Epidemiology

The devastating consequences of head injury have been recorded since ancient times. Early neurosurgical records were primarily observational, with very few suggestions for treatment (Fig. 41-1). Despite centuries of investigation and the development of new and better intensive care, we still have not discovered effective therapies that can be applied after the injury to reverse most pathologic aspects of traumatic brain injury (TBI).

In 1996, Congress approved the Traumatic Brain Injury Act (Public Law 104-166), which charged the Centers for Disease Control and Prevention (CDC) with “determining the incidence and prevalence of traumatic brain injury in all age groups in the general population of the United States.”¹

Each year, an estimated 1.7 million people sustain head injury in the United States.¹

Of these, 1.36 million (1.4% of all emergency department [ED] visits) undergo emergency evaluation, including approximately 470,000 children younger than age 14 years. TBI accounts for 15.1% of all injury-related hospitalizations in the United States. Overall, 80% sustain minor head trauma (Glasgow Coma Scale [GCS] score of 14 or 15), 10% have moderate head injuries (GCS score of 9-13), and 10% have severe head injuries (GCS score of 8). Almost 20% of all head-injured patients are hospitalized, and approximately 52,000 patients die each year from TBI (Table 41-1).

The leading causes of head injury in the civilian population are falls (43.7%) and motor vehicle collisions (MVCs) (21.5%).¹ TBI caused by blasts has been called the signature injury of the wars in Iraq and Afghanistan: TBI of any severity is estimated to affect as many as 10 to 20% of wartime service members.^2–4 Head injury is the leading cause of traumatic death in patients younger than 25 years and accounts for nearly one third of all trauma deaths.¹ Head injury from child abuse is common.⁵ New data suggest that with children younger than 12 months of age, TBIs and/or fractures attributable to abuse occurred in 1 of 2000 infants.⁶ The CDC estimates that there are at least 5.3 million Americans currently experiencing some degree of disability as a result of TBI. As veterans return to the United States, the number of patients experiencing the consequences of TBI has increased markedly.

These facts confirm that TBI is a major public health problem. The emergency physician sees patients with head injuries of different clinical severity caused by a variety of mechanisms. External physical signs of head trauma only confirm that injury has occurred; they are not always present in the patient who has sustained serious underlying TBI. The ultimate survival and neurologic outcome of the head trauma patient depend on the extent of TBI occurring at the time of injury, alone or in combination with secondary systemic insults, such as hypotension and hypoxia, that worsen the resulting neurochemical and neuroanatomic pathophysiology. Research aimed at reducing or preventing the neurologic consequences of head trauma is ongoing, but currently the clinical outcome after TBI depends on the circumstances of injury and early clinical management aimed at reducing the occurrence of secondary brain insults. No effective intervention has been found to reverse the pathologic events initiated by the traumatic event.

Anatomy and Physiology

Brain Cellular Damage and Death

Pathophysiology

History

Details regarding the mechanism of injury should be solicited from witnesses or the victim to determine whether the head-injured patient is at high risk for intracranial injury. The patient’s condition before trauma may give clues to important, otherwise unsuspected, comorbid factors such as preexisting coagulopathy (e.g., hemophilia). Past medical history, medications (particularly anticoagulants), recent drug or alcohol use, and complaints immediately before the traumatic event should be determined.

The patient’s current level of consciousness, as well as that immediately before and after the injury and at the arrival of first responders, should be determined. Witnessed PTSs or apnea should be reported. If the patient is now awake but was unconscious at some point, it should be determined if the patient has returned to baseline mental status.

Acute Neurologic Examination

Other Examination Findings

The head and neck should be carefully examined for external signs of trauma that may have also produced underlying TBI. A scalp laceration, contusion, abrasion, or avulsion may overlie a depressed skull fracture. Basilar skull fractures are usually diagnosed by the clinical examination (Box 41-1). Although not always related to severe brain injury, their presence implies that a significant impact force was sustained during head trauma. Carotid artery dissections caused by a hyperflexion-extension neck injury can occasionally be detected by auscultation of a carotid bruit.²⁴ In these patients, a careful neurologic examination should assess for subtle asymmetry between the carotid arteries. The percentage of concurrent cervical spine injury in patients with severe head trauma may be as high as 10.2%.²⁷ Often, other spinal regions are also injured.

Severe Traumatic Brain Injury

The neurosurgical literature defines severe head injury as TBI manifested by a postresuscitation GCS score of 8 or lower within 48 hours. In the emergency setting, however, this definition is not practical because the outcome for the patient beyond the initial resuscitation is not known. Most emergency medicine research defines severe head injury by a GCS score of 8 or lower at the acute presentation after injury. The presence of any intracranial contusion, hematoma, or laceration is also considered severe injury (see Fig. 41-5).

Approximately 10% of all head-injured patients who reach the ED alive have severe head trauma.1,30 The clinical prognostic indicators in the acute setting are initial motor activity, pupillary responsiveness, the patient’s age and premorbid condition, and the occurrence of secondary systemic insult during the acute period.^23,28,31 Up to 25% of these patients have lesions requiring neurosurgical evacuation.¹⁸ The prognosis cannot be reliably predicted by the initial GCS score or initial CT scan.

The overall mortality in severe head trauma has improved over the years and now remains stable at approximately 35%.32,33 Mortality for children is lower. For nonsurvivors of head injury who reach the hospital alive, the average time to death is 2 days after trauma. Adult survivors of severe head trauma are usually severely disabled; currently, only 7% have moderate disability or a good outcome. Children older than 2 years who survive a severe closed head injury have a better outcome than adults.

Moderate Head Trauma

Approximately 10% of all patients with head injury have sustained moderate TBI, defined as a postresuscitation GCS score of 9 to 13. Moderate TBI is often caused by MVCs. Most patients with moderate TBI do not die at the scene from their initial head injury and are brought to the ED for stabilization and evaluation.

Moderate TBI produces a number of physiologic abnormalities, including neuronal cell membrane dysfunction and a mild, brief acidosis with no concurrent depletion of adenosine triphosphate. These changes are probably reversible and therefore may be amenable to acute intervention to correct or prevent progression. The neuropathology of moderate brain injury probably represents the front end of the spectrum of pathophysiology seen with severe head trauma. Because of this, patients are vigilantly monitored to avoid hypoxia and hypotension and other secondary systemic insults that could worsen neurologic outcome.

