clinical signs of fracture of the skull base (basilar skull fracture) include CSF otorrhea or rhinorrhea, hemotympanum, retro-auricular ecchymosis (Battle’s sign), periorbital ecchymosis (“raccoon’s eyes”) in the absence of direct orbital trauma, and cranial nerve injury, particularly cranial nerves I, II, VI, VII, and VIII. Some of these findings may become apparent only after a delay.

Most skull fractures are readily identified on CT. Fractures of the skull base may be harder to visualize with standard head CT protocols. In these cases, specialized CT techniques may be required, including coronal imaging, thin slices, and bone windows. Figure 103-5 depicts a linear skull fracture through the left lambdoid suture with a small amount of adjacent pneumocephalus.

Figure 103-5 A, Computed tomographic head scan shows a linear skull fracture through the left lambdoid suture (arrow) with adjacent pneumocephalus. B, Close-up view of fracture.

A simple, linear, nondepressed skull fracture requires no specific treatment but does have some prognostic significance. In one large study of minor TBI, 3% of patients with a skull fracture deteriorated to the point of needing a neurosurgical procedure, whereas the risk of significant deterioration in patients without a skull fracture was less than 1%.⁶ This indicates that in cases of clinically mild TBI, the prognosis is worse in patients with a skull fracture than in those whose head CT does not reveal a fracture. These data have led some investigators to recommend that a skull fracture be an indication for overnight admission to the hospital for patients with clinically mild TBI.

Surgical repair is indicated for depressed skull fractures if there is a depression measuring more than 8 to 10 mm (or greater than the thickness of the skull) or for débridement of compound (open) fractures with dural laceration, CSF leakage, and parenchymal injury.

Placement of a nasogastric tube is contraindicated in patients with basilar skull fractures involving the anterior cranial fossa, because it would be possible for a nasogastric tube to pass through the incompetent skull base into the brain. If gastric drainage is needed in such cases, an orogastric tube should be placed.

Penetrating Cranial Trauma

Gunshot wounds to the head account for the majority of penetrating cranial injuries. Examination should include description of visible entrance and exit wounds, in addition to the usual assessments with GCS and of neurological function and general physical examination. The prognosis is generally poor, especially in high-velocity wounds. Patients with little cerebral function (in the absence of shock, alcohol overdose, or drug overdose) are unlikely to benefit from surgical intervention, and supportive care is most appropriate in these situations.

For patients who are believed to be capable of some recovery, the goals of surgery include débridement of devitalized tissue, evacuation of hematomas, removal of accessible bullet and bone fragments, obtaining hemostasis, and separation of the intracranial compartment from air sinuses that may have been traversed by the bullet. Any knives or other sharp objects protruding from the skull should not be removed in the field but, instead, should be left in place for extraction in the operating room under more controlled circumstances.

Adverse Effects of Anticoagulant Medications

It is crucial to know whether the patient is taking anticoagulant medications, such as warfarin or clopidogrel, or antiplatelet medications, such as aspirin, because these medications increase the risk of intracranial hemorrhage. A complete blood cell count with measurements of platelet counts, international normalized ratio, and prothrombin time should be obtained.

In patients taking warfarin, anticoagulation should be reversed with fresh-frozen plasma and phytonadione (AquaMEPHYTON). Depending on the level of anticoagulation, this reversal can take hours to days. Historically, this has presented a therapeutic dilemma in situations in which rapid reversal of anticoagulation is needed. A common example of this is the case of a patient with a large warfarin-related subdural hematoma causing cerebral herniation who needs an emergency craniotomy. If fresh-frozen plasma is given too rapidly, fluid overload and congestive heart failure may ensue. If the anticoagulation is not reversed fast enough, herniation may occur and the patient may die before surgery can safely be performed.

A significant advance in the care of these patients has been the introduction of recombinant factor VIIa (NovoSeven). Administered intravenously in doses of 15 to 100µg/kg, this product can reverse the anticoagulant effects of warfarin within a few minutes of administration. Rapid reversal of anticoagulant medications has two benefits: first, the risk of further enlargement of the hematoma is decreased, and, second, emergency surgery can be safely carried out in situations in which hematoma removal is warranted. Clotting parameters should be monitored, as additional doses of recombinant factor VIIa or fresh-frozen plasma may be required after initial reversal with the former.

