Glasgow Coma Scale

Ideally, using the GCS, a nurse, medical student, paramedic, physician assistant, intensivist, trauma surgeon, emergency medicine physician, neurologist, and neurosurgeon all should obtain the same score when assessing a patient. The GCS system is not perfect, but it has proved itself to be, overall, a practical, straightforward grading system that can be used by health professionals in various fields and at different levels to produce reliable results.25–30 The GCS has become the most widely used assessment tool and is considered the gold standard for the evaluation of patients with head injuries.¹²

The GCS is a measure of level of consciousness and does not take into account focal deficits. It is based on eye opening (1-4), verbal response (1-5), and motor response (1-6) (Table 66.1). A patient with a normal level of consciousness should have the highest possible score of 15. The lowest score possible is 3, not 0 as might be expected. An intubated patient technically gets a 1 for verbal response and is assigned 1T (for Tube) for the verbal score. It is important to identify the score for each observed variable tested. For example, a typical score for an intubated patient with decorticate posturing probably would be E1 + V1T + M3 = 5T (where E denotes eye opening, V is verbal response, and M is motor response). It also is important to realize the shortcoming of this system in evaluating patients with dementia or aphasia. A point to keep in mind is that the GCS attempts to put a numeric value on level of consciousness, with 15 being representative of normal. If a demented patient from a nursing home presents with a normal level of consciousness after a fall but doesn’t know what day it is, the GCS would be calculated as E4 + V4 + M6 = 14. A GCS score of 14 describes a patient with an abnormal level of consciousness but fails to accurately communicate this particular patient’s condition. Likewise, clinicians must use caution when applying the GCS to patients with aphasia. Conversely, patients with profound focal deficits and a normal level of consciousness should have a GCS score of 15. Another problematic case is that of a quadriplegic patient with a normal level of consciousness who is able to blink the eyes or stick out the tongue upon command, thereby giving a top score of 6 on the motor assessment.

The GCS has been used to predict outcome.³¹ The motor score itself has predictive value as well.³² The GCS score should be calculated after hemodynamic and pulmonary resuscitation and without sedatives or muscle relaxants.³³

Aggressive implementation of early sedation and intubation in severely head-injured patients compromises the ability to determine an accurate GCS score.³⁴

Computed Tomography Classification: Marshall Classification

A useful classification of brain injuries by findings on computed tomography (CT) has been devised by Marshall and colleagues. This CT classification, presented in Table 66.2, can serve as a guide in describing scans and has strong predictive power.^34,35

Maas and associates have proposed a scoring system with better predictive power (Table 66.3), with a sum total adjusted to be consistent with the GCS.³⁴ Table 66.4 presents a mortality prediction chart based on this classification.

This scoring system is best used as one piece of data in the overall clinical assessment in considering a patient’s prognosis.³⁶

Prediction of Outcomes

Severe brain injury outcomes can be accurately predicted using four variables: age, GCS score on admission (especially motor score), CT characteristics, and presence of ischemic and hemodynamic secondary insults. Using these four predictors, numerous investigators have used statistical modeling techniques to predict up to 80% or more of outcomes.³⁷

Head injuries generally are classified as mild (GCS score of 13 to 15), moderate (GCS score of 9 to 12), or severe,3–8 although the evidence may be sufficient to include a GCS score of 13 in the moderate category.³⁸

CT scanning is the diagnostic imaging study of choice in trauma. Plain x-ray films of the skull are rarely indicated as a screening study for head-injured patients. Outcomes with the strategy of obtaining CT scans in all head-injured patients are superior to those with other management strategies. The incidence of missed surgical lesions in mildly head-injured patients by CT scanning is 0.028%.39–42

Skull Fractures

The next layer involved in trauma is the skull, composed of outer and inner tables with the intervening vascular diploic space. Skull fractures are best considered as involving the cranial vault or the skull base. Cranial vault fractures are further divided into linear or depressed and open or closed. In general, closed, linear fractures of the cranial vault do not require any specific treatment.

Basilar skull fractures typically are linear and involve the anterior cranial base and the petrous part of the temporal bone. These fractures have the potential for an associated dural laceration adjacent to potentially contaminated paranasal sinuses, or the external ear canal if the tympanic membrane is disrupted. This allows the potential for a cerebrospinal fluid (CSF) fistula to develop, as well as meningitis. Clinical signs of a fracture of the petrous portion of the temporal bone include hemotympanum with or without tympanic membrane disruption, hearing loss, CSF otorrhea, and Battle sign. The cranial nerves that course through the temporal bone include the facial, acoustic, and vestibular nerves; therefore, associated vestibular dysfunction or facial weakness may be noted (Fig. 66.1). Anterior cranial base fractures may be associated with “raccoon eyes,” anosmia, and CSF rhinorrhea. It is important to remember that when a fracture of the floor of the anterior cranial base is suspected, a nasogastric tube should not be inserted, because of the risk of intracranial penetration (Fig. 66.2).

The use of prophylactic antibiotics in basilar skull fractures has been debated but generally is not recommended. When CSF leak does occur, the break in the tissue usually will heal with conservative treatment over the course of a week, unless the defect is very large or a bony spicule is identified. Keeping the patient’s head elevated and possibly using external CSF diversion after a few days are reasonable nonoperative methods; however, if the leak persists, surgical repair is indicated.⁴⁴

Most depressed skull fractures occur in men younger than 30 years of age.⁴⁵ Despite very little literature to support any particular management strategy, closed depressed skull fractures generally are operated on if the extent of depression is greater than the full thickness of the adjacent skull, with the theoretical benefits of improved cosmetic result, a decrease in late-onset posttraumatic epilepsy, and a reduction in the incidence of persistent neurologic deficit.⁴⁶ Most depressed skull fractures, however, are open⁴⁵ (Fig. 66.3), meaning that a scalp laceration with galeal disruption overlying the fracture is present.

