Traumatic Brain Injury

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38 Traumatic Brain Injury

It is estimated that 3.2 million people are living with long-term disability related to traumatic brain injury (TBI).¹ In addition to the personal toll, the direct and indirect costs of these disabilities are estimated to exceed $60 billion annually.² Americans sustain an estimated 1.6 million TBIs each year. Approximately 290,000 require hospitalization, and 51,000 die of their injuries.³ However, the true incidence of TBI is unknown because current surveillance methodologies do not capture those treated in non-hospital settings (e.g., primary care office) or those who do not seek treatment at all.

TBI is the leading cause of morbidity and mortality for Americans between the ages of 1 and 45 years. Teenagers and the elderly are most at risk, although the primary causes vary demographically. Motor vehicle crashes are the main cause of head injuries in those 5 to 64 years old, whereas falls are most common in people aged 65 years and older. The primary cause of penetrating head injury is gunshot wounds. Males have twice the risk of sustaining TBI as females across all age groups and are three times more likely to die as a result of their injury.

TBI death rates in the United States fell during the 1980s. A substantial decline in motor vehicle–related fatalities was primarily responsible. At the same time, the incidence of gunshot wounds to the head rose, and in 1990, firearms surpassed motor vehicle crashes as the single largest cause of death due to TBI in some urban areas. However, in-hospital mortality rose to 8% during the last decade, presumably because of the increase in hospitalization rates of severe and moderate TBI.⁴

Pathophysiology

Trauma to the head causes primary injury such as skull fracture, cerebral contusion, and hemorrhage that is a direct physical consequence of the impact. Hours or days after the traumatic incident, secondary injury usually occurs and may be a major determinant of the patient’s ultimate neurologic outcome.

Primary Injury

Injury to the brain is caused by external forces to the head that strain the tissue beyond its structural tolerance.⁵ These forces can be classified as contact or inertial.⁶ Contact forces typically produce focal injuries such as skull fractures, contusions, and epidural or subdural hematomas. Inertial forces result from the brain undergoing acceleration or deceleration (translational, rotational, or both) and can occur without head impact. Inertial forces can cause focal or diffuse brain injuries: pure translational acceleration leads to focal injuries such as contrecoup contusions, intracerebral hematomas, and subdural hematomas, whereas rotational or angular acceleration, common with high-speed motor vehicle crashes, usually causes diffuse injuries. Although external signs of head injury such as scalp abrasions, lacerations, and hematomas are common with blunt-force trauma, the brain can also be severely injured solely by inertial forces, without evidence of scalp or facial injuries.

Skull fracture results from a contact force to the head that is usually severe enough to cause at least brief loss of consciousness. Linear fractures are the most common type of skull fracture and typically occur over the lateral convexities of the skull. Most often, they are nondisplaced cracks in the skull (linear fractures), but a particularly intense impact can cause a gap (diastasis) between the edges of the fracture. A depressed skull fracture, in which skull fragments are pushed into the cranial vault, usually results from blunt force by an object with a relatively small surface area, such as a hammer (Figure 38-1). The base of the skull can be fractured by severe blunt trauma to the forehead or the occiput. Basilar skull fractures are most common in the anterior skull base and often involve the cribriform plate, disrupting the olfactory nerves (Figure 38-2). Posterior basilar skull fractures may extend through the petrous bone and internal auditory canal, thereby damaging the acoustic and the facial nerves.

Figure 38-1 Right frontal depressed skull fracture caused by an assault with a hammer (axial CT scan, bone window).

Figure 38-2 Basilar skull fractures through the anterior skull base typically cause cerebrospinal fluid rhinorrhea and tears in adjacent dura. CT scans through the base of the skull may not show the fracture itself but often show fluid in the sphenoid sinus or other paranasal sinuses (axial CT scan, bone window).

Skull fractures per se are less detrimental than the associated damage to underlying tissues or vessels. For example, linear skull fractures that involve the squamous portion of the temporal bone are frequently accompanied by a tear of the middle meningeal artery, causing an epidural hematoma. They may also cause facial nerve injury, exhibited as facial asymmetry that can present immediately or in a delayed fashion. Treatment may require steroids or in severe cases, surgical decompression of the facial nerve. Depressed skull fractures are often associated with contusions of the underlying brain tissue, and a scalp laceration overlying a depressed skull fragment can contaminate the fragment with bacteria from the scalp and hair. With a basilar skull fracture, the dura underlying the fracture is often disrupted, resulting in a cerebrospinal fluid (CSF) fistula and leakage of CSF from the nose or ear. Such fistulas allow bacteria to enter the intracranial space from the normally colonized nose, paranasal sinuses, or external auditory canal.

Common posttraumatic intracranial lesions are hemorrhage (epidural, subdural, and intraparenchymal), contusion, and diffuse brain injury. Subdural hematomas are seen in 20% to 25% of all comatose victims of TBI (Figure 38-3). They develop between the surface of the brain and the inner surface of the dura and are believed to result from the tearing of bridging veins over the cortical surface or from disruption of major venous sinuses or their tributaries. The hematoma typically spreads over most of the cerebral convexity; the dural reflections of the falx cerebri prevent expansion to the contralateral hemisphere. Swelling of the cerebral hemisphere is common in those with subdural hematomas, given the associated damage to underlying brain tissue. Underlying cerebral contusions were found in 67% of patients with subdural hematomas in one series.⁷ Subdural hematomas are classified as acute, subacute, or chronic, each having a characteristic appearance on computed tomography (CT): acute hematomas are bright white, subacute lesions are isodense with brain tissue and are therefore often overlooked, and chronic hematomas are hypodense relative to the brain.

Figure 38-3 Acute subdural hematomas (SDH) typically spread over entire surface of the hemisphere. Occasionally, mixed-density SDH is seen, indicative of injuries occurring at different times.

Epidural hematomas develop between the inner table of the skull and the dura, usually when the middle meningeal artery or one of its branches is torn by a skull fracture. They occur in 8% to 10% of those rendered comatose by TBI.^8,⁹ The majority of epidural hematomas are located in the temporal or parietal regions, but they can also occur over the frontal or occipital lobes and (rarely) in the posterior fossa. They appear as hyperdense mass lesions on CT. Unlike subdural hematomas, their spread is limited by the suture lines of the skull, where the dura is very adherent. Because an epidural space normally does not exist, the clot must strip the dura from the inner table of the skull as it enlarges, resulting in its classic biconvex or lenticular shape (Figure 38-4). Epidural hematomas are uncommon in infants and toddlers, presumably because their skulls are more deformable and less likely to fracture, and in TBI victims older than 60 years, because the dura is extremely adherent to the skull.

Figure 38-4 Epidural hematomas have a lens shape and smooth inner border because they strip the dura from the inner table of the skull as they enlarge (axial CT scan).

An intraparenchymal hematoma is a hemorrhage within the brain substance that occurs after a very severe TBI. It is usually associated with contusions of the surrounding tissue. Duret’s hemorrhage, or hemorrhage into the base of the pons or midbrain, is thought to result from disruption of the perforating arteries at the time of uncal herniation. Such brainstem hemorrhage almost always leads to death or minimally responsive survival.

Traumatic subarachnoid hemorrhage often results from tearing of the corticomeningeal vessels. Though common after severe TBI, subarachnoid hemorrhage does not produce a hematoma or mass effect.¹⁰ However, it may be associated with an increased risk for posttraumatic vasospasm, which may adversely affect clinical outcome.¹¹

Contusions are heterogeneous lesions comprising punctate hemorrhage, edema, and necrosis and are often associated with other intracranial lesions. One or more contusions occur in 20% to 25% of patients with severe TBI. Because they evolve over time, contusions may not be evident on the initial CT scan or may appear as small areas of punctate hyperdensities (hemorrhages) with surrounding hypodensity (edema) (Figure 38-5). Local neuronal damage and hemorrhage lead to edema that may expand over the next 24 to 48 hours. With time, contusions may coalesce and look more like intracerebral hematomas. Depending on their size and location, they may cause significant mass effect, resulting in midline shift, subfalcine herniation, or transtentorial herniation. Contusions are most common in the inferior frontal cortex and the anterior temporal lobes,¹² where the surface of the inner table of the skull is very irregular; they result from shifting of the brain over this irregular surface at the time of impact. Direct blunt-force trauma to the head can produce a contusion in the tissue underlying the point of impact (coup contusion). If the head was in motion upon collision with a rigid surface, a contusion may occur in the brain contralateral to the point of impact (contrecoup contusion).

