Chapter 19: Traumatic Brain Injury

The exact number of people who sustain TBI is unknown since some patients with severe systemic injuries do not survive long enough to undergo a thorough evaluation that would uncover the presence of brain injury. At the other end of the spectrum, many individuals suffering mild or moderate TBI choose not to seek medical care.

Many epidemiologic studies include only those TBI patients who receive medical care in an emergency department. By this criterion, approximately 1.4 million people per year suffer TBI in the United States. Approximately 1.1 million are treated and released, 240,000 are hospitalized, and 50,000 die.¹

Common causes of TBI include falls, motor vehicle collisions (MVCs), pedestrian impact, and assault. TBI has a bimodal age distribution, with the greatest risk in 0–4 and 15- to 19-year-olds. Falls predominate at the extremes of age, whereas MVCs are most common in teenagers and young adults. The incidence in males is 1.5-fold higher than in females. The youngest patients are often the victim of abuse and cannot protect themselves. Military personnel comprise a statistically small number of the overall volume of TBI patients, but combat operations cause them to have a higher incidence of penetrating and blast injuries.

TYPES OF INJURY

Classification and Management

Primary versus Secondary Injury

TBI is a dynamic process. Management priorities for a given patient may change rapidly as his or her underlying pathophysiology changes. Primary injuries result directly from the forces imparted at the time of the accident. These may include both focal disruption of tissue, such as contusions and hematomas, and diffusely distributed damage.

Secondary insults are defined as those occurring subsequent to the initial impact. These injuries may include hypoxemia, ischemia, seizures, fever, hypoglycemia, and other systemic (non-neurologic) events that can directly impact the brain’s ability to respond to a primary insult. A brief period of mild hypotension or hypoxia may be tolerated quite well by an uninjured brain, but the same minimal secondary insult can be devastating if it occurs soon after a brain injury. A neurosurgeon may spend several hours operating on an acutely injured patient, but the biggest determinant of outcome may be the management that the patient receives in the intensive care unit (ICU) in the days and weeks after admission.

Closed versus Penetrating Injury

Closed injuries are those in which the overlying scalp remains intact.

Penetrating Nonmissile Injury

Penetrating injuries to the central nervous system are generally considered to be of low velocity when caused by such objects as knives, arrows, lawn darts, and ice picks. High-velocity injuries are caused by missile-type projectiles. If an object is still embedded and protruding, great care should be taken to stabilize it during transport and evaluation. Physical examination should describe any visible wounds, but labeling these as “entry” or “exit” wounds is best avoided until all information is available, including results of detailed imaging studies. Clipping or shaving hair may be required for a complete assessment. Control of vigorous scalp hemorrhage may require suturing or tight wrapping of scalp wounds, which can bleed profusely.

Assessment and resuscitation proceed as in other types of TBI. Computed tomography (CT) scanning should be performed to localize any intracranial projectiles or indriven bone fragments and to characterize the extent of injury. If a foreign body has passed near the location of any major vessels, catheter angiography should be considered once more urgent evaluation and stabilization have been performed.

Evaluation, planning, and operative setup should be undertaken with the foreign body still embedded, and removal should proceed only in the operating room (Fig. 19-1). To help plan the removal, a similar or identical object may be useful to have on hand as a reference. Antibiotics and prophylactic anticonvulsants are usually administered.

FIGURE 19-1

CT scan showing ping-pong skull fracture. The multiple nondisplaced linear lucencies are normal calvarial sutures.

Penetrating Missile Injury

Gunshot wounds to the head (GSWH) make up the majority of penetrating cranial injuries. In some parts of the United States, GSWHs are the most common form of TBI. Some studies report an overall mortality rate greater than 90% if on-scene deaths are included, with a mortality rate exceeding 50% among those who are alive upon presentation to a hospital.

Traditionally, GSWH have been divided into those from high-muzzle-velocity rounds (approximately 750–1000 m/s, such as hunting rifles and military weapons) and those from low-muzzle-velocity rounds (approximately 200–500 m/s, as seen in most handguns). With escalating civilian firepower, however, these distinctions are becoming blurred. The above velocities reflect measurements taken as the projectile leaves the barrel of the weapon. As a bullet covers aerial distance, ricochets off objects, or passes through objects, it loses velocity and kinetic energy.