Minor Head Trauma

Minor or minor head trauma (MHT) is an injury to the brain resulting in a temporary and brief interruption of neurologic function after head trauma, which may involve a loss of consciousness (LOC).56,101 The neuropathology involved in producing signs and symptoms of minor TBI may remain at the neurobiochemical level without damage to the microstructure. Heightened ionic flux, surges in levels of glutamate transmitters, disruption of enzymatic pathways, and accumulation of lactate and nitric oxide have been reported in brain tissue after experimental minor TBI.¹⁷ Axonal stretching or twisting may occur with some mechanisms producing minor TBI. This injury pattern may promote glutamine-induced neurotoxic cascades that lead to the axonal damage typically described as DAI.¹⁰² Experimental models of blast injury also produce these same changes.¹⁰³

Most authorities, clinical policies, and decision rules now classify minor TBI as that producing a GCS score of 14 or 15.17,101,102,104–106 In fact, the GCS is not sensitive enough to be of prognostic usefulness in minor TBI; a perfect score of 15 in the ED does not take into account the level of alertness or neurologic status immediately after trauma or the presence or absence of focal neurologic injury.^31,102,107

From a practical standpoint, minor TBI is a clinical diagnosis. The diagnosis requires a credible mechanism of injury. In civilian life, most mechanisms that do not involve direct craniofacial impact cannot produce minor TBI. For example, belted drivers in low-velocity rear end–impact MVCs are not subjected to high enough acceleration-deceleration or rotary forces to the head to reach the force threshold needed to produce cerebral injury unless there is also direct impact to the head against a stationary object.102,108 It is therefore unlikely that a patient with a whiplash or “jolt” injury would also have minor TBI. Collision sports–related minor TBI can be caused by acceleration-deceleration. Although the extent of this mechanism is not yet known, forces generated in blast injuries in wounded service personnel are the most common cause of minor TBI without direct head impact. Mild TBIs from blast injuries have been called the signature injury of the wars in Iraq and Afghanistan.¹⁰³

Epidemiology

Approximately 650,000 to 1 million children are emergently evaluated yearly in the United States for head trauma, with 80 to 90% classified as mild.127,128 However, TBI accounts for the largest source of childhood mortality and morbidity after trauma. The etiology of TBI is age related; in infants and the very young, abusive injury is a major cause of TBI. In toddlers, abusive injury must be considered, but injury from falls appears more common. Once children enter school, injuries from physical activities (such as bicycle riding) and MVCs (especially pedestrians stuck by cars) are the most common causes of TBI.^129–131

Pathophysiology

Until the cranial sutures close, children’s skulls are more distensible than those of adults. As a result, young children often sustain less TBI after head trauma than adults with comparable nonfatal mechanisms of injury.¹³² However, children appear to have an age-dependent brain vulnerability. Very young children (younger than 1 year) have higher mortality after head trauma than older children with injuries with the same severity of injury. Many factors contribute to this. Medical attention is often delayed in children with nonaccidental injuries. Because of limited language and comprehension, an accurate formal neurologic examination in young children is sometimes difficult. Medical personnel tend to underestimate the extent of the injuries in small children and are often reluctant to initiate invasive procedures that may be necessary to aid in the diagnostic workup, such as intravenous access for sedation in CT scanning.

The types of TBI sustained after head trauma in children differ from those in adults. Children have fewer traumatic mass lesions (with the exception of SDHs in the very young), fewer hemorrhagic contusions, more diffuse brain swelling, and more diffuse axonal injury. Of head-injured patients younger than 20 years who talk and deteriorate, 39% have brain swelling only (i.e., no mass lesions), whereas 87% of patients older than 40 who talk and deteriorate have mass lesions.⁸⁹

Clinical Features

As with adults, an accurate description of the mechanism of injury, the appearance of the child immediately before and after the injury, and subsequent events can provide useful information to assist in the evaluation and management of the acutely head-injured child.

The initial physical presentation of a child with TBI may have minimal predictive value in terms of the severity of trauma sustained.¹³³ Therefore repeated examinations to detect changes in the neurologic status are paramount.

In principle, the acute neurologic assessment of head-injured children is the same as that of adults. Because of its reliance on developed language skills and the patient’s attention and cooperation, the GCS is difficult to apply to very young children. A modified scale (see Table 38-4) has been developed¹³⁴ and has been shown to accurately predict the need for neurosurgical intervention in head-injured preverbal children.¹³⁵

Children with severe or moderate head injury are clinically similar to adults with these degrees of injury, although children have an increased incidence of early (i.e., within the first week after trauma) PTSs after severe head injury.²³ Low GCS score and young age are associated with an increased early PTS risk. Even after adjustment for GCS score, children younger than 2 years have up to a threefold increased risk compared with older (i.e., older than 12 years) children.⁶⁶ Overall, up to 6% of all head-injured children and 20% of severely head-injured children have early PTS. Most PTSs occur within the first 24 hours and do not predict seizures later in the post-traumatic period. However, early PTS can exacerbate secondary brain injury by creating hypoxia and increasing cerebral metabolism and ICP. Although prophylactic use of anticonvulsants is not recommended to prevent late PTSs, acute anticonvulsant prophylaxis is a treatment option in severely head-injured infants and young children to prevent early PTSs.⁶⁶

The clinical presentation of post-traumatic intracranial lesions in infants who have sustained moderate or severe TBI can be extremely subtle, especially in those younger than age 6 months. Often these lesions are associated with scalp injuries and skull fractures but no other symptoms. Toddlers are also difficult to assess; the only symptom of an intracranial injury may be irritability.138,139 Recommendations are also offered regarding the ED workup in these very young children.

Inflicted head injury, also described as abusive head injury or nonaccidental head injury, is the most common cause of head injury deaths in infants. Child abuse is considered in all children with unexplained head injuries or injuries not consistent with the history provided. The shaken baby syndrome is most often seen in children younger than 1 year and is inflicted by violently shaking an infant while holding him or her by the torso or extremities. The uncontrolled head movement causes an acceleration-deceleration brain injury, with a rotary component, as the moving brain strikes against the interior of the skull. The resultant shearing injury causes widespread damage. Patients have a broad range of symptoms, from nonspecific complaints such as vomiting or sleepiness, to seizures and coma. Classically described findings include SDHs, and subarachnoid hemorrhage (SAH) without signs of external trauma. Diffuse retinal hemorrhages are seen in 50 to 100% of all patients with shaken baby syndrome; the extent of hemorrhage appears related to injury severity and may predict the prognosis.¹³⁰

Children who sustain minor head trauma often have more pronounced physical signs and symptoms than adults. Despite apparently trivial trauma, children may appear pale, be lethargic, and have frequent emesis and complaints of headaches and dizziness.