Figure 38-5 Contusions are most common in the inferior temporal and frontal lobes. In the first few hours after injury, they appear only as areas of hemorrhage mixed with edematous brain. Within 24 to 48 hours after injury, further hemorrhage may occur, causing significant enlargement of the contusion and hematoma (axial CT scan).

Diffuse axonal injury refers to lacerations or punctate contusions at the interface between the gray and white matter. Such punctate contusions are thought to result from the disparate densities of the gray and white matter and the consequent difference in centripetal force associated with a rotational vector of injury.¹³ Thus, diffuse axonal injury most often occurs after a high-speed motor vehicle crash, during which severe angular and rotational forces are applied to the head. Diffuse axonal injury was once thought to result solely from mechanical disruption at the time of impact; however, more recent research has identified cases in which the histologic footprints of diffuse axonal injury, such as fragmentation of axons and axonal swelling, do not appear until 24 to 48 hours after the incident, suggesting that some cases are a secondary manifestation of trauma.^14,¹⁵ Diffuse axonal injury is present in almost half of all patients with severe TBI and in a third of those who die, and it is a common cause of persistent vegetative or minimally conscious state.

Posttraumatic intracranial lesions cause neurologic dysfunction via direct and in some cases indirect mechanisms. By destroying brain tissue, contusions and intraparenchymal hemorrhage cause deficits directly related to the function of the damaged tissue. Uncal herniation is also an important mechanism of temporary or permanent neurologic deficits.^16,¹⁷ Semirigid dural reflections divide the intracranial contents into compartments. The tentorium cerebelli separates the anterior and middle cranial fossae from the posterior cranial fossa. The brainstem, specifically the midbrain, traverses an opening, the tentorial foramen, in the anterior central portion of this partition. The medial portion of the temporal lobe, the uncus, lies on both sides of the tentorial foramen. Because the most common TBIs, such as hematomas and contusions, are usually located over the lateral surfaces of the brain, and because the brain’s extreme lateral surface is the rigid skull, such lesions tend to depress the brain medially. Therefore, a subdural hematoma over the surface of the temporal lobe or a hemorrhagic contusion of the temporal lobe itself is likely to displace the medial portion of the temporal lobe (uncus) into the tentorial foramen (i.e., uncal herniation). Such displacement compresses the midbrain, which contains neurons that are part of the reticular activating system. At the base of the midbrain is the crus cerebri, which contains pyramidal fibers from the cortex, and the third cranial nerve, which exits the midbrain through the interpeduncular cistern. Midbrain compression due to uncal herniation damages the reticular activating system, causing loss of consciousness; stretches the third cranial nerve and its associated parasympathetic fibers, causing pupil dilatation and loss of the light reflex; and injures the pyramidal fibers in the crus cerebri, causing abnormal posturing responses in the contralateral arm and leg.

Medial displacement of a cerebral hemisphere resulting from hemispheric swelling or a subdural or epidural hematoma also can cause herniation of the cingulate gyrus under the falx cerebri. Permanent neurologic dysfunction usually does not result, however.

Intracranial hypertension is a major cause of posttraumatic neurologic morbidity and mortality.¹⁸ The intracranial pressure (ICP) is defined by the volume of CSF, blood, and brain tissue in the cranial vault. The volume of these components is dynamic, and the brain can accommodate moderate changes in any of the three. For example, the blood volume can rise or fall by as much as 30% to 40%, CSF absorption can increase to reduce the size of the ventricles by up to 90%, and brain tissue itself is compressible. Thus, the intracranial volume can gain 100 to 150 mL, equivalent to a moderate-sized subdural hematoma, without the ICP increasing significantly. When these buffering mechanisms have been exhausted, however, even a small increase in the size of a hematoma will cause a rapid rise in ICP. If appropriate treatment is delayed, the ICP may approach the mean arterial pressure (MAP), causing a hydrostatic block of blood flow to the brain and brain death. Intracranial hypertension, particularly if refractory to medical or surgical treatment, is the most common cause of death after severe TBI.

Secondary Injury

Posttraumatic ischemia initiates a cascade of metabolic events that lead to the surplus production of oxygen free radicals,¹⁹^–²¹ excitatory amino acids,^22,²³ cytokines,^24,²⁵ and other inflammatory agents.²⁶ Glutamate and aspartate are the excitatory amino acids most commonly implicated in excitotoxic injury,²⁷ which is mediated by activation of N-methyl-D-aspartate, α-amino-3-hydroxy-5-methylisoazole-4-proprionic acid, or kainic acid receptors.²³ Overactivation of these receptors causes an excessive influx of ionized calcium into the cytosol, and elevated amounts of ionized intracellular calcium play a key role in neurodegeneration after injury to the central nervous system (CNS).^28,²⁹ In addition, posttraumatic nonischemic events such as an increase in intracellular free Ca⁺⁺ via receptor-gated or voltage-dependent ion channels induce the release of oxygen free radicals from mitochondria.³⁰ Excessive levels of highly reactive oxygen free radicals cause lipid peroxidation of cell membranes, oxidation of intracellular proteins and nucleic acids, and activation of phospholipases A₂ and C, which hydrolyze membrane phospholipids, thereby releasing arachidonic acid. The liberation of arachidonic acid triggers the generation of free fatty acids, leukotrienes, and thromboxane B₂, all of which are associated with neurodegeneration and poor outcome after experimental TBI.³¹^–³³ Inflammatory cytokines, particularly interleukin (IL)-1, IL-6, and tumor necrosis factor, also are overproduced after TBI.³⁴^–³⁶ In animal models, posttraumatic activation of microglia is a principal source of these cytokines.²⁵ IL-1 and IL-6 provoke an exuberant cellular inflammatory response believed to be responsible for astrogliosis, edema, and tissue destruction.^26,³⁷

TBI also increases extracellular potassium levels,³⁸ leading to an imbalance of intracellular and extracellular K⁺, disruption of the Na⁺/K⁺-ATPase cell membrane regulatory mechanisms, and subsequent cell swelling.^39,⁴⁰ Astrocyte swelling has been attributed to the clearance of excessive extracellular K⁺.⁴¹ High levels of extracellular K⁺ have also been implicated as the cause of widespread neuronal depolarization and spreading depression seen after experimental TBI.^27,^38,⁴² Moreover, potassium stimulates increased oxygen uptake in glial cells, potentially depriving adjacent neurons of oxygen.^43,⁴⁴ Severe TBI also causes a substantial decrease in extracellular magnesium (Mg⁺⁺) levels, thereby impairing normal glycolysis, cellular respiration, oxidative phosphorylation, and the biosyntheses of DNA, RNA, and protein.⁴⁵^–⁴⁷ Because Mg⁺⁺ competes with Ca⁺⁺ at voltage-gated cell membrane–associated Ca⁺⁺ channels, reduced levels of Mg⁺⁺ will result in an abnormal influx of Ca⁺⁺ into the cell.