Primary injuries from gunshot wounds include direct injuries to face and scalp, pressure waves of gaseous combustion from the weapon if it is touching the target or fired at close range, coup and contrecoup injuries from missile impact, and destruction of brain or bone along the primary path of the original bullet or secondary paths created by fragments of bullets and bone. High-velocity projectiles also create secondary cavitation that pushes tissue away from the bullet in a cone of injury many times wider than the projectile itself. The vacuum that follows the cavitation may pull surface debris into the wound, potentially creating a nidus for infection. Some specially designed bullets mushroom, fragment, or tumble in order to increase the width of the destructive path. Projectiles can also ricochet off the inner table of the skull.

Secondary injuries from GSWHs mimic those seen in other types of head trauma and include edema, growth of contusions, disseminated intravascular coagulation (DIC), hemorrhage from vessel disruption, ischemia, infarction, and herniation. Late complications can include abscess or traumatic aneurysm formation, seizures, and migration of fragments of bone, bullet, or other debris.

The decision about whether to take a GSWH patient to the operating room may be difficult since many of these patients have devastating and irrecoverable injuries that will not benefit from surgery. The Glasgow Coma Scale (GCS) score is the most useful piece of information for triaging a GSWH patient.² Patients with GCS scores of 3–4 generally have a poor outcome regardless of CT findings, and for that reason some clinicians do not even obtain CT scans on these patients. Limited treatment is a reasonable course in such cases. Those with a GCS score of 5 are in an indeterminate category. If the GCS score is 6 or higher, most experts would opt for aggressive treatment in the absence of additional significant findings to suggest that a less aggressive course would be preferable. Poor prognostic factors include self-infliction of injuries, the presence of bilaterally fixed and dilated pupils, and the development of coagulopathy. Poor prognosis and high mortality have also been associated with bullet passage across the midline, through the geographic center of the brain, through the ventricles, or across more than one lobe of the brain.³

Basic principles of surgery for GSWH include evacuation of hematomas causing mass effect, meticulous hemostasis, thorough debridement of devitalized tissue and foreign debris, and watertight layered closure to prevent cerebrospinal fluid (CSF) leaks. A “chain of evidence” for forensic purpose should be preserved when bullet fragments are removed.

Diffuse Injury

Diffuse Axonal Injury

Diffuse axonal injury (DAI) refers to axonal damage that is caused largely by rotational and other mechanical forces. Mild cases result in axonal stretching and transient neuronal dysfunction. More severe cases may set into motion a complex series of cellular events that cause focal impairment of axoplasmic transport, culminating in axonal disconnection at the site of impairment. In humans, this sequence of events may occur over the course of roughly 6–12 hours, suggesting that a yet-to-be-developed therapeutic intervention might be administered within this time frame. More severe traumatic forces may cause direct mechanical disruption of tissue and immediate disconnection of axons. Subsequent axonal sprouting and attempts to re-establish connectivity may go awry when aberrant neural pathways are created, potentially contributing to the morbidity of severe brain injury. The development of DAI does not require direct impact to the head. It may result from rapid noncontact acceleration or deceleration in a linear or rotational fashion.⁴

Histologically, DAI-associated lesions are usually microscopic in size and nonhemorrhagic in composition. CT scans may be normal or may show hyperdense petechial hemorrhages. T2-weighted magnetic resonance imaging (MRI) scans may show multifocal hyperintense lesions at gray matter/white matter interfaces, especially in the frontal lobes, corpus callosum, and brainstem. When hemorrhagic DAI is visible on CT or MRI scanning, one must assume that the radiologically visible lesions are just the tip of the iceberg and that more widespread DAI exists.

Injury severity parallels the amount of force required to cause DAI. Prognosis worsens with increasing number of lesions or as lesion depth progresses from the cortex to corpus callosum to brainstem.

Blast Injury

Military personnel are at much higher risk than civilians for blast traumatic brain injury (bTBI). Brain injury accounts for approximately 20% of all combat-related injuries in modern wars,^5,6 including Operation Enduring Freedom in Afghanistan and Operation Iraqi Freedom. In these two conflicts, bTBI was frequently caused by improvised explosive devices (IEDs). Modern helmets, body armor, rapid transport of injured personnel, and forward-based field hospitals have provided unprecedented rates of warfighter survival and have allowed for a better understanding of the effects of bTBI.