Children with concussions tend to be symptomatic longer after mild TBI than adults. As in adults, postconcussive symptoms in children include neurocognitive changes. The severity and duration of postconcussive symptoms is related to the severity of initial injury, as well as personal and environmental factors. Children who have sustained LOC, post-traumatic amnesia, a GCS score less than 15 at presentation, or mental status changes are more likely to have prolonged postconcussive symptoms.140,141 Thus children should not return to sports or play activities until completely symptom free, and then only at the discretion of their primary physician.¹²⁰ Concussive injuries in children also produce two unique clinical circumstances. Many children experience a brief impact seizure at the time of relatively minor head injury. By the time the child is evaluated, he or she is at baseline neurologic function. Impact seizures do not appear to predict subsequent early PTSs. However, a post-traumatic impact seizure may confuse the initial assessment of the severity of the head injury and prompt a more aggressive workup than needed. Postconcussive blindness, another serious complication of concussive injuries in children, is usually associated with impact to the back of the head. Children experience a temporary loss of vision that can persist from minutes to hours before normal vision returns.

Diagnosis and Management

As with adults, pediatric head-injured patients should be assessed for other major trauma and assumed to have cervical spine injury until proved otherwise. Goals of ED management are also generally the same: to prevent secondary injury and systemic insults, to prevent increasing ICP, and to detect traumatic mass lesions requiring emergency surgery.

Children with severe TBI who are transported directly to a pediatric trauma center or an adult trauma center with pediatric capabilities have better outcomes than those transported to nontrauma hospitals.⁶⁶ Hypoxia and hypoventilation are common in pediatric head-injured patients, and they develop more rapidly in children than in adults. In children with a GCS score below 8, airway management should be aggressive to prevent hypoxia, aspiration, and hypercarbia and to allow mild hyperventilation if the patient has signs of herniation. There is no evidence to support the advantage of out-of-hospital intubation over bag-valve-mask ventilation of pediatric patients with TBI^66,142; scene time should not be prolonged with multiple attempts at endotracheal intubation.

Hypotension is a late finding in children in shock; poor perfusion should be clinically identified and corrected as soon as possible to ensure adequate CPP. There is no evidence to suggest that aggressive fluid resuscitation exacerbates cerebral edema in head-injured children. In children, unlike in adults, hypovolemic hypotension can occur because of head trauma. Hypotension from intracranial bleeding can occur in children younger than 1 year with a large linear skull fracture and an underlying large EDH.¹³² The intracranial blood can seep through the fracture and produce a large galeal or subperiosteal hematoma. Hypotension from intracranial bleeding can also occur in a child with hydrocephalus and a functioning shunt. Blood may accumulate without much evidence of increased ICP. Scalp lacerations can also produce significant hemorrhage and subsequent hypotension.

Up to 80% of children with severe head trauma have elevated ICP.¹³² In infants, a bulging fontanel suggests elevated ICP. Other signs of elevated ICP include bradycardia, papilledema, declining level of consciousness, and seizures. When increased ICP is indicated by physical examination, methods to reduce ICP should be initiated. As with adults, acute hyperventilation has immediate effects but is never indicated for prophylaxis or for prolonged management of increased ICP.⁶⁶ Hyperosmolar therapy is effective at reducing ICP. There have been no studies describing the superiority of one osmotic agent over another in the treatment of TBI, and no direct comparisons have been done. Although efficacy studies were based only on adults, mannitol at doses of 0.25 to 1.0 g/kg has become a mainstay in the treatment of elevated ICP in children with severe TBI. Bolus therapy has a theoretic benefit compared with continuous treatment; over prolonged periods, mannitol may accumulate in injured areas of the brain where the BBB is no longer intact, thus creating a reverse osmotic shift.^143,144 Several studies support the effectiveness of HTS in lieu of mannitol for elevated ICP in pediatric head-injured patients. Treatment is with a continuous infusion of 3% normal saline at 0.1 to 1.0 mL/kg body weight per hour, titrated to effect.⁶⁶

Severely head-injured children are less likely to have a surgically amenable lesion than adults. Because diffuse brain swelling is the most common finding in severely head-injured children, emergency burr holes are generally ineffective.

When minor head injury is considered in children, age is an important consideration in interpreting clinical and historical findings. Children younger than age 2 years are often difficult to assess and may have subtle clinical findings. In general, the literature supports the conclusion that younger patients are at higher risk for intracranial injury. One clinical sign of potential brain injury in children younger than age 2 years is the presence of a scalp hematoma, especially a large parietal scalp hematoma.143–145 In an observational cohort study involving children with low risk for brain injuries, scalp hematomas were present in 93% of children 2 years old or younger who had brain injuries.¹⁴⁴

More than 50% of children with head injury of all severities in the United States undergo emergent cranial CT scanning.127,146 Cranial CT is the diagnostic imaging modality of choice in the evaluation of moderate or severe pediatric TBI and should also be strongly considered in pediatric patients with high-risk minor TBI. However, potential risks are associated with childhood exposure to radiation. Children are more sensitive to radiation than adults because of rapidly dividing cells during normal growth. The younger the child, the more potential risk. Increased rates of solid tumor cancers¹⁴⁶ and decreased cognitive performance have been associated with radiation doses similar to that of a single head CT scan.¹⁴⁷ An additional safety concern is the frequent need to sedate young children in order to perform an adequate imaging study. In these circumstances, the risks of radiation exposure and sedation should be weighed against the likelihood of an intracranial lesion in the child with minor head trauma.

It is estimated that up to 98% of cranial CT scans done to assess head injury in children are negative.145,148 Several clinical prediction rules have been developed to assist in decision-making for emergent neuroimaging of children with minor TBI. Comparison of these various rules is difficult because of variable methods and inclusion criteria. Most have not been validated in a separate population.^148,149 Unless both sensitivity and specificity are high, such rules may actually result in an increased number of CT scans being performed. Kupperman and colleagues,¹⁴⁵ with a research network including 25 EDs and 4200 patients, have derived and validated a clinical prediction rule for minor head trauma that includes subsets of children younger than 2 years and from 2 to 18 years old. The rule performs well with a very low risk of missed clinically important TBI in both age subgroups. An algorithm suggested by this study is presented in Figure 41-7. The CATCH study derived a decision rule that identified two levels of risk for children with minor head injury.¹⁵⁰ The large cohort of 3800 patients was identified from 10 Canadian pediatric teaching institutions. Children with a GCS score below 15 at 2 hours after trauma, a suspected open or depressed skull fracture, a worsening headache, or persistent irritability were found to be at increased risk for the need for a neurosurgical intervention and considered high risk; moderate risk (brain injury on CT with no need for neurosurgical intervention) was associated with any sign of basal skull fracture, a large boggy scalp hematoma, or a dangerous mechanism of injury (e.g., MVC or fall greater than 3 feet).