Open depressed skull fractures may be associated with significant morbidity and mortality.45,47 Infection rates are reported to be between 1.9% and 10.6%,^46–50 with neurologic morbidity and mortality rates of approximately 11% each⁴⁶ and an incidence of late epilepsy up to 15%.⁵¹

By convention, open depressed cranial vault fractures are treated surgically, with debridement and elevation, primarily to attempt to decrease the incidence of infection. Open depressed cranial fractures may be treated nonoperatively if clinical and radiographic examination reveals no evidence of dural penetration, significant intracranial hematoma, depression greater than 1 cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination.⁴⁶

A special type of depressed fracture is fracture of the frontal sinus. Depression of the fracture may require surgery to prevent CNS infection and CSF leak (Fig. 66.4). Another special type of depressed fracture involves a major dural venous sinus (see Fig. 66.4). Under these circumstances, the risks associated with surgery are increased, and elevation of the fracture fragment generally is reserved for significant compromise of venous drainage.⁴⁴

Epidural Hematoma

The next anatomic layer after the skull is the dura, which is the periosteum of the inner table of the skull and, as such, is tightly adherent to the bone. The potential space between the inner table of the skull and the dura is the epidural space. Epidural hematomas (EDHs) form in this potential space between the skull and the dura. The most common mechanism for the development of an EDH is a motor vehicle crash (in 53% of the cases), followed by falls (in 30%) and assault (in 8%).52–60 Typically, bleeding results from damage to the middle meningeal artery, but an EDH also can occur from injury to the middle meningeal vein, diploic veins, or the venous sinuses.⁶⁰

EDHs generally occur in the temporal and temporoparietal regions (Fig. 66.5).^{52,57,61–64} A useful way to describe the development of an EDH is to follow the events that take place when a patient presents with an initial lucid interval following brief loss of consciousness after head trauma. A lucid interval occurs when a patient initially is rendered unconscious from a concussive head injury that causes a linear skull fracture involving the middle meningeal artery or one of its branches. The middle meningeal artery is a dural vessel that runs half in the dura and half through the groove in the inner table of the skull. When a fracture extends across the bony groove of the artery, it will tear and bleed. Because the dura is tightly adherent to the inner table of the skull, significant force is needed to push the dura off the inner table. An arterial hemorrhage generally has enough pressure to strip the dura off the bone, converting the potential epidural space into a mass. The bony attachment of the dura becomes progressively stronger with age; therefore, the dura of a younger patient requires less force to push it off the bone than would be required in an older patient. Not surprisingly, the mean age of patients with EDH is between 20 and 30 years of age,^{53–55,63–70} and EDHs are unusual in patients older than 50.⁶⁰

The growing epidural mass commonly compresses the anterior temporal lobe, which usually will not cause a major detectable neurologic deficit early in the course in the emergency department. During this so-called lucid component of the lucid interval, the patient regains consciousness from the concussive injury while the EDH is expanding and compressing the relatively silent anterior temporal lobe. The medial part of the temporal lobe, the uncas, lies just lateral to the brainstem at the level of the third cranial nerve (oculomotor nerve), which runs alongside the tentorial edge. When the EDH enlarges to the point at which it pushes the uncas of the temporal lobe over the tentorial edge, rapid development of a third nerve palsy, along with brainstem compression, is possible—which, at this level, will cause a contralateral hemiparesis from direct compression of the cerebral peduncle and a decrease in level of consciousness from the effect on the reticular activating system. The classic signs at this point are coma with a dilated pupil ipsilateral to the EDH and a contralateral hemiparesis. Occasionally, instead of directly compressing the ipsilateral cerebral peduncle, the herniating uncas can shift the brainstem into the contralateral tentorial edge, a relatively sharp rigid structure. This can damage the brainstem on the side opposite the EDH and cause a hemiparesis ipsilateral to the side of the hematoma. This is known as Kernohan’s notch phenomenon.

Taking a general view, the patient goes from unconscious at the time of impact from a concussive injury, to awake, to unconscious again secondary to brainstem compression—hence the term lucid interval. The lucid interval is observed in close to half of the patients undergoing surgery for EDH.*

Pupillary abnormalities occur in approximately 20% to 30% of patients with surgical EDH.52,54,59,60,67 Cranial fractures are present in between 70% and 95% of the cases.^{54,60,68,70,74,75} Associated intracranial lesions are found in 30% to 50% of adults with surgical EDHs,^† and subdural or parenchymal lesions in association with EDH lower the chance of a good outcome.⁶⁰

The overall mortality rate (for all ages and GCS scores) is approximately 10%.^‡ The time lapse between the onset of pupillary abnormalities and surgery determines outcome,^61,66,80 but the single most important predictor of outcome in patients operated on for EDH is the GCS score on admission and before surgery.^{52,53,55,61,81–83}

Not all EDHs, however, require surgery. No prospective randomized trials have been conducted to compare surgical treatment with nonoperative management, nor should there be. Available data describe nonsurgical management in selected cases. In one study, approximately 10% of the total number of EDHs were treated nonoperatively. All were conscious with a GCS score greater than 11 and a midline shift on CT scan of less than 10 mm. Not one of these nonoperative hematomas was in the temporal region.⁸⁴

Another study reported findings in a group of 57 selected patients treated nonoperatively with an initial GCS score of 10 or higher, with maximum hematoma thickness less than 13 mm, with five clots located in the temporal region, but only one patient had a midline shift on CT.⁵³

An interesting approach for dealing with thin, acute EDHs in an early stage has been reported in a small, isolated series of patients using endovascular techniques to occlude the middle meningeal artery.⁸⁵ Surgical decision making for an acute EDH is based on GCS score, pupillary findings, comorbid conditions, CT findings, age, and, in delayed decisions, ICP. Guidelines for the surgical management of acute EDH published in 2006 recommend surgical evacuation of an EDH less than 30 mL in volume. Smaller hematomas in patients with a GCS score greater than 8 and without focal deficits, clot thickness less than 15 mm, and less than 5 mm of midline shift may be considered for nonoperative management. Close neurologic monitoring and serial CT scanning are essential. Of importance, a temporal location for an EDH is associated with failure of nonoperative management and should lower the threshold for surgery.⁶⁰

Because time between neurologic deterioration and surgery is critical, the question of whether a patient with an acute EDH should receive treatment at the nearest hospital or should be transferred to a trauma center is important. The issue is whether or not a non-neurosurgeon should operate on a patient deteriorating from an acute EDH as a true emergency. One suboptimally controlled study reported worse outcomes in a small group of patients who underwent emergency operations by non-neurosurgeons and attributed this mainly to the technical inadequacy of the operation.59,60 Other studies have documented worse outcomes in patients transferred from outlying hospitals for surgery.^52,73 The take-home message is that EDHs are extra-axial hemorrhages located adjacent to the brainstem that can represent a true neurosurgical emergency, and that rapid, competent decompression makes a difference.