bTBI may be composed of four distinct types of injuries that often overlap. Primary blast injury occurs from overpressure. This has long been known to contribute to injuries in air-filled organs, such as the lungs, bowel, and middle ear. The potential contribution of overpressure to brain injury is currently the focus of much study. Secondary blast injury results from penetration of objects that are set into motion by the explosion. Tertiary blast injury results from a patient being thrown and striking the ground or other object. Quaternary blast injury refers to additional factors not included above, such as heat, toxic fumes and inhalational injury, or hypoxia. Blast injuries in an enclosed space produce an enhanced and complex pattern of forces as energy reflects off walls and objects to impact the head and body at multiple angles and to multiple degrees.

bTBI often includes closed and penetrating TBI components, and many of these patients also have additional serious injuries, such as traumatic limb amputations or hemorrhagic shock. This combination of factors makes it difficult to assess the true contribution of primary or quaternary blast effects on patients who present with TBI after an explosion. In milder cases, combatants may not recognize that they suffer delayed effects of bTBI, or they may knowingly hide their deficits in hopes of remaining with their combat unit.

bTBI can cause headache, confusion, amnesia, altered mental status, and other symptoms associated with concussions. Postconcussive symptoms may be difficult to differentiate from post-traumatic stress disorder, which often coexists with TBI.

Severe bTBI may cause hyperemia and severe cerebral edema early after injury, often requiring decompressive craniotomy. Higher rates of traumatic pseudoaneurysm formation and vasospasm are seen in comparison to civilian closed and penetrating TBI. These vascular pathologies may require more frequent endovascular or open vascular repair.⁷

Concussion

Concussion is the mildest form of mild traumatic brain injury (mTBI). It may be defined as a usually transient alteration of neurological function caused by nonpenetrating injury to the brain and characterized by normal imaging studies. Classic symptoms of concussion include headache, irritability, confusion, amnesia, nausea, vomiting, memory problems, difficulty concentrating, vertigo, alterations of balance, anorexia, insomnia, hypersomnolence, impaired coordination, anxiety, and depression. As many as 90% of concussed patients exhibit no loss of consciousness, and when this does occur, it is usually brief. Grading the severity of concussion is currently not recommended because the grading systems that have been described to date have not been shown to correlate with outcome, treatment recommendations, or duration of symptoms.

By definition, CT scanning is unremarkable in these patients. MRI may reveal abnormalities in up to 25% of cases in which CT scans are normal.⁸ Pathologic specimens show no gross or microscopic parenchymal abnormalities in patients who have suffered a single concussion.

“Second impact syndrome” is a rare but potentially catastrophic sequela of concussion. It is seen most commonly in children and teenagers. These patients are still recovering from the effects of a concussion when they suffer a second one. Within minutes, the patient develops cerebral vascular engorgement, possibly from impairment of cerebral autoregulation caused by the first concussion. Neurological deterioration quickly follows, usually culminating in cerebral herniation and death.

Most important for the treatment of concussion is the recognition of injury. Signs of concussion might be so subtle that they do not prompt the patient or family to seek medical attention. However, returning while still symptomatic to an activity that carries a risk of another concussion, such as contact sports, can be disastrous. All experts agree that a symptomatic player should not return to play until he or she has fully recovered.

Abusive Head Trauma

Nonaccidental trauma (NAT) is traumatic injury that is deliberately inflicted on infants and children. The concept was first described in infants as an injury triad consisting of long bone metaphyseal fractures, subdural hematomas (SDHs), and retinal hemorrhages⁹ and has become known in common parlance as “whiplash shaken infant syndrome” or “shaken baby syndrome.”¹⁰ Even though it is almost certainly underreported, it is nevertheless recognized as the primary etiology of brain injury death in children less than 2 years of age.

Some medical professionals find management of these cases to be difficult due to awkward discussions with the child’s parents, emotional attachment to the children, frequent lack of accurate information, rarity of admissions of guilt from perpetrators, and the medicolegal implications of child abuse accusations. However, a heightened level of suspicion must be maintained since missed recognition of NAT returns the child to a harmful environment, almost always results in continuation or escalation of the abuse, and may result in the patient’s death.

The two most commonly provided histories are trivial blunt trauma such as a short-height fall from bed or low surface, or complete denial of any history of trauma. Except for the rare epidural hematoma (EDH) with middle meningeal arterial bleeding, low-height falls (head-to-impact distance less than three feet) do not result in life-threatening brain injuries.^11,12 In the absence of a history of trauma, the existence of NAT may be indicated by feeding difficulty, emesis, lethargy, irritability, abnormal movements, seizures, unresponsiveness, or apnea.