The use of skull radiographs in the diagnostic workup of head-injured children is controversial but may be appropriate in some circumstances. As with adults, when a CT scan is indicated, skull radiographs are not necessary. Up to 11% of children younger than age 2 years will sustain a skull fracture associated with head trauma, and 15 to 30% of these will have TBI. Therefore in children younger than age 2 years, a skull fracture is a predictor of TBI.¹⁵¹ The presence of a skull fracture in children significantly increases the likelihood of intracranial pathology; conversely, a negative radiographic skull screen does not guarantee the absence of TBI. Parietal skull fractures are the most common. Often, fractures occur in infants who sustain relatively minor head injury. Skull films may be useful as a screening tool in determining the need for a CT scan, especially in children 2 years old or younger whose neurologic examination is difficult to obtain and interpret. In alert children younger than age 2 years with minor head injury, a low-risk history, normal findings on physical examination that includes a neurologic and mental status examination appropriate for age, and a scalp hematoma, skull radiographs may be a useful screen.¹³⁹ If the skull radiograph is negative for a fracture, a CT scan may be unnecessary. If the skull radiograph shows a fracture, CT imaging is indicated.

In older children, skull radiographs are rarely useful unless a specific lesion is suspected, such as a depressed skull fracture or a penetrating foreign object. Skull fractures are more clinically significant in children than in adults. Fractures, especially complex stellate or multiple injuries, are often seen in abused children, and skull films should be obtained if abuse is suspected. Ping-Pong fractures occur with concentrated forces that indent the skull. These fractures are unique to infants and appear as multiple indentations in the skull with no significant bone discontinuity. Skull fractures are common in children who have sustained deep scalp lacerations or who have a large scalp hematoma.

Post-traumatic leptomeningeal cysts or growing skull fractures are delayed complications of linear skull fractures in infancy. If a tear in the dura accompanies the linear fracture, the meninges may fill with CSF and prolapse through the fracture margins, thus preventing fracture healing.23,139 These cysts can grow in size and have the potential to cause a mass effect. If a linear fracture is found by skull radiography, close follow-up is indicated to assess for this rare delayed complication.

Overall, children who sustain severe head injury have lower mortality and a better neurologic outcome than comparably injured adults. This is probably because of the neuroplasticity of the young brain; however, in children younger than age 2 years, the prognosis after severe head injury is poor.¹⁵² Very young children have immature cerebrovascular autoregulation, which increases the risk of cerebral edema formation. The immature brain has increased susceptibility to permanent injury because of incomplete myelination.

The emergency evaluation of children with minor head injury is especially challenging, given their potentially dramatic presentation and the added difficulty of obtaining an accurate neurologic assessment. Evidence-based consensus guidelines have been proposed for the evaluation and management of minor head injury in children.23,127,138,139 Parents should be educated about the warning signs and symptoms of delayed complications of minor head trauma.

Epidemiology

Penetrating brain injury (PBI) occurs at a rate of 12 per 100,000 population and can be caused by missile injuries or impalement.¹⁵³ The United States has the highest penetrating head injury rate among developed countries in the world, with the most common cause being gunshot wounds (GSWs). These dramatic injuries are increasing in frequency, and the neuroscientific understanding of the complicated cerebral events that occur with penetrating head injury does not yet equal our understanding of the pathophysiology of blunt injuries.

Civilian GSWs to the head account for approximately 31,000 deaths per year, and up to 70% of all patients who sustain a GSW to the head are dead at the scene.154,155 Overall, the mortality caused by a GSW to the head is estimated to be 90%.¹⁵⁶ If the patient is hemodynamically stable, has not sustained secondary systemic insults such as hypoxia or hypotension, has no expanding mass lesions from the missile injury, and has not ingested intoxicants that may interfere with assessment, prognosis after a GSW to the head can be predicted by the GCS score and pupillary responsiveness at presentation.¹⁵⁷ If the GCS score at presentation is less than 5, mortality approaches 100%. If the GCS score at presentation is greater than 8 and the pupils are reactive, survival approaches 75%. Survivors of GSWs to the head tend to do well, with up to 60% returning to their former employment.¹⁵⁷

Pathophysiology

Missile injuries to the head can result in several different patterns of damage. Tangential wounds are caused by an impact that occurs at an oblique angle to the skull. If the missile has high velocity but low energy, it can travel around the skull under the scalp without passing through the skull. Intracranial damage, primarily cortical contusions, can occur at the initial site of impact because of pressure waves generated by the impact. In one study, 24% of patients with tangential GSWs also had intracranial hemorrhage, and 16% sustained skull fractures.158,159 Many patients with tangential GSWs have a GCS score of 15 on presentation.

Perforating wounds are usually caused by high-velocity projectiles, which cause through-and-through injuries of the brain with an entrance and an exit wound. This type of injury is largely discussed within the context of military GSWs to the head.

Penetrating missile wounds are produced with moderate- to high-velocity projectiles discharged at close range. The majority of the civilian PBI literature deals with penetrating missile wounds.¹⁵⁶ The penetrating object may travel through the entire skull, bounce off the opposite inner table of the skull and ricochet within the brain, or stop somewhere within the cranial cavity. Bullets that penetrate the skull do not travel in a straight path. The wounding capacity of a firearm is related to the kinetic energy of its missile on impact and how much energy is dissipated in the tissues. Low-velocity missiles tend to be deflected by intracranial structures. The final track is therefore erratic and occasionally bears no relation to the exit or entrance site of the missile.^160,161 High-velocity missiles can project straight through the tissues and easily fracture bones. Flight stability and the angle at which the bullet strikes its target affect the path through the brain. Within tissue, destabilizing motions include deviation of the longitudinal axis of the bullet from a straight line (yaw), forward rotation of the bullet around its center of mass (tumbling), and oscillatory motion of the bullet axis around its center of mass (rotation). As the bullet passes through the brain, a tissue cavity is created. This cavity can be as much as 10 times the diameter of the missile. A percussion shock wave is also created, lasting 2 msec but causing little tissue destruction.^156,160,161

The morbidity and mortality from missile injuries to the head depend on the intracranial path, speed of entry, and the size and type of the penetrating object. Projectiles that cross the midline or the geographic center of the brain, pass through the ventricles, or come to rest in the posterior fossa are associated with extremely high mortality.157,160,161 High-velocity wounds are associated with greater mortality than low-velocity injuries. Large missiles or missiles that fragment within the cranial vault are usually fatal. The design of the bullet and its fragmentation potential (capacity to deform or fragment) also contribute to final tissue destruction and patients’ morbidity and mortality.