Prehospital Care

The acutely injured brain is vulnerable to further damage from systemic hypotension, cerebral hypoperfusion, hypercarbia, hypoxemia, and elevated ICP. Preventing these physiologic insults is crucial to limiting secondary brain injury. Care of the TBI victim always should begin with evaluating and securing a patent airway and restoring normal breathing and circulation. Early endotracheal intubation usually benefits comatose patients. Securing and maintaining an airway are essential to optimal oxygenation and ventilation, and early intubation has been found to reduce mortality after severe TBI.⁴⁸

The airway is usually most easily and safely secured by orotracheal intubation, a method in which most emergency medical personnel are trained and experienced. Patients with severe maxillofacial trauma may require nasotracheal intubation, but this is less desirable because it is a relatively blind procedure. The nasal passageways can be irritated, causing blood pressure (BP) and ICP to surge, and in those with severe anterior skull base fractures, the tube can inadvertently be passed into the brain. A third alternative for securing the airway is the laryngeal mask airway, an easily learned and rapidly applied device that has undergone successful field trials.⁴⁹ However, it does not protect against aspiration and cannot be used to achieve high airway pressures. A surgical airway (cricothyroidotomy) should be performed only after other attempts to secure an airway have failed, and only by an experienced provider.

The patient should be sedated and pharmacologically paralyzed before intubation, because irritation of the oropharynx typically causes transient hypertension, tachycardia, increased ICP, and agitation that can interfere with the procedure. Fentanyl, a short-acting opioid agonist that produces analgesia and sedation, is the most commonly used sedative. The usual dose is 3 to 5 µg/kg body weight, administered intravenously (IV) 3 minutes before intubation. Etomidate, an alternative to opioids, provides adequate sedation and is less likely to cause hypotension. Some prefer thiopental because it is an ultra-short-acting barbiturate and is thus less likely to conceal the neurologic status when the patient reaches the trauma center; however, it is more likely than other agents to cause hypotension. Neuromuscular blocking agents commonly used for tracheal intubation include succinylcholine (1.5 mg/kg IV), which has the advantages of rapid onset, complete reliability, and very short duration of action. This last attribute is particularly important in the prehospital setting, where attempts at intubation sometimes fail. Vecuronium (0.01 mg/kg IV) is an alternative that offers the theoretical advantage of being a nondepolarizing muscle relaxant. Because it has a relatively long duration of action (1 to 2 hours), it is less forgiving of failed intubation attempts. Table 38-1 shows a recommended rapid-sequence intubation pathway.

TABLE 38-1 Recommended Rapid-Sequence Induction for Severely Head-Injured Patients

Supplemental oxygen should be provided before and immediately after intubation. Ventilatory rates of 10 to 12 breaths per minute for adults, 20 breaths per minute for children, and 25 breaths per minute for infants should supply adequate oxygenation. Therapeutic hyperventilation is inadvisable unless neurologic deterioration is clearly evident during evaluation and transport. Aggressive hyperventilation can cause cerebral vasoconstriction, reducing already low cerebral blood flow (CBF) and potentially causing or exacerbating cerebral ischemia.

Rapid fluid resuscitation and restoration of a normal BP are critical in the prehospital setting, because hypotension has been associated with doubling of the mortality rate after severe TBI.⁵⁰ The most likely cause of hypotension is hemorrhage, usually in the abdomen or chest; therefore, hypovolemia should be assumed. Lactated Ringer’s or normal saline solutions should be infused through a large-bore IV catheter as quickly as possible until normotension is achieved. Although preclinical studies suggest that hypertonic saline may be more effective than isotonic solutions for rapid volume resuscitation,^51,⁵² results of several small clinical trials have not been convincing.^53,⁵⁴

In all cases of severe TBI, defined as a Glasgow Coma Scale (GCS) score of 3 to 8 and an inability to follow commands, patients should be treated as if they have a spinal fracture until an adequate examination of the spine proves otherwise. Among those who survive long enough to reach the emergency department, the likelihood of a cervical spine fracture is 2% to 7%. More troubling, however, is that an estimated 10% to 25% of all posttraumatic spinal cord injuries are iatrogenic, occurring during transport to the hospital.⁵⁵ After respiratory and hemodynamic stabilization, the patient should be placed in a neutral position on a flat, hard surface. If the patient requires immediate tracheal intubation, it should be performed while another person provides in-line cervical spine immobilization. A rigid cervical spine collar should be placed as soon as possible. Next, the patient should be placed on a backboard; the cervical spine can then be further immobilized with a buttress of foam or towels placed on both sides of the head. To prevent any movement during transport, the patient should be strapped to the board in several locations.

The organization of emergency medical services and regional trauma programs has improved outcomes for victims of trauma, particularly those with severe TBI.⁵⁶ A very large prospective study of the cost and outcomes associated with trauma center designation found more than a 25% reduction in in-hospital mortality for those with severe TBI who were initially treated at a level I trauma center compared to similarly injured patients treated at hospitals of similar size that were not designated trauma centers.⁵⁷ This is likely because designation as a level I or II trauma center by the American College of Surgeons Committee on Trauma or a state health department ensures the availability of immediate neurosurgical care when the patient arrives. Therefore, every effort should be made to transport severely injured patients directly to a designated trauma center. Nonetheless, if an adequate airway or venous access cannot be obtained in the field, some patients may need to undergo respiratory or hemodynamic stabilization at a nearby emergency department en route to the trauma center. Once hemodynamic and airway stability is achieved, immediate transport to a designated trauma center should occur without delays for imaging or secondary surveys.

Emergency Department Care

Upon arrival at the trauma center, the emergency medical personnel should concisely report their prehospital assessment and management, including mechanism of injury, stabilizing maneuvers, medications given, initial vital signs, GCS score, and hemodynamic stability during transport. A thorough physical and radiographic examination to identify all life-threatening injuries should then be performed. Most trauma centers follow the Advanced Trauma Life Support protocol, a comprehensive routine that has proved successful in quickly detecting all major injuries.⁵⁸ First the airway is reassessed, and the need for tracheal intubation is carefully reconsidered. For patients intubated in the field, proper placement of the tracheal tube is verified both clinically and radiographically. When the airway is secure and adequate oxygenation is confirmed using a percutaneous oxygen saturation monitor or arterial blood gas analysis, two large-bore IV catheters are inserted to provide sufficient venous access for high-volume fluid resuscitation. An isotonic saline solution is infused to continue volume replacement, which probably began at the scene. Any life-threatening injuries such as overt hemorrhage, tension pneumothorax, or cardiac tamponade should be treated immediately upon discovery. A brief neurologic examination is performed, including assessment of the GCS score (Table 38-2), pupillary size and reaction to light, and symmetry and extent of extremity movements. The head is palpated to detect fractures, lacerations, or penetrating wounds, and lacerations are probed gently to ascertain the presence of a depressed skull fracture or foreign body. Large lacerations are compressed with pressure dressings or temporarily sutured to prevent further hemorrhage. Careful inspection of the head should reveal hemotympanum, periorbital or mastoid ecchymosis, and CSF rhinorrhea or otorrhea.

TABLE 38-2 Glasgow Coma Scale ⁵⁹

Response	Points
Speech
Alert, oriented, and conversant	5
Confused, disoriented, but conversant	4
Intelligible words, not conversant	3
Unintelligible sounds	2
No verbalization, even with painful stimulus	1
Eye Opening
Spontaneous	4
To verbal stimuli	3
To painful stimuli	2
None, even with painful stimuli	1
Motor
Follows commands	6
Localizes painful stimulus	5
Withdraws from painful stimulus	4
Flexor posturing with central pain	3
Extensor posturing with central pain	2
No response to painful stimulus	1

Data from Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;2(7872):81-84.

Oxygen saturation is monitored continually, and BP is measured frequently during this primary examination. A Foley catheter is placed to help monitor the fluid status, and an orogastric tube is inserted and connected to suction to decompress the stomach. Blood specimens are obtained and analyzed for glucose, electrolytes, complete blood count, platelets, prothrombin and partial thromboplastin times, and International Normalized Ratio (INR). Type and crossmatch of a blood specimen should be considered, and an arterial blood gas obtained. Serum and urine toxicology screens are advisable if alcohol or substance abuse is suspected, and women of child-bearing age should undergo a pregnancy test.