On imaging studies, NAT may appear as multiple brain injuries that are more severe than expected given the reported history. Injuries may appear to vary in age (some recent, some remote). Impact injuries include skull fractures and superficial scalp lacerations or swelling, in addition to injuries to the underlying brain. There is a high association with other organ injuries. Historically, some fracture patterns have been incorrectly considered suspicious for child abuse. Fractures that are multiple, compound, diastatic, midline, or nonparietal, or that cross suture lines, may denote a greater degree of imparted force, but they are not pathognomonic for NAT.

A shaking mechanism can result in diffusely distributed SDH. The most frequent hemorrhagic finding is a combination of convexity and interhemispheric SDH, often located posteriorly. Some experts believe interhemispheric SDH has the highest degree of specificity for abuse of any intracranial injury. SDH, subarachnoid hemorrhage (SAH), and retinal hemorrhages are far more commonly seen in abused children than in nonabused children. EDHs can occur, but they are much more commonly associated with accidental injury. Retinal hemorrhages are seen in 65–95% of children with inflicted head injuries and may be unilateral or bilateral. However, severe bilateral retinal hemorrhages are occasionally seen in accidental trauma, usually after major application of force via a well-defined mechanism, such as MVC.

In the appropriate circumstances, practically any pattern of hemorrhage or fracture can result from either accidental or inflicted trauma. However, inflicted injury is the only known illness or condition associated with the combination of acute SDH, skeletal fractures, and severe bilateral retinal hemorrhages. The burden of injury is staggering, with 15–38% overall mortality and 60% mortality if the patient is comatose on presentation. Survivors face a 60–70% likelihood of significant neurological handicap.

Focal Injuries and Their Management

TBI varies widely in both severity and specific subtype. During a single traumatic event, a patient may be subjected to multiple forces that differ in magnitude, direction, and duration. Although the following injuries are discussed individually, it must be remembered that multiple types of injury may, and often do, occur in the same patient. Furthermore, focal and diffuse injuries often coexist. Thus, initial treatment efforts may focus on immediate evacuation of a patient’s large SDH, but associated DAI may have an even greater influence on ultimate neurological outcome.

Skull Fracture

Skull fractures can be categorized by the state of the overlying scalp (closed or open), the number of bone fragments (simple or compound), the relationship of bone fragments to each other (depressed or nondepressed), the widening or entry of a fracture into an existing cranial suture (diastatic), and involvement of the cranial vault or skull base. In general, lower-force impacts like falls from standing will create fractures that tend to be linear, closed, and without dural laceration. Higher-force impacts like motor vehicle accidents, falls from heights, or penetrating trauma are more likely to produce comminuted, open fractures with a greater likelihood of underlying dural or cerebral injury. “Ping-pong” fractures are greenstick-type fractures usually seen in newborns due to the plasticity of the skull (Fig. 19-2). They show a local concavity of the skull, without sharp edges, and usually do not require intervention because the skull remodels during growth, with gradual resolution of the cosmetic deformity.¹³

FIGURE 19-2

CT scan showing growing skull fracture from leptomeningeal cyst in child. Note displaced bone and expansion of CSF-filled soft tissue.

Clinical signs suggestive of the presence of calvarial fractures include gross deformity and palpable step-offs. Basilar skull fractures may show postauricular or periorbital ecchymosis, hemotympanum or laceration of the external auditory canal, and CSF rhinorrhea or otorrhea. Cranial nerve injuries may be seen with fractures of the cribriform plate (CN I, anosmia), optic canal (CN II, visual deficit), and temporal bone (CN VII, facial weakness; or CN VIII, hearing loss). Severe basilar skull fractures may result in pituitary gland or stalk injury and resultant endocrinopathies. Direct injury to vasculature that penetrates the skull base may result in arterial dissection, traumatic aneurysm formation, or traumatic carotid-cavernous sinus fistula formation and resulting cranial neuropathies, chemosis, bruit, and stroke. Fractures of air sinuses or mastoid air cells may result in meningitis, even years after the initial event.