Subdural Hematoma

Proceeding deep to the skull, the next space is the subdural space. Unlike the potential epidural space, the subdural space is a real space. It is a compartment that follows the contour of the brain, which is how it appears on a CT scan (Fig. 66.6). Anatomically, bridging veins course through the subdural space from the cerebral hemispheres to the superior sagittal sinus. As the brain accelerates within the skull after impact, these veins can stretch and tear.⁸⁶

The source of bleeding also can be from a cortical artery87,88 or vein. These hematomas typically form over the surface or between the cerebral hemispheres, along the tentorium, or between the temporal lobe and base of the skull.

An acute subdural hematoma (SDH), as defined by Bullock and colleagues, appears within 14 days of injury,⁶⁰ although some authors consider an SDH to be subacute when signs and symptoms develop between 3 and 20 days after trauma.⁸⁹

Acute SDHs consist of clotted blood, which is fibrous and often adherent to adjacent tissue. The blood remains clotted for several days. After this time, the clot gradually and progressively lyses, resulting in a mixture of clot and fluid. After several weeks, the clot is liquefied and becomes a chronic SDH. Chronic SDHs may manifest weeks or months after what may have been mild or insignificant trauma. Chronic SDHs occur more often in elderly patients and individuals who have more intracranial space because of cortical atrophy. A membrane often surrounds these hematomas, and the collection of fluid may slowly grow in size because of repeated small bleeds or accumulation of fluid transudate from the membrane.⁸⁶

The incidence of acute SDHs is approximately 20% in severe traumatic brain injury,60,90–93 and the mean age is between 31 and 47 years, with most of the patients being men.^60,94–97 The mechanism of injury differs between age groups, with patients older than 65 more commonly presenting after a fall, and younger patients being involved more often in a motor vehicle crash,^60,98–100 which, among comatose patients with acute SDH, is the most common mechanism of injury.^60,91,93,101

Between 37% and 80% of patients with acute SDH present with a GCS score of 8 or lower,60,65,71,94,97,102 and the overall mortality rate is between 40% and 60%.* Mortality rates among comatose patients requiring surgery are somewhat higher, with reported rates between 57% and 68%.^† Acute subdural hematomas frequently are associated with other brain injuries,^97,102 which is one of the reasons why the mortality rate is relatively high.

A simple acute SDH is a subdural, extra-axial hematoma without any other associated brain injury (Fig. 66.7). A complex SDH is associated with parenchymal injury (Fig. 66.8).^107,108 Fewer than half of acute SDHs requiring surgery are isolated, simple lesions.^60,97,102

One useful method to identify the presence of associated injury is to measure the thickness of the subdural clot relative to the amount of brain shift on the CT scan. If the amount of shift is directly proportional to the thickness of the extra-axial clot, the injury is likely to be simple and only the brain compressed. However, if the amount of shift is more than expected as indicated by the size of the hematoma, then additional parenchymal brain injury probably is present under the clot, causing additive mass effect. Not surprisingly, the mortality for complex injuries is higher than that for simple SDHs.107,108

In addition to the obvious compressive effects that an SDH generates, the available evidence points to a direct toxic effect of the blood itself on the underlying cortex, thereby compounding the problem.109,110

Age is an important factor in acute SDHs. There is a significant increase in poor outcome among patients older than 60 years of age with severe head injury in general.93,98–101,111,112 Older patients with an acute SDH and a low GCS score do especially poorly.^{98–101,111,112}

The decision for immediate surgery is dependent on GCS score, age, pupillary examination, comorbidities, CT findings, and salvageability with respect to the patient’s level of injury. In addition to all of these factors, decision making for delayed surgery is dependent on clinical course and ICP.⁶⁰

On the basis of a contemporary search of the literature, Bullock and colleagues found that CT parameters of a midline shift greater than 5 mm and a clot thickness greater than 10 mm were independent factors requiring surgery in salvageable patients. They also identified a select group of comatose patients with smaller SDHs who could be managed nonoperatively if the patients remained neurologically stable with normal pupils and ICP of 20 mm or less.⁶⁰

Traumatic Subarachnoid Hemorrhage

The subarachnoid space is a CSF-filled compartment within which are the major cerebral blood vessels. The CSF within the subarachnoid space fills the basal cisterns and interdigitates into the cortical sulci. Traumatic SAH can be caused by bleeding of cortical arteries, veins, or brain surface cerebral contusions.¹¹³

In contrast with hemorrhages in other locations, SAH is not a discrete surgical clot that requires evacuation. Trauma is the most common cause of SAH; a ruptured aneurysm is the most common cause of a spontaneous SAH. Aneurysmal SAH generally involves the suprasellar cistern, where the circle of Willis lies. Traumatic SAH can be found as small-volume hemorrhages in the sylvian fissures and especially in the interpeduncular cistern. Traumatic SAH also commonly involves the cerebral convexity and can fill cortical sulci, which can sometimes mimic sulcal effacement¹¹⁴ (Fig. 66.9A).