Coagulopathy resulting from TBI is thought to occur when hypoperfusion causes activation of the protein C pathway, thereby inducing alterations in the clotting cascade.⁶⁰ It is also commonly seen as a result of therapeutic anticoagulation with warfarin, especially in the geriatric population. Rapid identification and correction of coagulopathy is critical to prevent expansion of intracranial hematomas and allow surgical intervention. Fresh frozen plasma and cryoprecipitate can be used to correct the INR to 1.3 or less. Recombinant factor VIIa has been shown to decrease blood product requirements and costs associated with correction of coagulopathy.⁶¹ Other studies demonstrate more rapid correction times compared to blood product administration, although differences in outcomes have not been significant. Product expense and concern for thromboembolic complications have limited the routine use of recombinant factor VIIa.

The initial x-ray evaluation is usually performed in the trauma bay during the primary survey and includes chest, pelvis, and lateral cervical spine films. If the lower cervical spine is not visible on the lateral cervical spine film, a swimmer’s view can be obtained, or this area can be imaged with axial CT.

After all life-threatening injuries have been identified and stabilized, the immediate concern is whether the patient requires a craniotomy to evacuate an intracranial mass lesion. A CT scan of the head should be performed at intervals of 10 mm or less from the C2 vertebra to the vertex. In addition to posttraumatic intracranial lesions, the scan should be examined for brain swelling, patency of the basal cisterns, and other characteristics that will guide subsequent treatment. If no surgical intracranial mass lesion is evident on the scan of the head, CT scans of the chest and abdomen can be performed to detect occult hemorrhage in these cavities. If a surgical mass lesion is seen on the head CT scan, however, it should be evacuated immediately, postponing any other imaging studies. Diagnostic peritoneal lavage is often performed during the craniotomy to detect abdominal bleeding. Conversely, if hemodynamic instability necessitates an emergent laparotomy or thoracotomy before a head CT scan can be obtained, several diagnostic procedures can be performed in the operating room to confirm a suspected intracranial injury. These procedures include an air ventriculogram or diagnostic burr holes and are most appropriate if the patient has lateralizing neurologic deficits, particularly a unilateral fixed and dilated pupil.

Definitive Treatment

Critical to determining the severity of the brain injury and appropriate treatment are CT findings combined with a reliable postresuscitation GCS score and assessment of pupil size and reactivity. In the case of an acute subdural hematoma, for example, a patient with a moderate-sized lesion who has normal pupil size and reactivity and is able to follow commands might safely be treated nonoperatively. Conversely, surgery is unlikely to benefit an elderly patient with fixed and dilated pupils and a GCS score of 3 or 4, regardless of the CT findings. Other determining factors include size and location of the hematoma, presence and extent of an underlying contusion or brain swelling, and results of the neurologic examination. Neurologic deterioration, particularly a decline in mental status, suggests enlargement of the hematoma, and a new CT scan should be obtained promptly. Hematomas less than 10 mm thick that cause a midline shift of less than 5 mm can usually be observed, especially if they do not involve the middle cranial fossa.⁶² If nonoperative management is chosen for an intracranial hematoma, the patient should be monitored with frequent neurologic assessments in the intensive care unit (ICU). If the patient cannot follow commands, ICP monitoring is recommended.

The classic presentation of a patient with an epidural hematoma is a period of unconsciousness immediately after impact to the head, followed by a so-called lucid interval in which consciousness returns for a few minutes to an hour or more before the patient lapses into a coma. This lucid interval actually occurs in less than a third of patients with epidural hematomas, however; most either remain conscious after the injury (smaller clots) or remain comatose.

A hematoma that compresses the temporal lobe is particularly ominous and can rapidly cause uncal herniation with minimal enlargement. Thus, such lesions warrant a lower threshold for evacuation compared with hematomas in other locations. If the clot is small enough to not require evacuation, it should be monitored with frequent CT scans during the first several days after injury. Enlarging middle fossa hematomas, even those large enough to cause herniation, do not always cause an increase in the ICP; therefore, ICP monitoring should not be relied on to follow their status.

The initial signs and symptoms of contusions vary greatly, depending on their size and location and the presence of other associated lesions. A small contusion may cause only a headache or no symptoms at all. If located in an eloquent area of the brain, such as the speech or motor areas, it may cause focal neurologic symptoms. Larger contusions, especially those involving the frontal or temporal lobes, typically cause elevated ICP and coma. Patients with small or deep-seated contusions without mass effect initially can be managed nonoperatively. The contusion should be followed closely with serial CT scans, however, because there is a 20% to 30% risk that the contusion will enlarge during the next 24 to 48 hours. The ICP should be monitored if the patient cannot follow commands. As with hematomas in the middle cranial fossa, contusions of the temporal lobes should be closely watched with CT scans. A temporal contusion can enlarge to the point of uncal herniation without a significant rise in ICP, so the threshold for evacuation of these lesions should be low (Figure 38-6). Unilateral frontal or temporal lobectomies are usually well tolerated and do not cause measurable neurologic deficits, while allowing space for further brain swelling.

Figure 38-6 Temporal lobe contusions must be monitored closely because even a slight enlargement can cause uncal herniation, often without an increase in intracranial pressure (ICP) (axial CT scan).

In the ICU, the primary goal is to prevent cerebral ischemia and thereby limit secondary brain injury. The most common preventable causes of cerebral ischemia are hypotension, hypoxemia, and intracranial hypertension. Comprehensive physiologic monitoring should be performed so that these physiologic insults can be detected and treated promptly.

Physiologic Monitoring

Continual monitoring of the end-tidal partial pressure of carbon dioxide (PCO₂) and frequent analyses of arterial blood gases enable the early detection of deteriorating ventilatory status, which should prompt appropriate ventilator adjustments. Oxygen saturation should also be monitored continually with pulse oximetry. BP monitoring is best accomplished with an indwelling arterial catheter coupled to a pressure transducer. The catheter is usually inserted into the radial artery and can also be used to obtain arterial blood samples for blood gas analysis. Hypovolemia is a common cause of posttraumatic hypotension. It can result from overt hemorrhage, usually detected soon after injury; from occult hemorrhage, which may not be recognized for several hours or days; or from soft-tissue inflammation and swelling. Consequently, central venous pressure (CVP) monitoring should be considered for patients with severe TBI, particularly those with significant non-CNS injuries. Indwelling subclavian or internal jugular venous catheters are used, coupled to pressure transducers. In elderly patients or those with severe pulmonary contusions, intravascular volume may be more accurately assessed by pulmonary artery catheterization with a Swan-Ganz catheter. Monitoring urine output with an indwelling Foley catheter is essential for determining the patient’s fluid status.

Continuous ICP monitoring is essential for all patients who have severe TBI and abnormal CT findings, because intracranial hypertension develops in 53% to 63% of such patients.⁶³ ICP monitoring is also recommended for comatose patients who are older than 40 years and have unilateral or bilateral motor posturing or a systolic blood pressure (SBP) less than 90 mm Hg, even if no abnormalities are seen on the initial CT scan.⁶⁴ The gold standard for ICP monitors is the ventricular catheter coupled to an external strain-gauge transducer.⁶⁵ It is accurate, reliable, and far less expensive than newer self-contained pressure-sensing devices. In addition, ventricular pressure is considered more reflective of global ICP than is subdural, subarachnoid, or epidural pressure. Catheters placed in these extracerebral spaces are more prone to occlusion and, owing to the effects of compartmentalization, typically record a pressure that is lower than the global ICP. Other advantages of the ventriculostomy method of ICP monitoring are that the system can be re-zeroed after insertion—not possible with most of the newer self-contained devices—and CSF can be withdrawn to treat intracranial hypertension. The overall complication rate for ventricular ICP monitoring is 7.7% (infection, 6.3%; hemorrhage, 1.4%),⁶³ and some studies indicate that the infection rate increases significantly when a catheter remains in place for more than 5 days.⁶⁶

Alternatives to the ventriculostomy technique have been developed that provide relatively accurate measurements of global ICP, are easier to insert, and may cause fewer complications. They include devices that contain a pressure-sensing transducer (either strain-gauge or fiber-optic technology) within the tip of the catheter.⁶⁵ These pressure sensors provide reliable ICP measurements even if they are inserted into the white matter and are often used when a ventricular catheter is difficult to insert because of small or collapsed ventricles. The primary disadvantage is that CSF drainage is not possible. In addition, these devices can be calibrated only once, before insertion, and with some of them, measurement drift is as much as 1 to 2 mm Hg per day.