Many GSWs to the head are intentionally self-inflicted injuries. The percentage of penetrating head injuries caused by self-inflicted GSWs ranges from 13 to 88%.¹⁵⁷ Characteristics of self-inflicted GSWs include injury on the dominant side, powder burns at the entrance site, and large stellate scalp lacerations caused by dissection of the subgaleal layer by exploding gases released close to the scalp. In suicide attempts, GSWs to the head tend to traverse the midline in the coronal plane and often involve major vascular structures. If the self-inflicted GSW has an entrance through the mouth, injury to the hard palate may occur with potential upper airway compromise. The careful aim and close range of self-inflicted GSWs to the head make these injuries particularly devastating; mortality is higher than with non–self-inflicted penetrating injuries, and odds ratios of death vary from 1.63 to 5.83.¹⁵⁷

Clinical Features

Physical assessment of the patient with a missile wound to the head focuses on the presenting GCS score and pupillary responsiveness. The entire scalp is carefully inspected for occult GSWs. In addition to the physical damage to brain tissue caused by the penetrating injury, other devastating physiologic changes occur immediately after injury. ICP increases, the BBB breaks down, CBF is altered, and cerebral edema develops. Cerebral autoregulation is lost, and CPP may fall.

Management

The ED management is directed at reducing the occurrence of the secondary systemic insults of hypoxia and ischemia, with emergent intervention if signs of herniation syndrome develop and the patient is viable. Management should be aggressive until the prognosis can be established by examination and neuroimaging data. When penetration of the cranial vault is established, the patient should be intubated. If the physician waits for coma before intubating the patient, mortality approaches 100%.

Emergency treatment should include intravenous antibiotics because penetrating missiles are contaminated with skin, bone, and hair. Tissue contamination may be widespread because of the cavitation caused by the missile as it passes through the brain.¹⁶² Approximately 90% of all CNS infections associated with penetrating TBI injuries occur within 6 weeks. Most neurosurgeons do not automatically débride bone and missile fragments owing to a growing body of literature that shows no evidence that removal of these foreign bodies decreases infection rate.^18,156

Between 30 and 50% of patients with PBI develop seizures; 10% of these occur in the first week.18,156 Anticonvulsants should be given in the acute setting to prevent early PTSs in the patient with PBI, especially if the patient is to be transported to another institution after acute stabilization. Anticonvulsants should not be given beyond the first week after PBI because this has not been shown to prevent the development of late seizures.

Skull radiographs may be useful in determining the number of penetrating fragments and their track. A CT scan defines the precise location of the missile, its intracranial path, the presence of bone or missile fragments, extra-axial or intracerebral blood collections or other traumatic lesions, and pneumocephalus. CT scanning is the radiologic test of choice for PBI.¹⁶³ Pneumocephalus is often associated with missile wounds that penetrate the sinuses but can be caused by free air sucked into the penetration cavity behind the projectile.

All tangential GSWs should be evaluated with a head CT scan secondary to the high incidence of associated intracranial injury.¹⁵⁹ When a penetrating head injury is caused by impalement, the penetrating object should be left in place to be removed at surgery. A skull radiograph shows the size of the object, the angle of impalement, and the depth of penetration. Angiography may be indicated to better discern location referable to key vascular structures.

Neurologic Complications

Medical Complications

Scalp Wounds

Scalp lacerations are extremely common after head injury and may be a source of significant bleeding because hemostasis may be difficult to achieve. Methods to achieve hemostasis include direct digital compression of the bleeding vessel against the skull, infiltration of the wound edges with lidocaine with epinephrine, and ligation of identified bleeding vessels. If the galea is lacerated, it can be pulled up with a clamp and its edges folded over the lacerated skin edges to tamponade the bleeding vessels. Raney scalp clips applied to the edges of the wound are also effective. In stable patients, quick closure of the wound, after proper débridement and irrigation, is the most effective way to stop a bleeding scalp laceration and prevent the tissue crush injury that may occur if other compressive methods are used for too long.

When hemostasis is obtained, the wound should be irrigated to rinse away any debris. The emissary vessels of the subgaleal layer of the scalp drain directly into the diploë veins of the skull. These in turn drain into the venous sinuses. Contaminated or infected scalp wounds therefore have the potential to cause serious intracranial infections. Blood clots and other debris should be removed and the galea and underlying cranium palpated to detect any remaining debris, disruptions, or bone step-offs. Shear injuries to the scalp may deposit contaminants at sites distant from the apparent injury. The complexity of stellate lacerations often interferes with thorough inspection and débridement; stellate lacerations are particularly susceptible to infection. Digital exploration of a scalp wound should be carefully performed; if it is done too vigorously, comminuted or depressed bone pieces may be depressed further.

It is easy to confuse a disruption in the galea or a tear in the periosteum with a skull fracture. The base of the laceration should therefore be directly visualized. Clipping away a small area of hair parallel to the edges of the wound may facilitate this. Alternatively, an antibiotic ointment can be applied to the hair immediately surrounding the wound and used to plaster the hair away from the injury site. If the laceration begins on the forehead and extends upward beyond the hairline, surrounding hair should not be removed. Removal obliterates a useful landmark for cosmetic closure and may result in malalignment of the two laceration edges. If hair is accidentally embedded within the repaired laceration, it can delay healing by producing an inflammatory reaction or by serving as a nidus of infection.

Disruption of the galea results in a gaping scalp laceration. Large lacerations of the galea are closed to prevent the edges of the wound from pulling apart as the muscles within the galea contract. The skin, dermis, and galea can usually be repaired in a single layer with interrupted or vertical mattress sutures of 0-3.0 nylon or polypropylene.¹⁷⁸ Several recent studies have evaluated the use of staples versus sutures to close scalp lacerations that do not involve the galea. For both adult and pediatric scalp lacerations that begin beyond the hairline, staples have been shown to be cheaper, take less time, and have the same outcome than sutures if used in the appropriate manner.^179–181 Staples cannot be used to close the galea and may not be effective alone when hemostasis is a problem.¹⁸¹ Recently an alternative method of scalp laceration closure has been described in which bundles of the patient’s hair on each side of the wound are twisted together and then secured with tissue glue.^182,183 This may provide another method of effective repair and prevent the need to remove the closure material after the wound has healed.