Occasionally, the distribution of the hemorrhage may be hard to differentiate from an aneurysmal hemorrhage. Under this circumstance, a vascular study should be obtained (Fig. 66.9B). Cerebral vasospasm following aneurysmal SAH is a common, well-described problem with an unclear pathogenesis. Increasing evidence suggests that SAH from trauma also may cause clinically significant cerebral vasospasm, which may be responsible for ischemia and infarction.^115,116

Clearly the incidence of clinically relevant cerebral vasospasm is less than what is seen in aneurysmal SAH; however, posttraumatic SAH may cause ischemia during the acute as well as the delayed phase.115,117

In severe nonpenetrating head injury, the degree of SAH can be predictive of outcome,118,119 and although traumatic SAH can be an isolated finding, it is commonly associated with other intracranial injuries.¹²⁰

Traumatic SAH can be a marker of severe primary injury and the amount of blood can also be an independent predictor of the development and progression of intraparenchymal contusions¹¹³ (Fig. 66.9C).

Intraparenchymal Contusions and Hematomas

Traumatic parenchymal mass lesions are common and are reported in 13% to 35% of severe traumatic brain injury.121–127 Contusions consist of heterogeneous areas of necrosis, pulping, infarction, hemorrhage, and edema.^89,128,129 Hemorrhagic contusions are mixtures of blood and edematous cerebral parenchyma that also have a heterogeneous appearance on CT.⁸⁹ Contusions commonly occur in the frontal and temporal lobes both at the poles and on the inferior surfaces as a result of contact with the rough, bony skull base¹³⁰ (Fig. 66.10A).

Contusions typically involve the crests of the gyri but in more severe injury may extend into the substance of the white matter. If the pia-arachnoid is torn, contusions are classified as cortical lacerations.130–132

Contusions represent one end of a spectrum of injury on which hematomas, which are well-defined, homogeneous collections of blood, are the other end (Fig. 66.10B). The amount of energy delivered may have only been enough to cause failure of small vessels, resulting in contusions. If more energy is delivered, failure of larger vessels may occur, resulting in hematomas. Alternatively, the hemorrhagic component of a contusion may continue to bleed and coalesce into a more discrete hematoma. In general, the most common traumatic parenchymal lesions are contusions,⁸⁹ and they tend to evolve.^{122,126,127,133,134}

Risk factors for the progression of intraparenchymal hemorrhage include the presence of SAH (see Fig. 66.9C), and subdural hematoma, as well as the size of the clot on the initial CT scan. Enlargement of contusions occurs approximately 40% of the time, which justifies early follow-up CT scanning.¹³⁵ In addition to the problem of progressive enlargement of existing contusions is a phenomenon of delayed appearance of traumatic intracerebral contusions (DITCH). DITCH is defined as a new contusion identified on a CT scan in an area of brain that was normal on the admission CT scan. These delayed hemorrhages are reported to occur in up to 7% of patients with severe head injuries.⁹⁰

Contusions can be subdivided into two groups. Coup contusions occur in the brain tissue under the impact site and usually are associated with an acceleration injury. Contrecoup contusions are located away from the point of impact and usually are associated with a deceleration injury.130,131,136–138

Understanding the biomechanics of how a contrecoup contusion develops is useful. In general, biologic tissues tolerate strain better if they are deformed slowly rather than quickly. For example, a 150-mL hematoma with accumulation of blood over minutes is likely to be lethal, whereas a 150-mL slow-growing meningioma may have no appreciable effect on the patient’s level of consciousness. In trauma, the cause of tissue damage may be any of three types of induced strains: compression, tension, and shear. The skull, brain, and blood vessels will tolerate compression better than tension, and tension better than shear. These strains are induced by contact or inertia (relative to acceleration-deceleration), or both. Contact injuries are a result of impact, which may cause inward deformation of the skull with local effects, and of shock waves, which can produce remote effects. As a consequence of contact the head is set in motion, which leads to inertial injury. Inertial injuries may cause damage by differential acceleration of the skull and brain. In addition, acceleration-deceleration can independently produce strains in the brain itself. The two clinically relevant types of acceleration are translational (when the brain moves in a straight line) and angular. Most injuries are a combination of both.¹³⁹

These effects are best illustrated by a case example of a 37-year-old man who falls from a height onto the back of his head and presents with a deteriorating level of consciousness. His CT scan (Fig. 66.11) reveals soft tissue swelling at the point of impact in the right occipital region with a small underlying hemorrhage, as well as a large, hemorrhagic contusion in the left frontal lobe. The mechanism involved is primarily translational (linear) deceleration. The skull stops suddenly as it hits the ground, but the brain continues to move toward the impact site, where compression is induced (Fig. 66.12).

As the brain is moving toward the inner table of the skull at the impact site, it also is moving away from the skull on the opposite side, creating regions of low pressure and tensile strains. Contributing to the extensive tissue damage in the left frontal lobe also may be movement of the brain across the rough surface of the anterior cranial base.89,139

The same amount of energy is delivered to the brain in nearly a straight line, with the compressive injury at the point of impact resulting in much less damage than the contrecoup injury caused by tension. In view of the dramatic differential susceptibilities of the brain and blood vessels to compressive and tensile strains induced in trauma, it is understandable that diffuse injuries can be caused by seemingly less violent trauma when the head undergoes an injury with a large component of angular acceleration-deceleration. This is the motion that can induce shearing strains, which the tissues tolerate poorly (see “Diffuse Axonal Injury” later on).

Surgical decision making is more straightforward for epidural and subdural types of hematomas, in which the extra-axial mass causing compression is simply on the surface of the brain. Contusions and hematomas, however, are intra-axial masses intimately associated with surrounding regions of brain that may be salvageable. It is one thing to surgically evacuate an extra-axial hematoma compressing the dominant frontal lobe, and quite another to operate on a large contusion within the dominant frontal lobe.