The cerebral perfusion pressure (CPP), defined as the difference between MAP and ICP, is a calculated physiologic measurement that is used to describe actual cerebral perfusion. Some have suggested that maintaining the CPP above a certain threshold is more important than any particular MAP or ICP.⁶⁷

Devices that monitor the oxygen partial pressure of oxygen (PO₂) of brain tissue can be used to determine whether cerebral oxygenation is adequate. These monitors continually measure the tissue PO₂ in the small region of brain into which they are inserted. Studies suggest that mortality may be decreased in those undergoing oxygen directed therapy.⁶⁸ Although no methods are available for continuously monitoring global CBF, transcranial Doppler insonation of the middle cerebral arteries can provide indirect information. Positron emission tomography (PET) or CBF measurements with xenon, either as a radiolabeled agent or as a CT contrast medium, can provide periodic snapshots of the blood flow.

Medical Treatment

Hypoxemia is best avoided with the use of tracheal intubation and mechanical ventilation. The fraction of inspired oxygen should be titrated to provide an arterial PO₂ of 100 mm Hg. Maintaining an arterial PCO₂ of approximately 35 mm Hg is advised to avoid the cerebral vasoconstriction associated with aggressive hyperventilation. A form of acute respiratory distress syndrome (ARDS) can develop in patients with severe chest injuries. In such cases, adequate oxygenation requires the use of positive end-expiratory pressure (PEEP). Concern has been raised that the use of PEEP in patients with TBI may increase the ICP. However, clinical studies have shown that in the presence of ARDS, up to 14 to 15 cm H₂O of PEEP can be used without measurable changes in ICP, most likely because ARDS significantly reduces pulmonary compliance.

Hypotension, defined as a MAP of less than 90 mm Hg, should be treated aggressively. Normovolemia should be restored by infusing isotonic saline as needed to achieve a central venous pressure of 7 to 12 cm H₂O. Hypotonic intravenous solutions can exacerbate cerebral edema and should be avoided. If the patient is anemic, packed red blood cells should be transfused to restore the hematocrit to at least 30%. If hypotension is refractory to volume resuscitation, the patient should be given a continuous IV infusion of a vasopressor medication, with the dose titrated to raise the MAP above 90 mm Hg. Norepinephrine has been shown to be most efficacious at maintaining MAP and CPP without deleteriously affecting ICP.⁶⁹

Although some advocate the used of induced hypertension to raise the CPP above 70 mm Hg, particularly if the ICP is elevated and difficult to reduce,⁷⁰ others do not support this practice. A prospective, randomized clinical trial of patients with TBI compared a group whose CPP was kept above 70 mm Hg via induced hypertension with a group whose CPP was allowed to drift to 60 mm Hg.⁷¹ Six-month clinical outcomes did not differ between the two groups. Moreover, the group whose CPP was kept above 70 mm Hg required more vasopressor agents and had a significantly higher incidence of ARDS and other pulmonary complications. Others have found that the brain tissue PO₂ in patients with TBI typically does not fall until the CPP drops below 60 mm Hg.⁷² Based on these findings, the current recommendation is to maintain a CPP above 60 mm Hg.

Intracranial hypertension is defined as sustained ICP greater than 20 mm Hg. Several clinical studies have found that mortality and morbidity increase significantly when the ICP persistently remains above this threshold.⁷³ Based on this association and the widely accepted premise that elevated ICP can compromise cerebral perfusion and cause ischemia, the aggressive treatment of intracranial hypertension is almost uniformly endorsed. Before beginning therapy for intracranial hypertension, however, medical or physiologic conditions that can increase ICP should be considered and, if present, treated. These include seizures, fever, jugular venous outflow obstruction (e.g., poorly fitting cervical collars), and agitation.

Several medical and surgical options are available to reduce ICP. Depending on the type of brain injury, some may be more effective than others, and each is associated with potential adverse effects. A stepwise approach is usually followed, with the least toxic therapies utilized first and more toxic therapies added only if the initial treatment is unsuccessful. Sedation and neuromuscular blockade are often an effective first treatment, particularly if the patient is agitated or posturing. Narcotics (e.g., morphine, fentanyl), short-acting benzodiazepines (e.g., midazolam), or hypnotic agents such as propofol can be used for sedation, and vecuronium bromide as the paralytic agent. Narcotic-induced hypotension can be averted by using relatively low doses and ensuring the patient is normovolemic before treatment. Because the ability to obtain an accurate GCS score is lost during this treatment, the pupil status, ICP, and CT scans must be closely monitored.

If intracranial hypertension is refractory to sedation and neuromuscular blockade, intermittent ventricular CSF drainage is used. Intermittent rather than continuous drainage enables reliable measurement of the ICP. If these measures fail to reduce the ICP, a bolus administration of mannitol is recommended (0.25 to 1 g/kg every 3 to 4 hours as needed). This osmotic diuretic lowers ICP and increases CPP by expanding the blood volume, reducing the blood viscosity, and increasing CBF and oxygen delivery to the tissues within a few minutes of infusion. Its duration of effect averages 3 to 5 hours. Continuous infusion is less desirable than bolus infusion, because the former is more likely to lead to extravasation of the drug into brain tissue, causing a reverse osmotic gradient and increased edema and ICP.⁷⁴ The serum osmolarity and sodium level should be monitored frequently during mannitol administration. The drug should be discontinued if the serum sodium level exceeds 160 mg/dL or the osmolarity exceeds 320 mOsm in order to minimize the risk of acute tubular necrosis and renal failure. The intravascular volume should also be closely monitored to prevent dehydration. Recent studies have shown that hypertonic saline may also be effective at reducing ICP. Hypertonic saline appears to create osmotic mobilization of water across the blood-brain barrier. Concentrations ranging from 3% to 23.4% have been used to decrease ICP.⁷⁵

If despite these measures the ICP remains above 20 mm Hg, the ventilatory rate can be adjusted to reduce the arterial PCO₂ to 30 mm Hg. Hyperventilation should be used cautiously during the first 24 to 48 hours after injury, however, because it will cause cerebral vasoconstriction at a time when CBF is already critically reduced. Evidence also suggests that even brief periods of hyperventilation can lead to secondary brain injury by causing an increase in extracellular lactate and glutamate levels.⁷⁶ Prophylactic hyperventilation is always contraindicated in the absence of elevated ICP.⁷⁷ If hyperventilation is used, the brain tissue PO₂ or jugular venous oxygen saturation should be monitored to detect any cerebral ischemia that the treatment might cause. The risk of tissue ischemia and poor outcome may increase if the brain tissue PO₂ falls below 10 mm Hg.⁷²

If intracranial hypertension persists despite all these treatments, particularly if the ICP rises rapidly or if the patient’s initial CT scan showed a small contusion or hematoma, another CT scan should be obtained immediately to determine whether there is a new mass lesion or a preexisting lesion has enlarged. Even if the lesion has enlarged only slightly, an emergent craniotomy and evacuation of the contusion or hematoma may be the best way to reduce the ICP quickly and effectively.