Because of the rich blood supply of the scalp, even very large scalp avulsions can survive. If the avulsion remains attached to the rest of the scalp by a tissue bridge, it should be reattached to the surrounding tissue. If the avulsion is completely detached from the scalp, it should be treated as any other amputated part and reimplanted as soon as possible.¹⁷⁸ Scalp abrasions are often contaminated with pieces of dirt or other debris. The wound should be cleaned as thoroughly as possible and inspected for puncture wounds or other areas that penetrate beyond the superficial layers of the skin to ensure the removal of unsuspected foreign bodies. A careful inspection often reveals a small scalp laceration within the abraded area. Antibiotics are usually not needed for carefully managed scalp wounds because rapid healing is facilitated by the rich blood supply of the scalp.

Skull Fractures

Diffuse Axonal Injury

Prolonged traumatic coma not caused by mass lesions, ischemic insult, or nontraumatic causes of coma is thought to result from DAI. DAI or diffuse traumatic axonal injury is a pathologic process in which axons sustain a primary insult in which they are torn (axotomy) and secondary insults that can result in progressive cellular pathologic changes and eventual axon death (Fig. 41-8).¹⁵⁵ Affected axons are dispersed between areas of undamaged cells (Fig. 41-9). Badly damaged axons become edematous and eventually begin to separate from one another, causing widespread disruption of cortical physiology and microanatomy in the white matter of the brain and brainstem. Complete separation of axons does not always cause cell death; acute uncoupling of CBF and metabolism and apoptosis are thought to be the primary factors linked to axonal cell death after DAI.^21,155 Experimental laboratory data have indicated that neurons can partially repair and regenerate damaged axons. Recovery depends on the reversal or correction of structural and physiologic abnormalities.¹⁷

DAI is thought to be the cause of persistent traumatic coma that begins immediately at the time of trauma; however, some patients with DAI may recover consciousness briefly before lapsing into prolonged coma. No specific acute focal traumatic lesions are noted on a head CT scan. MRI is more sensitive in detecting subtle injury in DAI, but it is often not practical to perform MRI on critically injured patients. Occasionally, small petechial hemorrhages in proximity to the third ventricle and within the white matter of the corpus callosum or within the internal capsule of the brainstem are detected. DAI is the most common CT finding after severe head trauma, estimated to occur in 50% of all comatose head-injured patients.¹⁶⁶

Because diagnostic studies cannot predict the extent of the axonal damage, the severity of the injury is determined by the clinical course. Patients with mild DAI are in coma for 6 to 24 hours. Approximately one third of patients with mild DAI demonstrate decorticate or decerebrate posturing, but by 24 hours they are following commands.¹⁶⁶ The mortality in this group is 15% and is associated with infectious complications or concurrent intracranial injuries. Most patients who recover have mild or no permanent disabilities.

Moderate DAI is the most common clinical picture. Patients with moderate DAI are in coma for longer than 24 hours. Often, they are victims of falls or vehicular crashes and have associated basilar skull fractures. Patients may exhibit transient decortication or decerebration but eventually recover purposeful movements. On awakening, patients have prolonged severe post-traumatic amnesia and moderate to severe persistent cognitive deficits. Almost 25% die of complications of prolonged coma.¹⁶⁶

Severe DAI is almost always caused by vehicular crashes. Patients remain in coma for prolonged periods and demonstrate persistent brainstem dysfunction (posturing) and autonomic dysfunction (e.g., hypertension and hyperpyrexia). Diffuse brain swelling subsequent to injury causes intracranial hypertension. Herniation syndrome can occur if elevated ICP does not respond to medical or surgical intervention. Some patients with severe DAI eventually awaken but are severely disabled. Some patients remain in a persistent vegetative state, but most with severe DAI die from their head injury. All patients with DAI have an identical presentation of coma. Recent research has identified several biomarkers that may have clinical relevance in the future.¹⁵⁵ However, currently no early clinical or biomarker predictor exists that differentiates patients with mild, moderate, or severe DAI.

Cerebral Contusions

Contusions are bruises on the surface of the brain, usually caused by impact injury. Most often, contusions occur at the poles and the inferior surfaces of the frontal and temporal lobes where the brain comes into contact with bone protuberances in the base of the skull. If the contusion occurs on the same side as the impact injury, it is a coup injury; if it occurs on the opposite side, the contusion is a contrecoup injury. Contusions also often develop in the brain tissue that underlies a depressed skull fracture. Multiple areas of contused tissue may be produced with a single impact, often in association with other intracranial injuries.

Contusions are produced when parenchymal blood vessels are damaged, resulting in scattered areas of petechial hemorrhage and subsequent edema. Contusions develop in the gray matter on the surface of the brain and taper into the white matter. Often, subarachnoid blood is found overlying the involved gyrus. With time, the associated hemorrhages and edema of a contusion can become widespread and serve as a nidus for hemorrhage or swelling, thus producing a local mass effect. Compression of the underlying tissue can cause local areas of ischemia, and tissue infarction is possible if the compression is significant and unrelieved. Eventually, these ischemic areas become necrotic, and cystic cavities form within them.

The clinical presentation of patients with contusions is frequently delayed. They may have sustained only a brief LOC, but the duration of post-traumatic confusion and obtundation may be prolonged. If contusions occur near the sensorimotor cortex, focal neurologic deficits may be present. Many patients with significant contusions make uneventful recoveries, but contusions may cause significant neurologic problems, including increased ICP, PTSs, and focal deficits. Agrawal and colleagues¹⁸⁹ showed that significant progression of cerebral contusions is not an infrequent occurrence. Patients with lower GCS scores and larger cerebral contusions are at higher risk for needing delayed surgical intervention.¹⁸⁹

Non–contrast-enhanced CT is the best diagnostic test to discover contusions in the early post-traumatic period. These appear heterogeneous and irregular because of mixed regions of hemorrhage, necrosis, and infarction. Often, the surrounding edematous tissue appears hypodense. By post-trauma days 3 and 4, the blood located within the contusions has begun to degrade, and MRI becomes more useful.

Epidural Hematoma

EDHs are blood clots that form between the inner table of the skull and the dura. Most EDHs are caused by direct impact injury that causes a forceful deformity of the skull. Often, a fracture occurs across the middle meningeal artery, vein, or a dural sinus. The temporoparietal region is the most likely site for an EDH.¹⁵⁹ The high arterial pressure of the bleeding vessel dissects the dura away from the skull, permitting the formation of the hematoma.