In 2006, guidelines were published after a thorough review of the relevant but scientifically weak literature. The reviewers reported that patients with parenchymal mass lesions and signs of progressive neurologic deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on CT scan should be treated operatively. Patients with GCS scores of 6 to 8 with frontal or temporal contusions greater than 20 cc in volume with midline shift of at least 5 mm or cisternal compression on CT scan and patients with any lesion greater than 50 cc in volume should receive operative treatment. Patients with parenchymal mass lesions who do not show evidence of neurologic compromise, whose ICP is controlled, and who demonstrate no significant signs of mass effect on CT scan may be managed nonoperatively with intensive monitoring and serial imaging. For patients with refractory intracranial hypertension and diffuse parenchymal injury with clinical and radiographic evidence for impending transtentorial herniation, the guidelines also recommended, as treatment options, subtemporal decompression, temporal lobectomy, or hemispheric decompressive craniectomy (Fig. 66.13). With regard to timing of surgery, the literature supports a bifrontal decompressive craniectomy within 48 hours of injury as a treatment option for patients with diffuse, medically refractory posttraumatic cerebral edema and resultant intracranial hypertension.¹²⁷

Hypothalamic-Pituitary Injury

Injury to the pituitary and hypothalamus can complicate head injury. A prolonged loss of consciousness often is reported in patients with such injuries. Up to 80% of cases are associated with a fracture through the skull base. Injuries include (in decreasing order of frequency) pericapsular hemorrhage, hypothalamic infarction, posterior pituitary hemorrhage, anterior pituitary infarction, and rupture of the infundibulum.140–142 Clinically measurable decreases in pituitary hormone production are not seen until at least 75% of the gland is destroyed. Complete loss of production requires destruction of at least 90% of the gland.

Derangements in pituitary function can result in decreased production of any of the pituitary hormones. Of particular clinical significance is impairment of adrenocorticotropic hormone release that can result in secondary adrenal insufficiency (Addison’s disease). Physiologic stressors such as trauma, surgery, or infection can result in addisonian crisis, with potentially life-threatening results. Diabetes insipidus has been reported in a significant number of severe head injuries, with a high percentage of cases remaining permanent.¹⁴³ Injuries to the pituitary often are not suspected in the acute period, and the diagnosis of hypopituitarism is therefore often delayed (Fig. 66.14).

Diffuse Axonal Injury

The term diffuse axonal injury (DAI) describes brain damage in a group of patients who become immediately unconscious or go into coma at the time of the head trauma.⁸¹ Depending on the severity of the injury, patients may have mild, moderate, or severe DAI. A large number of patients with severe head injury will have DAI. Because of the gradient acceleration difference of certain brain areas during primary impact, shearing forces at the gray-white junction, corpus callosum, or brainstem may occur.^131,144 The result of these forces will be diffuse tearing of axons and small blood vessels. These lesions initially may be hemorrhagic, but as they become chronic, shrinking, softening, and scarring ensue, often with cyst formation.^42,145 The lesions usually are microscopic but can be large and macroscopic. Although small, focal, petechial hemorrhages may be visualized, the initial CT scan often is normal.¹⁴⁶ Most of the clinical and experimental studies support that the diffuse injury occurs at the time of initial impact and is not the result of other adverse factors, such as decreased brain oxygenation, increased ICP, or brain swelling,^145,147 although these factors tend to accentuate the amount of damage.

The term gliding contusions originally was introduced by Lindenberg and Freytag¹⁴⁸ to describe hemorrhagic lesions in parasagittal white matter; this brain injury concept has been reanalyzed.¹⁴⁹ Gliding contusions frequently are found in association with DAI and acute subdural hematomas. Two mechanisms have been considered in relation to the formation of these contusions. First, during angular acceleration, more movement and displacement of the cortical gray matter occur than of the deep white matter; accordingly, most of the tissue injury occurs at the gray-white junction because shearing strains predominate. The second mechanism involves excessive displacement of the bridging veins during brain acceleration. Patients with severe DAI who survive may be profoundly disabled, but some patients with mild or moderate DAI may recover with mild or no disability.⁸¹ The importance of recognizing DAI in the initial evaluation cannot be overstressed; this will affect the management and outcome. Clinically, these patients will have impaired consciousness secondary to bicortical damage, possibly in association with unremarkable imaging findings and normal ICP.

Penetrating Brain Injury

It is estimated that between 6000 to 7000 people die each year in the United States from gunshot wounds to the brain.130–139,150–152

Basic Concepts

Management of primary head injury generally entails the surgical management of head-injured patients and typically is driven by the presence of pathologic masses (hematomas) in anatomic spaces. Management of secondary head injury usually involves the nonsurgical management of these patients and deals with the pathologic derangement of physiologic processes.

The three functional volumetric compartments in the head are blood, brain, and CSF. The volumes of these three functional compartments are approximately 1200 mL for brain, 150 mL for CSF, and roughly 150 mL for the variable blood compartment. The total volume of the intracranial compartment is relatively fixed and relatively incompressible. Therefore, if volume is added to one of these three compartments, a compensatory loss of volume from another compartment will occur; otherwise, ICP will rise. To illustrate this point, a pressure-volume curve for the intracranial compartment is shown in Figure 66.16. Initially, as volume is added to the system, no significant change in pressure occurs. With cerebral edema, for example, as the brain compartment increases in volume, venous capacitance vessels collapse, which moves blood volume out of the system; therefore, overall net volume does not change and ICP remains stable. As the brain continues to swell and increase in volume, the ventricles become smaller as CSF moves out of the system, again keeping overall net volume and ICP relatively stable. At some point the system loses this buffering capacity, and as more injury-related volume accumulates, ICP starts to rise. The rise in ICP is gradual, progressive, and nonlinear. As the system continues to get stressed with additional volume, it progressively loses compliance and, in effect, gets stiffer. The result is that increasingly smaller volumes introduced into the system result in higher changes in ICP. Using MRI methods to study cerebral edema, Marmarou and colleagues noted a rise in ICP when edema was only 1% higher than the normal water content of brain tissue. These investigators also showed that when water content increased in a contused hemisphere, ICP increased exponentially. These findings demonstrate the importance of small changes in intracranial volume, particularly when the buffering capacity of the system has been exhausted.¹⁹⁸

Increased ICP may be associated with mass effect secondary to unbalanced forces, causing direct, mechanical compressive damage to involved structures. This condition generally necessitates surgical decompression in the operating room. Increased ICP also may result in inadequate perfusion. This condition generally requires medical management in the ICU (Fig. 66.17).