If the CT scan does not reveal an intracranial mass lesion requiring surgery, the next recommended treatment for intracranial hypertension is high-dose barbiturates. Barbiturates are thought to be effective by reducing cerebral metabolic demand and blood flow, and preclinical studies suggest significant cerebral protective effects.⁷⁸ Pentobarbital is the most commonly used drug for this purpose and is administered as an IV loading dose of 10 to 15 mg/kg over 1 to 2 hours, followed by a maintenance infusion of 1 to 2 mg/kg per hour. The dose can be increased until intracranial hypertension subsides or MAP begins to fall. Continuous electroencephalographic monitoring is recommended while increasing the dose until a burst suppression pattern is observed. Hypotension, the most common adverse effect of barbiturates, can usually be averted by ensuring a normal intravascular volume before administering the drug.

Only a few options remain when intracranial hypertension is recalcitrant to all these measures, and they are controversial and not uniformly embraced. Therapeutic moderate hypothermia has been used in several clinical trials over the past decade. The body temperature is lowered to 32°C to 33°C as soon as possible after injury and kept at that temperature for 24 to 48 hours using surface cooling techniques. Although some clinical trials have not found that this treatment improves neurologic outcome compared with normothermia, they have consistently shown that hypothermia significantly reduces ICP.^79,⁸⁰ Moreover, hypothermia does not cause significant medical complications when used for no longer than 48 hours.

Some advocate the use of decompressive craniectomies, such as large lateral or bifrontal bone flaps, with or without a generous temporal or frontal lobectomy In one study of patients with severe TBI, 6-month outcomes were similar for a group that had large decompressive craniectomies and a group that did not, even though the craniectomy group had lower initial GCS scores and more severe radiographic injuries.⁸¹ Importantly, the craniectomy group did not have a higher incidence of persistent vegetative state. Two studies reported good outcomes in 56% to 58% of patients whose refractory intracranial hypertension was treated with decompressive craniectomy as a last resort,^82,⁸³ and another study suggested that decompressive temporal lobectomy, when performed soon after injury, improves the outcome for young patients.⁸⁴ However, others found that decompressive craniectomy does not improve ICP, CPP, or mortality rates.⁸⁵ The decision to perform decompressive surgery should take into account the patient’s ultimate prognosis. Because age has such a profound impact on the likelihood of a meaningful recovery, these therapies are recommended only for patients who are younger than 40 years old.

Failure to control intracranial hypertension may result in brain death, the irreversible cessation of cerebral function. Clinically, this is manifested by loss of motor function and brainstem reflexes including pupillary response, corneal reflex, cough reflex, and oculovestibular reflexes. Once these criteria are met, confirmatory testing such as apnea testing or nuclear medicine perfusion studies can be performed. Federal law requires notification of the local organ procurement office prior to formal brain death testing. However, medical staff should avoid mentioning organ donation to family members to minimize the appearance of conflict of interest; this is best left to designated requestors after decoupling has occurred.

Patients who have TBI, particularly those who are comatose or have significant non-CNS injuries, are at high risk for pneumonia and other infections, fever, malnutrition, seizures, deep venous thrombosis (DVT), pulmonary embolism, and other maladies endemic to the ICU. Most of these complications cause secondary brain injury and should be diagnosed and treated without delay. Fever is very common in the ICU and occurs in more than 79% of patients within the first week following injury.⁸⁶ Preclinical studies have found that there is a log increase in neuronal death in ischemic brain regions for every degree of brain temperature above 39°C,⁸⁷ and this effect is observed for 24 hours or more after injury.⁸⁸ Clinical studies of TBI patients have shown that the brain temperature is often 1°C to 2°C higher than body temperature,⁸⁹ though the effect of hyperthermia on ICP is less clear.^90,⁹¹ Consequently, the body temperature should be kept below 37°C at all times, and infectious or other causes of fever should be aggressively sought and treated.

Patients who are comatose, those being maintained on neuromuscular blocking agents, and those with pelvic or long-bone fractures are at high risk for deep venous thrombosis and pulmonary embolism. They should receive early prophylaxis, which typically includes the use of lower extremity sequential compression devices as well as subcutaneous heparin or enoxaparin. The early (2 to 3 days after injury) use of minidose heparin or low-molecular-weight heparin is safe and has not been found to cause or worsen intracranial hemorrhage after TBI.^92,⁹³ DVT is prevalent in TBI patients despite early use of prophylaxis.⁹⁴

Malnutrition is also common after severe TBI. The resting metabolic expenditure typically increases by 140% in a non-paralyzed patient with severe TBI.⁹⁵ Branched-chain amino acids from muscle protein are used preferentially for energy metabolism, potentially compromising the effectiveness of physical therapy. Nitrogen wasting is also increased, with excretion of as much as 9 to 12 g/day. Thus, early enteral or parenteral feeding is advisable, with the aim of providing at least 140% of the daily basal metabolic caloric requirements by the third or fourth day after injury.⁹⁶ A normal-sized adult patient usually needs 2000 to 3000 kcal/day. Because parenteral feeding increases the risk of infection, continuous enteral administration is preferable. For a patient expected to be in a prolonged coma, a percutaneous gastrostomy or surgical jejunostomy provides a convenient and well-tolerated route to administer tube feeding. Hyperglycemia is associated with TBI and is associated with prolonged hospital stays and increased mortality.⁹⁷ Aggressive management of hyperglycemia has been shown to decrease complications and improve long-term outcome,⁹⁸ but the optimal blood glucose range in patients with severe TBI remains controversial, and tight glucose control may be problematic.^99,¹⁰⁰

Posttraumatic contusions and subdural hematomas are well-known causes of generalized seizures which can precipitate secondary injury. Anticonvulsant prophylaxis, usually with phenytoin, is therefore recommended for patients with these lesions. The drug should be given for the first 7 days after injury; a prospective clinical trial found no advantage to longer prophylactic treatment.¹⁰¹ A common side effect of phenytoin is fever; this should be considered if infectious causes of fever have been ruled out. If a patient has seizures, especially if they are prolonged, the associated cerebral hypermetabolism will cause secondary brain injury. Seizures should thus be treated aggressively, up to and including the use of general anesthesia if necessary. Subclinical seizures may occur in up to 33% of patients in the first week following TBI.¹⁰² Therefore, EEG should be considered for those with unexplained depressed mental status, abruptly deteriorating cerebral oxygenation, or a sudden increase in ICP; however, enlarging intracranial mass lesions remain the most likely cause.

Physical Therapy and Rehabilitation

The number of survivors of TBI is increasing because of greater success in understanding and treating the disease and improved motor vehicle safety devices. Accordingly, the demand for high-quality, well-organized TBI rehabilitation programs is also increasing. The primary goal of these programs is to reintegrate patients into their communities by either restoring normal or near-normal ability to function or teaching them alternative strategies to function well despite their disabilities. Such programs should involve a multidisciplinary team of physical, occupational, and speech therapists, neuropsychologists, and social workers, ideally coordinated by a physiatrist or a neurologist with special training in physical medicine and rehabilitation. The team should be experienced in TBI rehabilitation and thoroughly understand the special needs of these patients. Programs that focus exclusively on TBI rehabilitation are far preferable to those that mix patients with TBI, stroke, neurodegenerative diseases, and tumors, because the typical age groups are very different, as are their rehabilitative needs.

Rehabilitation of TBI patients should begin in the ICU during the first few days after injury, in consultation with a physiatrist, and include passive range-of-motion exercises and functional splinting of the extremities. Mobilization helps prevent DVT, and studies indicate that early sitting of comatose patients may hasten the return of consciousness. Supplementing physical therapy with central neurostimulant medications is being investigated for those with more severe injuries and minimal responsiveness.¹⁰³ Rehabilitation after TBI entails many other factors that are critical to optimizing outcome, but a thorough review is beyond the scope of this chapter.