An EDH is usually unilateral, and 20% of patients have other intracranial lesions, usually SDHs or contusions.²³ The deterioration of a patient who has an EDH from arterial bleeding can be rapid and dramatic. Because of their rapid formation, EDHs from arterial bleeding are usually detected within hours after injury and often earlier in children. EDHs that develop from a dural sinus tear develop more slowly, and clinical manifestations may be delayed, with resultant delays in detection.

EDH is primarily a disease of the young and accounts for 2.7 to 4% of all patients who have experienced TBI.23,190 EDHs are rare in elders and children younger than 2 years of age because of the close attachment of the dura to the skull in both patient populations. The classic presentation of an EDH is described as head trauma producing a decreased level of consciousness followed by a “lucid” interval. Although the patient’s consciousness is less decreased during the lucid interval, a completely normal mental status may not return before a second episode of decreased consciousness occurs. The lucid interval is not pathognomonic for an EDH and occurs in patients who sustain other expanding mass lesions. Approximately 47% of patients with EDHs present classically.¹⁹⁰ The development of symptoms and signs of EDH is entirely dependent on how quickly the EDH is developing within the cranial vault. Patients with an EDH often complain of a severe headache, sleepiness, dizziness, nausea, and vomiting. A small EDH may remain asymptomatic, but this is rare.

If the patient is not in coma when the diagnosis of EDH is established and if the condition is rapidly treated, the mortality is 5 to 10%. If the patient is in coma, the mortality from EDH is approximately 20%. The mortality in pediatric patients undergoing surgical evacuation is 5%.¹⁹⁰ If the EDH is rapidly detected and evacuated, the functional outcome is excellent.

On CT scan, an EDH appears hyperdense, biconvex, ovoid, and lenticular. The EDH does not usually extend beyond the dural attachments at the suture lines. The margins are sharply defined, and the hematoma usually bulges inward toward the brain (see Fig. 41-9). EDHs of mixed density on CT may be actively bleeding.

A posterior fossa EDH is the most common traumatic mass lesion of the posterior fossa and accounts for 5% of EDHs.²³ Direct occipital trauma resulting in a skull fracture that disrupts a venous sinus is the usual cause, and most patients have external evidence of occipital injury. Most patients become symptomatic within 24 hours after injury, with complaints of headache, nausea, vomiting, and nuchal rigidity. Most patients eventually have a decreased level of consciousness. On CT scan, a posterior fossa EDH looks similar to other EDHs, but it may cross the midline and extend above the tentorium to the supratentorial compartment (Fig. 41-10). Expert consensus guidelines support rapid surgical evacuation for any patient who has mass effect on CT or progressive neurologic deterioration.¹⁷⁵ Mortality approaches 26%.²³

Recent studies have investigated the indications for immediate operative intervention for EDHs. Epidurals greater than 30 cm³ in volume should be evacuated surgically, regardless of the patient’s GCS score. Furthermore, it is strongly recommended that comatose patients with an acute EDH and anisocoria on pupillary examination undergo surgical evacuation as soon as possible.¹⁹⁰

Subdural Hematoma

SDHs are blood clots that form between the dura and the brain. Usually they are caused by the movement of the brain relative to the skull, as seen in acceleration-deceleration injuries. These hematomas are common in patients with brain atrophy, such as alcoholic or elder patients. In these patients, the superficial bridging vessels traverse greater distances than in patients with no atrophy. As a result, the vessels are more likely to rupture with rapid movement of the head. Once they are ruptured, blood can fill the potential space between the dura and arachnoid.

SDHs are more common than EDHs, occurring in up to 30% of patients with severe head trauma.¹⁵⁹ The slow bleeding of venous structures delays the development of clinical signs and symptoms. As a result, the hematoma compresses the underlying brain tissue for prolonged periods and can cause significant tissue ischemia and damage.

The patient’s clinical presentation depends on the amount of brain injury sustained at the time of trauma and the rate of SDH expansion. If the patient with an SDH was rendered unconscious at the time of trauma, the prognosis is poor; these patients often have concurrent DAI. The signs and symptoms after injury that produces an SDH are initially related to the other intracranial injuries that may have been sustained and then to the slow expansion of the SDH.

SDHs are classified by the time to clinical presentation. Acute SDHs are symptomatic within 24 hours after trauma. Patients with acute SDHs often have a decreased level of consciousness. Most patients with an SDH have a GCS score less than 8. Approximately 12 to 38% of patients will have a lucid period at some point in their presentation. The overall mortality of patients who have an SDH and require surgical intervention is 40 to 60%.¹⁵⁹

Because of associated brain injury caused by the SDH, the delay in clinical signs and symptoms, and the more advanced mean age of the at-risk population, the mortality associated with SDH is much higher than that associated with EDH. Pupil inequality, motor deficit, and other signs consistent with increased brain swelling may be present on the initial examination. If the patient is deeply comatose at presentation with flaccidity and without signs of brainstem activity, supportive care should be considered in the ED. Subsequent management decisions should be discussed with the patient’s family and the attending neurosurgeon.

If the SDH is very small (only a few millimeters thick at its widest point on CT scan), some neurosurgeons may choose careful observation for these patients. Even a small SDH may be accompanied by extensive brain tissue damage that can cause an increase in ICP sufficient to precipitate a herniation syndrome. Current consensus guidelines recommend that acute SDHs with a thickness greater than 10 mm or a midline shift of more than 5 mm on CT should be evacuated surgically, regardless of the patient’s GCS score.¹⁵⁹ Research indicates that the longer the time between clinical worsening and operative treatment, the worse the patient’s clinical outcome. In these cases, surgical evacuation should be performed as soon as possible.¹⁵⁹

Unlike EDHs, SDHs often extend beyond the suture lines (Fig. 41-11). An SDH may follow the contour of the tentorium and be detected within the interhemispheric fissure (Fig. 41-12). Many patients with an acute SDH also show CT evidence of intracerebral lesions contralateral to the SDH.

A subacute SDH is symptomatic between 24 hours and 2 weeks after injury. It may appear hypodense or isodense on CT scans. Contrast increases detection of isodense lesions. Patients complain of a headache, altered mental status, or focal deficits. Most patients with subacute SDH require surgical evacuation of the lesion.