The heart delivers blood at a given mean arterial blood pressure (MABP), the systemic perfusion pressure, to the base of the skull. The blood pressure then has to overcome whatever pressure is inside the head for blood flow to get in, and whatever is left over will be the pressure that perfuses the brain—that is, cerebral perfusion pressure (CPP). Simple in concept and calculation, CPP is defined as the mean arterial blood pressure minus ICP (CPP = MABP − ICP). It is the physiologic variable that defines the pressure gradient driving cerebral blood flow (CBF) and metabolic delivery and is therefore closely related to ischemia.199,200

Technically, the MABP should be measured as the mean carotid pressure with the arterial line transducer zeroed at the level of the foramen of Monro (as opposed to the right atrium),²⁰¹ but this approach is not common in clinical practice. Normal values generally are considered to be 60 to 80 mm Hg for CPP and approximately 10 mm Hg or less for ICP.

The ultimate cause of secondary injury is typically ischemic, and the fundamental goal in dealing with severe traumatic brain injury is to ensure adequate CBF relative to the metabolic demand of the brain. It is, however, impractical to continuously measure CBF at the bedside. Fortunately, CBF is dependent on CPP—which can easily and continuously be measured at bedside. Therefore, a fundamental management strategy for treating a head-injured patient is to maintain adequate CPP by lowering ICP, accomplished by reducing intracranial volume.

Surgical methods for reducing intracranial volume include evacuating an intracranial hematoma, removing part of the frontal or temporal lobe, and placing a ventriculostomy to drain CSF. Other methods for reducing intracranial volume are applicable in the ICU setting, where management strategies are directed at treating volume in the blood and brain compartments.

Cerebral Blood Volume

In discussing cerebral blood volume, it is useful to divide this topic into the arterial and venous compartments.

Brain Compartment

Another functional volumetric compartment is the brain itself. One of the consequences of traumatic brain injury is an acute increase in total brain water.²⁴⁶

The volume of the brain parenchyma can be affected by therapeutic dehydration induced with the use of osmotic agents. These agents can be used to treat cerebral edema in an effort to remove a pathologic accumulation of fluid. Dehydration also can be used to manipulate the volume status of an otherwise normal but threatened brain compartment in order to emergently manage an increase in ICP as a temporizing measure before surgery, such as with extra-axial hematoma or hydrocephalus. The agents most commonly used to effect these changes are mannitol and hypertonic saline.

Cerebrospinal Fluid Compartment

CSF is produced mostly by the choroid plexus located in the ventricles. CSF flows from the lateral ventricles (first two ventricles) through the foramina of Monro into the third ventricle, and from there the fluid moves through the aqueduct of Sylvius to the fourth ventricle. From the fourth ventricle, CSF moves out of the ventricular system through the foramen of Magendie in the midline and the foramina of Luschka laterally. CSF then enters the subarachnoid space of the brain and spinal cord and circulates around the surface of the cerebellum and brainstem as it comes up through the tentorial hiatus, thus forming the basal cisterns. The clear and colorless fluid migrates over the cerebral hemispheres toward the midline, where, through a semiactive process, it is transported from the subarachnoid space into the superior sagittal sinus.

CSF is made at a continuous rate of approximately 0.3 mL per minute. With a total volume of approximately 150 mL (roughly 10% of intracranial volume), the entire CSF volume is replaced three times a day. A little less than one third of the total volume is in the ventricular system.

In severe head injury, CSF can be displaced out of the intracranial compartment as pressure differences between the superior sagittal sinus and the intracranial compartment increase (see Fig. 66.16). The spinal CSF compartment also is an important physiologic sink, and this contribution of CSF flow to ICP is another justification for nursing traumatic brain-injured patients with the head elevated.³⁰⁰

A standard way of managing the CSF compartment in the trauma patient is by draining CSF through an indwelling ventricular catheter (ventriculostomy). This has proved to be a relatively safe and effective tool in lowering intracranial volume and pressure, although ventricles in younger trauma patients commonly are smaller and harder to access and have less CSF to drain. Ventricular drainage is discussed further in Chapter 17.

Craniectomy

Craniectomy is an alternative to the medical and direct surgical methods for reducing intracranial volume. This is a surgical strategy for managing a dangerous increase in intracranial volume by expanding the size of the intracranial compartment. The necessary expansion is accomplished by removing a large portion of the skull and opening the dura (see Fig. 66.13).

Intractable intracranial hypertension despite maximal medical therapy is associated with a high risk of morbidity and death.301–303 In one multicenter trial, an 86% mortality rate was found among patients whose condition failed to respond to an induced pentobarbital coma³⁰⁴—the last line of defense in medical management. Similarly, a significant relationship has been recognized between an ICP higher than 25 mm Hg and a poor outcome.³⁰⁵

Because of these ominous facts, craniectomy to increase the space available for the swollen brain has been used to lower ICP, although early outcome studies of hemicraniectomy yielded poor results.306–308 More contemporary experiences, however, have achieved better results. In 2006, Aarabi and colleagues reviewed 10 reports published since 1988, with a total of 323 patients treated with decompressive craniectomy for posttraumatic brain swelling and intractable intracranial hypertension, and calculated a collective mortality rate of 22.3%, with good outcomes in 48.3%, with the rest of the patients (29.4%) remaining severely disabled or vegetative. These results compared favorably with six previous reports in which the mortality rates ranged from 42% to 100% when ICP greater than 20 mm Hg remained refractory to medical management. Reported complications included subgaleal collections, which resolved over the course of weeks to months; delayed wound healing; bone flap resorption and infections; increased swelling and hemorrhagic contusions; and parenchymal lucencies, possibly due to ischemia.*