There is a seemingly small risk of thrombotic complications related to the use of recombinant factor VIIa. The major drawback to this medication is its cost. A 1.2-mg vial costs about $1000. However, in cases of life-threatening intracranial hemorrhage, the benefits of this product clearly outweigh the expense and risks of its use.

The clinician must also inquire about the use of alcohol or illicit drugs, which could impair consciousness. Appropriate drug screens of blood and urine should be obtained.

Physical Examination

The physical examination should include assessment of vital signs, GCS assessment, neurological examination, and general examination for evidence of systemic injury and spinal column injury. The scalp should be inspected for evidence of scalp laceration and underlying skull fracture. It may be necessary to shave a portion of the scalp in order to perform an adequate evaluation. Careful examination of a scalp laceration may reveal a depressed skull fracture with dural laceration and exposed cerebral tissue, even in cases of clinically mild TBI.

Tachycardia and hypotension are indicative of hypovolemic shock, which should prompt a search for systemic injury, such as intra-abdominal hemorrhage or pelvic fracture. Hypotension is not observed with TBI, with two exceptions: profound blood loss from a scalp laceration (which is uncommon) and in the agonal phase of severe TBI with brain death. Bradycardia and hypertension are known as Cushing’s response and are indicative of raised ICP. Bradycardia and hypotension are suggestive of a cervical spinal cord injury.

Coexisting Spinal Injury

The unconscious patient should be assumed to have a cervical spine injury until proven otherwise. A rigid cervical collar should remain in place until the cervical spine can be judged stable by appropriate clinical and radiographic assessment. Flaccid limbs and priapism are worrisome signs that suggest a high likelihood of spinal cord injury.

“Talk and Die” Injuries

It is now well known that patients with seemingly mild TBI can have a brief period of stability, or even improvement, followed by dramatic neurological deterioration. This ominous clinical scenario was first reported by Reilly and associates in 1975.⁷ This initial report focused on patients who talked at some point after the injury and then died. These injuries came to be known as “talk and die” injuries and, in their milder form, as “talk and deteriorate” injuries.

Neurological worsening, as documented by a decline in the GCS score, immediately raises concern about an expanding intracranial hematoma; however, several other possibilities must be considered as well, including hydrocephalus, pneumocephalus, cerebral edema, metabolic abnormalities (hyponatremia, hypoglycemia, adrenal insufficiency), drug or alcohol withdrawal, seizures, meningitis, and carotid or vertebral artery dissection.

In the event of neurological deterioration, head CT should be repeated, with a search for hematoma, hydrocephalus, pneumocephalus, and cerebral edema. If results of CT are unremarkable, electrolytes, metabolic parameters, and arterial blood gases should be measured. Electroencephalography is useful in selected cases. A lumbar puncture with CSF examination is needed if meningitis is a strong consideration; however a lumbar puncture is contraindicated in the presence of raised ICP. Dissection of the carotid or vertebral arteries is a rare complication of trauma to the head and neck. Dissection should be considered if there is major neurological deterioration that cannot be explained by the testing described previously. This diagnosis can be established by ultrasonography or magnetic resonance angiography.

Figure 103-6 illustrates the dramatic worsening that may occur with TBI. The case involved a 72-year-old woman who presented to the emergency department with a clinically mild TBI (GCS score, 15) after a fall at home. Figure 103-6A shows the initial computed tomographic head scan, which was unremarkable, aside from extracranial soft tissue swelling in the right parietal region. The patient was dismissed from the emergency department in the care of her family. Later that day, the patient exhibited marked deterioration and was brought back to the hospital by her family. She was deeply comatose, and the GCS score had decreased from 15 to 6. Figure 103-6B shows the follow-up computed tomographic head scan, obtained 10 hours after the initial scan, which reveals interval development of a large acute right subdural hematoma. Emergency craniotomy was required. This was an example of a “talk and deteriorate” injury.

Figure 103-6 A, Initial computed tomographic head scan is unremarkable. There is mild generalized cerebral atrophy, consistent with age. Right parietal extracranial soft tissue swelling is seen. B, Follow-up computed tomographic head scan 10 hours later shows a large acute subdural hematoma with midline shift. The black arrow indicates the component of the hematoma over the cerebral convexity. The white arrow indicates an interhemispheric component of the hematoma along the falx cerebri.