Penetrating Injuries

Gunshot wounds to the head, the predominant cause of penetrating head injury, usually cause massive destruction of brain tissue, severe brain swelling, and if transcranial trajectory, death. The wounding potential of a bullet depends primarily on its velocity at impact and its mass, although the shape of the bullet and its lateral movements also play a role. The relationship of bullet mass and velocity to the energy imparted to the head is described by the equation KE = 1/2MV², where KE is kinetic energy, M is the mass of the bullet, and V is the impact velocity of the bullet. According to this equation, the impact velocity is by far the most important determinant of a bullet’s wounding potential. Consequently, high-velocity rifle wounds to the head are invariably fatal, whereas low-velocity open-chambered handgun wounds often are not. When a bullet enters the skull, it creates a variety of pressure waves within the brain, some of which can cause tissue pressures of nearly 100 atmospheres, resulting in further tissue injury. In addition to forward velocity, the bullet’s lateral motion before and after impact affects the severity of tissue destruction. Such motion is described as yaw, or the angle between the bullet’s path of flight and its long axis, and precession and nutation, which are circular rotations of the bullet around the center of its mass. These movements increase the bullet’s relative surface area at the point of impact and enable it to pass more of its kinetic energy to the surrounding tissue. They increase the size of the entrance wound and cause greater cavitational injury. Bullets often fragment after they strike the skull, fracturing a portion of the skull into multiple fragments. Both the bullet and the bone fragments then become numerous secondary missiles that cause additional tissue damage.

Low-velocity missile wounds, such as those from knives, ice picks, or arrows, do not cause the massive brain injuries seen with bullets, as might be predicted by the kinetic energy equation. Usually, only the tissue in the immediate path of the missile is damaged, and patients often have a complete neurologic recovery after the missile is surgically extracted. Rarely, a missile injures a major intracranial artery or venous sinus, and these vascular injuries can result in large intracranial hematomas. Nonetheless, vascular injuries are always possible with high- or low-velocity missile injuries to the head, especially those in or near the skull base or the sylvian fissures.

The initial assessment and resuscitation of patients with penetrating head injuries are the same as for those with closed head injuries, as detailed earlier in this chapter. Prompt and aggressive cardiopulmonary resuscitation is critical. Knives or other missiles protruding from the head should never be removed in the field or emergency department; if they are tamponading a damaged intracranial vessel, removal could lead to massive intracranial hemorrhage. Wounds with active bleeding should be sutured immediately, as this is a source of ongoing blood loss and can contribute to hemodynamic instability. When a patient has a gunshot wound to the head, the neck, chest, and abdomen should be inspected carefully for other gunshot wounds, because wounds to the heart or great vessels in the chest or abdomen may be even more life threatening. A postresuscitation GCS score should be obtained as soon as possible to guide future therapeutic decision making. A CT scan of the head defines the intracranial path of the missile and related skull and tissue damage. More importantly, it identifies any large intracranial hematomas or contusions that may significantly affect outcome. If the missile trajectory is in or near the skull base or sylvian fissures and the patient is deemed salvageable, cerebral angiography should be performed because this injury pattern is associated with development of pseudoaneurysm.

Most patients who are expected to survive a penetrating head injury require at least limited operative treatment. Large intracranial hematomas should be evacuated promptly. A craniotomy is required for low-velocity missile wounds in which the object is still protruding from the head. After removing a segment of skull containing the missile and large enough to allow for intracerebral exploration, the surgeon can seek and immediately repair or occlude any vascular injuries caused by the missile. For gunshot wounds to the head, the surgeon should perform a limited débridement of the scalp and skull wound, removing scalp, bone, and bullet fragments penetrating the brain only if they lie near the surface. Easily accessible necrotic brain should be débrided and meticulous hemostasis achieved. Dural closure is important because it reduces the risk of CSF leak and infection, but it usually requires a pericranial graft. Artificial dural substitutes and allografts increase the risk of infection and therefore are not recommended.

Subsequent medical management of penetrating injuries is as described previously for closed head injuries. In addition, patients should receive prophylactic antibiotics for at least 14 days, because the missile usually carries skin and hair into the brain. Because a penetrating TBI by definition disrupts and contuses brain tissue, all patients with these injuries should also receive anticonvulsants for at least 7 days.

Mild and Moderate Injury

A mild TBI or concussion is defined by an initial GCS score of 14 or 15; a moderate TBI by a GCS score of 9 to 13. These injuries typically involve a brief loss of consciousness or alteration of consciousness at the time of impact to the head and some degree of retrograde or posttraumatic amnesia; however, patients with such injuries can follow commands. They usually do not have the complex intracranial pathology associated with severe TBI and therefore are unlikely to die from the injury; mortality rates are near zero for those with mild TBI and approximately 4% for those with moderate TBI. Nonetheless, these injuries can cause long-term cognitive and neuropsychological impairment. As many as 10% of those with mild injuries and 66% of those with moderate injuries suffer prolonged or permanent disabilities that prevent them from returning to work or school.

Rotational, acceleration, and deceleration forces are common causes of these injuries, particularly those that result in loss of consciousness. The impact usually is not intense enough to cause intracranial hematoma, cerebral contusion, skull fracture, or brain swelling. Although a small amount of subarachnoid hemorrhage may be present, usually in the sulci over the frontal or temporal lobes, CT findings are usually normal. Abnormal magnetic resonance imaging (MRI) findings have been reported in as many as 30% of these patients, most commonly diffuse hyperdense lesions on T2-weighted images. These lesions are thought to represent focal or punctate contusions.^104,¹⁰⁵ Functional MRI often shows abnormal activation patterns, particularly if the patient has lost consciousness or is symptomatic at the time of the study.¹⁰⁵

Several factors determine the appropriate level of medical evaluation and treatment after mild or moderate TBI. Any loss of consciousness at the time of impact or retrograde or antegrade amnesia of at least several minutes warrants a thorough medical assessment, as do persistent headache, confusion, dizziness, diplopia, blurry vision, weakness, or numbness. A formal examination in the emergency department is generally advisable. Patients who are neurologically normal and asymptomatic after at least one hour of observation and serial evaluations can usually be safely discharged, with clear instructions to return immediately if symptoms or signs of TBI develop. Ideally, these instructions are given to both the patient and a responsible companion.

A patient with persistent symptoms or neurologic deficits should have a CT scan of the head and be admitted to the hospital for observation. This is particularly important for those with GCS scores of 13 or less, because the risk of an intracranial hematoma or contusion large enough to require emergent craniotomy increases as the GCS score decreases among patients whose initial GCS scores are 9 to 13. As many as 40% have CT abnormalities, and 8% require neurosurgical intervention.¹⁰⁶

Athletes—especially those involved in contact sports such as boxing, football, soccer, wrestling, and field hockey—are at high risk for mild and moderate TBI. One report found that 47% of high school football players sustained a concussion, with 35% sustaining multiple concussions.¹⁰⁷ Multiple concussions are much more likely to cause prolonged or permanent neurologic disability than a single concussion, particularly if they occur over a short time span. Second impact syndrome is a rare but potentially lethal problem first noted in athletes in 1973 and later implicated as the cause of sudden death in several high school football players.¹⁰⁸

Because sports-related concussions are associated with such disabling and potentially life-threatening consequences, coaches and athletic trainers must carefully consider whether an athlete should be advised to return to play or retire from athletic competition after a concussion. Several groups have devised concussion grading scales to evaluate concussion severity and developed guidelines to determine when an athlete can safely resume play. The most widely adopted scales are those developed by Kelly and colleagues at the University of Colorado,¹⁰⁹ Cantu,¹¹⁰ and the American Academy of Neurology¹¹¹ (Tables 38-3 and 38-4). Most authorities recommend that athletes abstain from play for at least one season if, during that season, they sustain three or more grade I or II concussions or two grade III concussions.¹¹² In addition, many athletic organizations at the high school, college, and professional levels have adopted neuropsychological testing as a means of objectively evaluating the cognitive and neuropsychological consequences of each concussion.¹¹³ Comparison of postinjury and preseason scores is a powerful tool for guiding return-to-play decisions.