In addition to the demonstrated improvement in outcome, contrast-enhanced ultrasonography has been used to assess cerebral perfusion after decompressive craniectomy and found an average fivefold improvement in microvascular blood flow.³¹⁹ A technical point worth emphasizing is that a decompressive craniectomy must be sufficiently large in order to be helpful.³²⁰

Management of Intracranial Hypertension

Acute, severe traumatic brain injury is a dynamic process with the potential for dangerous changes that can evolve over hours to days; therefore, all patients need to be observed closely. Ideally, ongoing assessment by neurologic examination should be at least hourly. In most patients with a GCS score of 8 or less, however, airway protection mechanisms will be impaired, necessitating intubation and, therefore, sedation, which makes an accurate neurologic assessment problematic. An ICP measuring device usually is needed at this point to adequately monitor the patient, in lieu of a reliable examination (see Chapter 16 on ICP monitoring).

The medical management of intracranial hypertension in the ICU generally occurs after surgical decompression of hematomas causing unbalanced forces, or in patients without a surgical lesion. This management strategy generally is divided into tiers of therapy. The first tier is sedation, analgesia, and intubation without hyperventilation, keeping the head elevated and the neck straight and uncompressed. The routine use of paralytics may increase the risk of pulmonary complications; therefore, muscle relaxants should be used for ICP control when sedation is inadequate.³²¹ If ICP exceeds 20 mm Hg³²² despite these maneuvers, moving to the next level of care is indicated, which includes CSF drainage if a ventriculostomy is being used, mannitol, or hypertonic saline. Beyond the first 24 hours, mild hyperventilation to keep Pco₂ in the mid-30s can be used. Throughout the clinical course it also is necessary to maintain an adequate CPP of at least 60 mm Hg by ensuring normovolemia and a safe MABP. If ICP is refractory to these treatments, the next step is use of decompressive hemicraniectomies or barbiturate coma (or both). Historically, surgical decompression has been reserved as a radical, end-of-the-line treatment after the patient has failed to respond to burst suppression barbiturate coma; however, craniectomy is moving up in the treatment algorithm of most centers (Fig. 66.20).

When ICP goes up, it is important to understand why and then try to correct the underlying problem if possible. In any given head-injured patient in whom the brain has lost its buffering capacity, with resultant poor compliance, small increases in intracranial volume can cause a significant rise in pressure. When ICP rises, CPP goes down. This usually will result in a decrease in CVR and vasodilation, with its attendant increase in cerebral blood volume and increase in intracranial volume. This of course leads to a further increase in ICP, and the cycle perpetuates itself. This is the mechanism of a plateau wave.²⁴⁵

In managing these patients, it is critical to try to determine the source of the problem. Perhaps the patient became hypovolemic and the blood pressure dropped, or a ventilator change caused hypercarbia or hypoxia. Maybe the patient is inadequately sedated or having an unrecognized seizure while pharmacologically paralyzed. The problem may be as simple as a high fever or a rigid cervical collar compressing the jugular veins. Whatever is driving this process must be corrected to break this dangerous plateau wave.

If the cause cannot be determined, a new CT scan may need to be taken, and therapeutic maneuvers should be employed to help turn things around, such as increasing sedation, further head elevation, ventricular drainage, administration of mannitol or hypertonic saline, pressors when needed, and brief periods of gentle hyperventilation.

Anticoagulation

It is intuitive that severe coagulopathy is associated with increased mortality after head injury.323–331 Penetrating or blunt brain injury can be associated with the massive release of thromboplastin from neuronal tissue, thereby initiating the coagulation process, which evolves to an exaggerated fibrinolytic response and disseminated intra-vascular coagulopathy (DIC).³²⁴ This brain injury–induced coagulopathy may lead to significant secondary injury and delay the invasive monitoring necessary for the aggressive management of intracranial hypertension.³³² The criteria for the diagnosis of DIC include abnormal clotting studies, thrombocytopenia, low fibrinogen, and, in some cases, elevation in levels of products of fibrinolysis (D-dimer or fibrin degradation products).³²⁷ The DIC caused by head trauma is relatively common and frequently is detected by a prolonged prothrombin time and elevated international normalized ratio (INR). Its presence may be an indication for more intense clinical observation and follow-up CT scanning. An important component of DIC is coagulation; however, in the setting of active bleeding, anticoagulation is not indicated. The therapeutic focus is on hemostasis and replacement of diluted or consumed blood elements and components.^328–329

Typical treatment of coagulopathy consists of fresh frozen plasma (FFP) administration; however, use of FFP can be problematic. This product takes time to administer, so that a relatively large volume of fluid may be given to a head-injured patient when it is important to avoid hypervolemia. Other concerns are the possibility of blood-borne disease transmission and, as reported in a rare case, transfusion-related acute lung injury. Another important issue is the variable effect FFP can have on brain injury–induced coagulopathy, such that it ultimately may fail to correct the coagulopathy.

Preliminary data indicate that recombinant activated factor VII (rFVIIa) provides a rapid and successful correction of coagulopathy in head-injured patients.³²⁶ Originally developed for the treatment of hemophiliacs, rFVIIa also may be helpful in reversing the effects of anticoagulants and antiplatelet drugs.^{326,330–340} It is a vitamin K–dependent glycoprotein, similar to the human plasma-derived factor VIIa, which appears to promote hemostasis by activating the extrinsic pathway of the coagulation cascade.³⁴¹ Its mechanism of action is not fully understood but includes interaction with platelets or tissue factor to augment thrombin generation and platelet activation.^{330,332,334,335} Factor VIIa seems to be the bottleneck, the critical factor most depleted when patients are profoundly anticoagulated.³⁴² The use of rFVIIa to correct a coagulopathy before neurosurgical intervention was reported in 1998 in a hemophiliac patient with an EDH requiring craniotomy for evacuation.³⁴³ Although not specifically evaluated for use in DIC, rFVIIa has been administered to neurosurgical patients in whom DIC was likely to be present.^329,338 Recombinant FVIIa has been used in the absence of hemophilia for neurosurgical emergencies such as EDH and SDH, SAH and intracerebral hemorrhage, tumor resection, and during placement of ICP monitors.^{333,336,338,340} A retrospective study found improved outcomes, without complications, when rFVIIa was used for coagulopathic patients requiring urgent neurosurgical intervention.³⁴⁴ The incidence of thrombosis after rFVIIa is low, but thrombosis is an extremely important potential complication^{334,338,339,345,346} and of particular concern in DIC.³²⁸ Precise dosing for conditions other than hemophilia has not been confirmed³³²; the Food and Drug Administration (FDA) has approved rFVIIa only for use in hemophilia; other uses are considered off-label.