Hospital Admission

In cases of clinically mild TBI, one of the first decisions to be made is whether to admit the patient to the hospital for observation or to have the patient observed at home. There is no evidence that hospital admission improves the outcomes of patients with mild TBI. Two large clinical series in which investigators compared outcomes of observation of inpatients and outpatients with mild TBI failed to show a benefit of inpatient care.^8,9 Nevertheless, large numbers of patients with mild TBI are admitted to the hospital for overnight observation, generally for medicolegal reasons.

Dozens of guidelines have been published, but no consensus exists about which patients with minor TBI should be admitted for in-hospital observation, nor is there any consensus regarding the duration of hospital stay for admitted patients. Some guidelines specify 24- or 48-hour hospital admission. Others recommend “overnight admission,” but this vague and nonspecific. For example, a patient who is admitted to the hospital in the late evening or early morning hours and is then discharged on morning rounds may actually be in the hospital for only a few hours.

The most important consideration is for the patient to be in an environment where he or she can be observed carefully for any evidence of neurological deterioration. The decision to admit or observe on an outpatient basis depends on clinical judgment, results of CT in selected patients, and consideration of a patient’s social situation. As a general rule, the patient with a GCS score of 15, no evidence of skull fracture on CT, and a responsible parent or other adult available to monitor the patient may be observed at home. In pediatric patients, the possibility of child abuse is an additional consideration. A child should not be discharged home if the clinical and radiographic findings are at all suggestive of nonaccidental injury.

All patients with moderate and severe TBI require hospital admission. More severe injuries should be monitored in an intensive care unit or a dedicated neurosurgical unit. The majority of patients with severe TBI require endotracheal intubation for airway control and mechanical ventilation.

Surgical Issues

The initial computed tomographic scan should be carefully scrutinized for any acute surgical problems, including intracerebral hemorrhage, subdural hematoma, epidural hematoma, and depressed skull fracture. Any hematoma causing significant mass effect on the brain should be promptly evacuated. Smaller hematomas and small areas of contusion can be monitored but may necessitate surgery on a delayed basis if there is subsequent enlargement.

There is no precise size threshold above which the hematoma must be evacuated and below which the lesion may be safely monitored. These decisions must be made on a case-by-case basis, guided by the patient’s clinical course and findings on CT.

Intracranial Pressure Monitoring

ICP monitoring should be considered for clinically severe TBI (GCS score, 3 to 8). There are various types of ICP monitors, including intraventricular, intraparenchymal, subdural, and epidural devices. Intraventricular monitors are more accurate and have the added advantage of allowing withdrawal of CSF to lower ICP. The main drawback to intraventricular monitoring is difficulty with catheter placement if the ventricles are severely compressed as a result of cerebral edema caused by severe TBI. In these cases, it may not be technically possible to cannulate the ventricles. Other concerns with the intraventricular technique include the risk of intraparenchymal hemorrhage associated with passing a catheter through brain tissue and the risk of infection. An intraventricular ICP monitor is visible in Figure 103-7.

Figure 103-7 A, Lateral scout view from a computed tomographic head scan in which an intraventricular intracranial pressure monitor is visible. B, Axial computed tomographic image showing catheter position in the ventricles.

Subdural and epidural monitors are technically easier to place and have a lower risk of hemorrhage and infection, but they provide less accurate readings of ICP and do not enable CSF withdrawal.

In view of all benefits and risks, intraventricular monitors are generally preferred. ICP monitors may be placed in the surgical suite or in the intensive care unit.

Management of Raised Intracranial Pressure

The normal ICP is 10 to 15 mm Hg in adults and older children. Various threshold values are used at different centers, above which treatment measures are instituted. This threshold is usually 20 to 25 mm Hg.

A related concept is that of cerebral perfusion pressure (CPP), which equals the mean arterial pressure (MAP) minus ICP; that is,

Normal adult CPP is higher than 50 mm Hg. Because of cerebral autoregulation, large fluctuations in systemic blood pressure produce only small changes in cerebral blood flow. However, when CPP falls below 40 mm Hg, cerebral blood flow is impaired. Thus, a major goal of TBI care is to maintain CPP within a normal range through appropriate management of systemic blood pressure and ICP.