A chronic SDH becomes symptomatic 2 weeks or more after trauma. The signs and symptoms may be very subtle or nonspecific, but many patients demonstrate unilateral weakness or hemiparesis.²³ Most report an altered level of consciousness, but some patients are unable to recall their head injury or describe only a minor injury. In 20% of cases, chronic subdurals are bilateral. A chronic SDH may have initially been a small asymptomatic SDH that eventually expanded owing to a combination of recurrent hemorrhage and escape of plasma into the hematoma. At some point, a critical mass is reached and the chronic SDH becomes symptomatic. On CT scan, a chronic SDH may appear isodense or hypodense to brain parenchyma. In these cases, indirect evidence of the lesion includes a midline shift, effacement of the ipsilateral cortical sulci, and ventricular compression. Contrast may increase the likelihood of identifying a chronic SDH that has become isodense. On CT scan, blood of various ages is seen as a mixed-density lesion. On MRI, a chronic SDH appears hyperdense. The treatment of chronic SDHs is controversial. If they become symptomatic, chronic SDHs require surgical evacuation. Most patients have a good outcome after surgery. Overall, the mortality from surgically drained chronic SDH approaches 4%, with decreased survival in elders.²³

The prognosis of SDH does not entirely depend on the size of the hematoma but rather on the degree of brain injury caused by the pressure of the expanding hematoma on underlying tissue or by other intracranial injury caused by the initial impact. Mortality is highest in older people, in patients who have a GCS score of 8 or less, and in those with signs of acute herniation syndrome on initial ED presentation. Posterior fossa SDHs make up less than 1% of all reported SDHs. They are caused by occipital trauma that tears bridging vessels or venous sinuses. Clinical manifestations of posterior SDH vary but usually include nausea, vomiting, headache, and decreased level of consciousness. Occasionally, CN palsies may be found, as well as nuchal rigidity, cerebellar signs and symptoms, and papilledema. On a CT scan, a posterior fossa SDH does not cross the midline or extend above the tentorium. The outcome of a posterior SDH is very poor.

In children the presence of an SDH should prompt consideration of child abuse. Many types of injury can produce SDH in children, but the infant who is repeatedly and forcibly shaken is especially susceptible.¹³⁰ Infants may have SDH because of birth trauma. In these cases the initial clinical manifestation may be a generalized seizure within the first 6 months of life. On examination the infant may have a bulging fontanel or an enlarged head circumference. A careful history may elicit long-standing constitutional symptoms, such as failure to thrive or lethargy.

Subdural Hygroma

A subdural hygroma (SDHG) is a collection of clear, xanthochromic blood-tinged fluid in the dural space. The pathogenesis of an SDHG is not certain. It may result from a tear in the arachnoid that permits CSF to escape into the dural space or effusions from injured vessels through areas of abnormal permeability in the meninges or in the underlying parenchyma. They may accumulate immediately after trauma or in a delayed manner. Clinically, an SDHG cannot be distinguished from other mass lesions. Often, patients have a decreased level of consciousness or focal motor deficits. They may complain of headaches, nausea, and vomiting. The ICP can increase because of the mass effect, and signs of increased ICP may be present on examination.

On CT scans, SDHGs appear crescent shaped in the extra-axial space. The CT density is the same as that of CSF. Bilateral SDHGs are common. If SDHGs are asymptomatic, observation is reasonable management. Otherwise, they are surgically evacuated. Mortality approaches 20% and appears to depend on the severity of other intracranial injury.²³

Traumatic Subarachnoid Hemorrhage

Traumatic subarachnoid hemorrhage (TSAH) is blood within the CSF and meningeal intima and probably results from tears of small subarachnoid vessels. TSAH is detected on the first CT scan in up to 33% of patients with severe TBI and has an incidence of 44% in all cases of severe head trauma. It is therefore the most common CT scan abnormality seen after head injury. Data from the National Traumatic Coma Data Bank demonstrate a 60% unfavorable outcome in severely brain-injured patients in the presence of TSAH compared with a 30% unfavorable outcome if no TSAH occurs.¹⁹¹ An increased incidence of skull fractures and contusions is found in patients with TSAH compared with patients with no TSAH. The amount of blood within the TSAH correlates directly with the outcome and inversely with the presenting GCS score.

Patients may complain of headache and photophobia. A noncontrast CT scan allows the diagnosis to be made, with increased density noted within the basilar cisterns. Blood can also be seen within the interhemispheric fissures and sulci.

TSAH with no other brain injury does not generally carry a poor prognosis. The most serious complication of TSAH is worsening of cerebral vasospasm, which may be severe enough to induce cerebral ischemia. Post-traumatic vasospasm is common, occurring approximately 48 hours after injury and persisting for up to 2 weeks. Calcium channel blockers (e.g., nimodipine and nicardipine) have been used in the acute intensive care unit setting to prevent or reduce vasospasm after TSAH.

Intracerebral Hematoma

Intracerebral hematomas (ICHs) are formed deep within the brain tissue and are usually caused by shearing or tensile forces that mechanically stretch and tear deep small-caliber arterioles as the brain is propelled against irregular surfaces in the cranial vault. Resulting small petechial hemorrhages subsequently coalesce to form ICHs. Approximately 85% are in the frontal and temporal lobes. They are often found in the presence of extra-axial hematomas, and in many patients multiple ICHs are present.192,193 Isolated ICHs may be detected in as many as 12% of all patients with severe head trauma.

The clinical effects of ICH depend on size, location, and whether the bleeding is continuing. ICHs have been reported with all degrees of severity of head trauma. More than 50% of patients with ICH sustain LOC at the time of impact. The patient’s subsequent level of consciousness depends on the severity of the impact and coexisting lesions. Combined with contusions, other concurrent lesions, and subsequent perilesion edema, an ICH can produce substantial mass effects and precipitate a herniation syndrome (Fig. 41-13).

An ICH may be detected on the first CT scan immediately after injury but often is not seen for several hours or days. Unlike contusions, ICHs are usually deep in the brain tissue and often become well demarcated over time. On CT scan, an ICH appears as a well-defined hyperdense homogeneous area of hemorrhage (Fig. 41-14).

Many patients with an ICH require emergent intervention or surgery to control elevated ICP. Mortality is low in patients who are conscious before surgery; in unconscious patients, mortality approaches 45%.192,193 ICHs that bleed into the ventricles or cerebellum also carry a high mortality rate.

Traumatic Intracerebellar Hematoma

Primary traumatic intracerebellar hematomas are rare but can occur after a direct blow to the occipital area. Often, these patients also have a skull fracture or a posterior fossa EDH or SDH. Supratentorial contrecoup hematomas and contusions are also common associated findings.

The clinical presentation of an isolated traumatic cerebellar hematoma is similar to that of other posterior lesions. When other traumatic lesions are present, the picture may be quite confusing. The acute management should first address the most clinically significant lesion. The mortality from isolated traumatic intracerebellar hematoma is very high. Emergent neurosurgical consultation is indicated.

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