In addition to the coagulopathy induced by a brain injury, neurosurgeons and intensivists often are faced with managing patients with traumatic intracranial hemorrhage who are pharmacologically anticoagulated. The use of these drugs is expected to increase as the population ages.³²⁹ These patients must have normal coagulation rapidly restored to prevent further bleeding and to make surgical intervention possible. One of the more common drugs encountered in clinical practice is warfarin; a typical scenario is one in which an elderly patient on warfarin sodium (Coumadin) falls and hits her head. It takes about 4 days to normalize coagulation if warfarin is stopped. With vitamin K, full reversal begins 4 to 6 hours after administration and takes about 24 hours to lower the INR. FFP contains vitamin K–dependent factors, is rapidly effective, and is given intravenously. Recombinant factor VIIa also can be used to normalize coagulation in these patients.^{329,336,347,348}

In hospitalized patients on heparin, reversal occurs approximately 60 minutes after an intravenous infusion is stopped. If it needs to be reversed faster, protamine is recommended. Desmopressin also has been recommended to reverse the effects of heparin. Subcutaneous heparin is usually not reversed.³²⁹

With low-molecular-weight heparin (LMWH), a partial thromboplastin time (PTT) is variably altered and not a reliable measure of its effect. Reversal of LMWH effect with protamine is variable in humans.³²⁹

A common situation is the presentation of a head-injured patient on an antiplatelet agent such as aspirin or other nonsteroidal anti-inflammatory drug (NSAID). Acetylsalicylic acid (ASA) inhibits platelet aggregation for the life of the affected platelet, which is approximately 10 days. This occurs even at the lowest dose of 81 mg per day. A period of 5 to 6 days typically is needed after stopping aspirin to replace approximately half of the circulating platelets (10% per 24 hours). The effect of ASA on platelets is complete and irreversible. If treatment is necessary, platelet transfusion is given to provide unaffected platelets as long as no ASA remains in the circulation. Desmopressin (DDAVP) may secondarily improve platelet adhesion to endothelial defects and is therefore also recommended to overcome aspirin-induced platelet dysfunction. Other NSAIDs have various anticoagulant effects. If significant NSAID use has occurred before a neurosurgical emergency, the same interventional strategy may apply. Data confirming efficacy in counteracting an anticoagulant effect, however, are not available.³²⁹

Other antiplatelet agents include adenosine diphosphate (ADP) and glycoprotein receptor-blocking agents. Clopidogrel and ticlopidine irreversibly alter platelet aggregation349–352 through a mechanism that is additive to the antiplatelet effects of aspirin. The platelets are permanently affected; once the drug is stopped, recovery of normal platelet function requires about a week until new platelets are produced. Rapid correction requires platelet transfusion, and DDAVP also may have a beneficial, short-term effect.³²⁹

Abciximab, eptifibatide, and tirofiban are highly effective in generating 80% to 95% reversible inhibition in platelet aggregation.349,350,352–355 Stopping the medication allows return of normal platelet function in approximately 48 hours for abciximab and in 4 to 8 hours for the others. Platelet transfusion increases the proportion of unaffected platelets and is the primary intervention.³²⁹

Fibrinolytic and thrombolytic agents disrupt formed clots.355–357 These drugs have a prolonged half-life and frequently are used in combination with heparin or other agents to ensure continued therapeutic anticoagulation. Because circulating fibrinogen is decreased during thrombolysis, cryoprecipitate, a source of concentrated fibrinogen, is the basis for reversing treatment.³²⁹ Although these agents have well-recognized applications for cardiac³⁵⁸ and neurologic^359,360 problems, their use generally is not seen in patients presenting with head injury.

Hypothermia also is known to cause and worsen coagulation abnormalities,332,361 the treatment for which is rewarming. Certain medical conditions also may affect coagulation, and therefore may be important as underlying factors in patients with a head injury. DDAVP increases the release of factor VIII and von Willebrand factor and is used to treat mild hemophilia A, von Willebrand disease, and chronic renal and liver disease, as well as acquired and congenital platelet disorders.^{361,362–365}

DDAVP has a significant antidiuretic effect and will increase free water reabsorption in the kidney, potentially leading to overhydration and hyponatremia. This may cause serious problems in a severely head-injured patient with cerebral edema, poor compliance, and high ICP.

Unintended, iatrogenic worsening of coagulopathy may result with use of hetastarch solutions, which may be administered to increase intravascular volume. These solutions may lower von Willebrand factor levels and alter platelet function. Low-molecular-weight hetastarch preparations are available that may cause less severe changes; however, if the patient requires correction of a coagulation abnormality, these solutions should be avoided if possible.365–368

Nutritional Support

Replacement of 140% of resting metabolic expenditure in nonparalyzed patients and 100% resting metabolic expenditure in paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as protein by the seventh day after injury is recommended.3,369

Role of Steroid Therapy

On the basis of class 1 evidence originating from a prospective randomized trial comparing dexamethasone and placebo in 300 head-injured patients, dexamethasone was found to be ineffective in improving outcome or reducing ICP in patients with severe brain injury.3,312 Methylprednisolone, when given in high doses to moderate and severe head-injured patients, is associated with increased mortality.³⁷⁰ Therefore, the use of steroids is not recommended in their management.

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