After placement of the ICP monitor, efforts are made to keep ICP lower than 20 mm Hg and CPP higher than 50 mm Hg. General measures include elevating the head of the bed 30 to 45 degrees, avoidance of hypoxia, maintenance of normocapnia (carbon dioxide tension, 35 to 40 mm Hg), and light sedation. If raised ICP persists, the follow measures may be needed: heavy sedation with fentanyl and paralysis with vecuronium; drainage of CSF in 3- to 5-mL increments; mannitol, 0.25 to 1 g/kg, followed by 0.25 g/kg every 6 hours; and mild hyperventilation to a carbon dioxide tension of 30 to 35 mm Hg. If mannitol is used, serum electrolytes and osmolality must be monitored closely. Mannitol must be discontinued if serum osmolality exceeds 320 mOsm/L. Head CT should be repeated if there is a persistent problem with raised ICP. Finally, high-dose barbiturate therapy (barbiturate coma) should be considered as a last resort for raised ICP that is refractory to all other measures.

Anticonvulsant Therapy

Post-traumatic seizures are a recognized complication of TBI. Post-traumatic seizures are classified as being early if they occur within 1 week of injury and late if the onset is more than 1 week after injury. There may be justification for a third category of “immediate” seizure, occurring minutes to hours after injury.

Total prevention of seizures would obviously be of great benefit to the patient. Administration of an anticonvulsant medication to prevent a first seizure (prophylactic anticonvulsants) has been the subject of considerable investigation. Data indicate that in adults, prophylactic anticonvulsants lower the risk of early seizures but do not improve outcomes. Prophylactic anticonvulsants also do not lower the risk of late seizures.¹⁰ In Guidelines for the Management of Severe Head Injury, the American Association of Neurological Surgeons has rated various treatments as standards, guidelines, or options. Prophylactic anticonvulsants are considered by this organization to be an option of unclear benefit to the patient.¹¹ This means that the clinician may choose to prescribe or withhold this treatment, on the basis of clinical judgment. If prophylactic anticonvulsants are being considered, the decision to prescribe must be made in view of the known potential for serious complications associated with these medications. Prophylaxis, when prescribed, is usually phenytoin, and the usual duration of therapy is 1 week.

If late seizures occur, long-term anticonvulsant therapy is needed, usually starting with phenytoin or carbamazepine and progressing to other agents in the event of therapeutic failure or toxicity.

Immediate seizures may complicate an otherwise trivial injury, especially in children. In these cases, a period of observation, without initiation of anticonvulsant therapy, may be appropriate.

Patients with clinically severe TBI (GCS score, 3 to 8), penetrating brain injury, and a history of alcohol abuse are at higher risk for developing post-traumatic seizures.

Steroids

The use of glucocorticoids in severe TBI dates back to the 1960s. Early laboratory and clinical work suggested that glucocorticoids improved cerebral edema, lowered ICP, and had other beneficial effects. As a result, these agents became a standard part of the management of severe TBI. However, more recent investigation indicates that glucocorticoids do not lower ICP or improve outcome in patients with severe TBI. Therefore, the routine use of glucocorticoids is no longer recommended for any type of TBI.¹¹

Post-traumatic Syndrome

This is a well-known and yet poorly understood complication of mild or moderate TBI. Patients report somatic symptoms, including headache, dizziness, blurred vision, tinnitus, and balance difficulties; cognitive symptoms, including difficulty concentrating and impaired judgment; and psychosocial symptoms, including depression, emotional lability, personality changes, insomnia, and fatigue.

Treatment for these symptoms is largely supportive. The clinical course is usually one of improvement, although progress is quite variable.

In some cases, further evaluation is warranted. Head CT, MRI, and neuropsychological testing may be needed. Imaging studies occasionally identify a late complication of TBI, such as hydrocephalus, that can be helped with surgical intervention. Electroencephalography should be considered when there is a question of seizure activity.

A more severe form of post-traumatic syndrome is chronic traumatic encephalopathy, also known as dementia pugilistica or punch drunk syndrome, which results from repeated concussions, as described previously.