TABLE 38-3 Grading Scales for Concussion

TABLE 38-4 Recommendations for Return to Play

A common sequela of mild or moderate TBI is postconcussion syndrome, a constellation of symptoms that can be disabling for weeks or even months. The most common symptoms are headache, irritability, dizziness, tinnitus, lethargy, and sleep disturbance. One or more of these symptoms develop in approximately 30% of patients 1 week after a mild or moderate TBI, but they usually subside within 3 months.¹¹⁴ After 1 year, only 7% of patients report residual symptoms, most commonly persistent headache. Postconcussion syndrome is best treated by a primary care physician or neuropsychologist who thoroughly understands the disorder. Cognitive testing is recommended for patients whose symptoms last more than a few weeks, because symptoms such as frustration and irritability are often linked to an inability to resume normal daily activities. Neuropsychological testing often indicates deficits in attention and concentration rather than memory. If such testing identifies specific deficits, cognitive rehabilitation is recommended.¹¹⁵ Persistent headaches, dizziness, and tinnitus should be treated symptomatically after a CT scan of the head establishes the absence of intracranial lesions. Posttraumatic disturbances of the ossicles of the inner ear semicircular canals can cause severe positional vertigo which can be immediately improved with canalith repositioning. In other cases, dizziness is more complex and may result from problems with the vestibular-ocular reflex, so patients with vertigo or tinnitus may benefit from evaluation by an otolaryngologist. Factors associated with an adverse long-term outcome after a concussion include old age, prolonged posttraumatic amnesia, and a below-normal premorbid intellectual capacity.¹¹⁴

Prognosis

Predicting outcome soon after a TBI can help guide acute and chronic care and help prepare family members for the typically protracted recovery process. Equally important is that further treatment may be deemed futile, and expensive critical care or surgery can be reserved for those who are likely to benefit. Of course, early prognostication must be reliable, especially when withdrawal of life support is a consideration.

Several clinical and radiographic characteristics have proved useful for outcome prediction, but they must be used in concert.¹¹⁶ Moreover, these criteria are more reliable for predicting death or vegetative survival than for accurately predicting mild or no dysfunction and a complete return to normalcy. The most powerful outcome predictors are age, initial GCS score (particularly the motor component), pupil size and reaction to light, ICP, and the nature and extent of intracranial injuries.

Old age correlates most consistently with a poor outcome after TBI. In the Traumatic Coma Data Bank study of more than 700 patients with severe TBI, the incidence of death, persistent vegetative state, or severe disability was 92% for those older than 60 years, 86% for those older than 56 years, and 50% for younger patients.¹¹⁷ The older groups had a higher incidence of traumatic intracranial mass lesions, midline shift, and subarachnoid hemorrhage, and the presence of these insults correlated strongly with poor outcome. Subsequent studies confirmed the low probability of a good recovery for patients older than 60 years whose initial GCS scores are 8 or less.¹¹⁸

The second most important predictor of outcome is the initial postresuscitation GCS score. Among patients with severe closed head injuries in the Traumatic Coma Data Bank study, good outcomes occurred in 4.1% of those with an initial GCS score of 3, in 6.3% whose score was 4, and in 12.2% whose score was 5. Again, later clinical studies corroborated the strong direct correlation between initial GCS score and outcome.¹¹⁹

Unilaterally or bilaterally dilated pupils that are unreactive to light usually reflect uncal herniation and significant brainstem compression and damage, so this sign is ominous. Several large clinical studies found that patients with bilaterally fixed and dilated pupils had a greater than 90% likelihood of death or vegetative survival.^120,¹²¹ Also, intracranial hypertension refractory to medication is associated with a 43% mortality rate and 0% chance of a functional outcome.¹²²

Various studies have analyzed the effect of the type and size of posttraumatic intracranial lesions on outcome in terms of both the specific lesions and the CT-defined characteristics of their mass effect. Subdural hematomas are associated with the worst prognosis. One study found that only 26% of patients with these clots had a functional recovery.¹²³ However, the prognosis for patients with subdural hematomas is also related to how soon after injury the clot is evacuated, with the best outcomes in those who have surgery within 2 hours.⁷

Epidural hematomas pose a much lower risk of mortality because, unlike subdural hematomas, they usually are not associated with underlying cerebral contusions or swelling. If left untreated, however, epidural hematomas can cause uncal herniation and death. One report noted an increase in mortality from 17% to 65% if an epidural hematoma was not evacuated within 2 hours after the onset of coma.⁸

The presence of traumatic subarachnoid hemorrhage is associated with a 50% greater risk of death.¹⁰ The link between traumatic subarachnoid hemorrhage and worse outcomes is controversial, however. Many believe that this condition merely indicates a more severe TBI and has no direct association with outcome.

Marshall and colleagues devised a CT-based classification scheme that proved prognostically useful when applied to the patients in the Traumatic Coma Data Bank study (Tables 38-5 and 38-6).¹²⁴ The classification emphasizes the mass effect of posttraumatic intracranial lesions. Not surprisingly, these investigators found the worst outcomes among patients with large intracranial mass lesions and uncal herniation.

TABLE 38-5 Computed Tomographic Classification of Traumatic Brain Injury

Category	Definition
Diffuse injury I	No visible intracranial pathology
Diffuse injury II	Cisterns present, with midline shift 0 to 5 mm; no high-density lesion >25 mL
Diffuse injury III (swelling)	Cisterns compressed or absent, with midline shift 0 to 5 mm; no high-density lesion >25 mL
Diffuse injury IV (shift)	Midline shift >5 mm; no high-density lesion >25 mL
Evacuated mass lesion	Any lesion surgically evacuated
Nonevacuated mass lesion	High-density lesion >25 mL; not surgically evacuated

Data from Marshall LF, Marshall SB, Klauber MR, Clark M. A new classification of head injury based on computerized tomography. J Neurosurg. 1991;75(Suppl):S14-S20.

TABLE 38-6 Relationship of Computed Tomographic Classification to Outcome at Discharge

Based on these studies, one can say with certainty that an 80-year-old patient who presents with bilaterally fixed and dilated pupils, a GCS score of 3 or 4, and a large subdural hematoma will not have a functional outcome regardless of treatment. However, the prognosis is much better for young patients with higher GCS scores, and aggressive surgical and medical management is usually warranted.

The patient’s salvageability and prognosis after a penetrating injury are far clearer than for those with closed head injuries. Most victims of gunshot wounds to the head die before or shortly after hospital admission. Among 314 patients with civilian craniocerebral gunshot wounds, 92% died; 73% of them were pronounced dead at the scene of the injury, and 12% died within 3 hours of injury.¹²⁵ In the Traumatic Coma Data Bank study, the mortality rate was 88% for the 151 patients with gunshot wounds to the head.¹²⁶ No patient with an initial GCS score of 8 or less regained normal neurologic function, and only three recovered to the level of moderate disability, suggesting that the initial GCS score is an even more powerful predictor of outcome for these patients than for those with closed TBI. A meta-analysis of recent clinical studies examining civilian gunshot wounds to the head found that favorable outcomes (Glasgow Outcome Scale scores of 4 or 5) occurred in only 5 of 490 patients with initial GCS scores of 3 to 5.¹²⁷ Mortality rates ranged from 51% to 87% for patients with scores of 8 or less. In contrast, those whose initial GCS scores were 13 to 15 all survived and had favorable outcomes. Other clinical signs associated with death or a poor outcome are fixed and dilated pupils, intracranial hypertension, and hypotension. Also, a gunshot wound is more likely to be lethal if self-inflicted.

The CT-defined extent of intracranial injury caused by the missile also has prognostic significance. Hyperdense lesions with a volume greater than 15 mL, midline shift of more than 3 mm, compressed or absent basal cisterns, subarachnoid hemorrhage, and intraventricular hemorrhage are all associated with mortality rates of 80% to 90%, as is a bullet trajectory that traverses both hemispheres, the basal ganglia, or the posterior fossa.^126,¹²⁸