Most skull fractures can be seen on CT scans. Plain films may be superior to CT for discovering linear calvarial fractures parallel to the skull base (in the plane of CT slice acquisition). They can be differentiated from vascular grooves or normal cranial sutures by the characteristics listed in Table 19-1.¹⁴ CT scans provide better visualization of facial and orbital fractures, temporal bone fractures, and pneumocephalus, as well as better detection of air-fluid levels and varying degrees of opacification that may indicate injury to air sinuses and mastoid air cells. Thin-cut bone windows can be reconstructed in coronal and sagittal planes and via three-dimensional surface modeling to aid in fracture characterization and surgical planning. CT angiograms and venograms are useful for assessing fractures involving skull base foramina containing important vasculature, such as the carotid canal and foramen magnum, or fractures that cross major venous sinuses.

TABLE 19-1Differential Diagnosis of Fractures on Skull X-Rays

TABLE 19-1 Differential Diagnosis of Fractures on Skull X-Rays

Linear skull fracture

Vascular groove

Suture line

Density

Course

Branches

Width

Black

Straight

Usually none

Very thin

Gray

Curving

Often branching

Thicker than fracture

Gray

Follows known suture course

Joins other suture lines

Jagged, wide

Fractures must be assessed and treated in concert with management of any underlying brain injury. The following discussion of skull fracture treatment assumes that evaluation has been conducted and appropriate treatment instituted for subdural or epidural hematomas, parenchymal hemorrhages, contusions, and/or cerebral edema, and that clinical criteria do not separately mandate operative intervention for these lesions.

Closed, nondisplaced fractures do not normally require intervention. Open skull fractures may require debridement and careful inspection, along with prophylactic antibiotics. Those with obvious underlying dural laceration or CSF leakage require layered surgical repair to reduce the risks of meningitis or brain herniation through a dural defect. In the pediatric population, laceration of the underlying dura may rarely lead to development of a growing skull fracture (or leptomeningeal cyst) in 0.05–0.6% of skull fractures.¹⁵ Over time, pulsations of the underlying rapidly growing brain widen the dural laceration and fracture line (Fig. 19-3). These are most common in children under 1 year of age, and over 90% occur in children less than 3 years old. Surgical repair includes wide bony exposure to repair the dural edges that often retract beyond the limits of the visible fracture.

FIGURE 19-3

CT scan showing a depressed skull fracture that required surgical elevation and dural repair. The patient also had an underlying brain contusion and presented with a receptive aphasia.

Relative indications for surgical elevation of a depressed skull fracture include depression of more than 8–10 mm or more than the thickness of the adjacent skull (Fig. 19-4), a focal neurological deficit clearly attributable to compression of underlying brain, significant inward intrusion of bone fragments (implying possible dural laceration), and persistence of cosmetic deformity after overlying scalp swelling has subsided. For simple depressed fractures without dural violation, there is no evidence that post-traumatic seizure (PTS) risk¹⁶ or neurological outcome¹⁷ is improved by surgical elevation of the fracture. At least in very young patients, cosmesis may not be improved by surgery because, over time, the growth of the child’s brain induces remodeling of the overlying skull.¹⁷ Fractures that cross a major dural venous sinus may warrant a more conservative approach given the increased risks of bleeding and air embolism that may occur during surgical repair.

FIGURE 19-4

CT scan of acute epidural hematoma. Note the biconvex- or lenticular-shaped hemorrhage. This hematoma was subjacent to a diastatic left lambdoid suture.

Current recommendations support surgical repair of open fractures depressed greater than the thickness of the cranium. Surgery is also supported in the presence of significant intracranial hematoma, depression greater than 1 cm, significant frontal sinus or nasofrontal duct involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination. In the absence of gross contamination, primary bone fragments may be replaced without excessive risk of infection.¹⁸ Nonoperative management may be preferred for management of open depressed cranial fractures if there is no evidence of dural penetration.

Epidural Hematoma

EDH occurs when blood collects in the potential space between the dura and inner table of the skull. Although classically described EDHs arise from arterial bleeding caused by a temporal bone fracture that lacerates the middle meningeal artery, the advent of CT scanning has revealed that many EDHs originate from bleeding of the bony edges of skull fractures. Another common cause is injury to a venous sinus.

On CT scanning, an EDH usually appears as a hyperdense, biconvex (lenticular) mass adjacent to the inner table of the skull (Fig. 19-5). Unless sutural diastasis is present, the EDH is often externally bounded by cranial sutures and may cross the falx or tentorium. Additional associated findings may include SDHs and cerebral contusions. A significant percentage of EDHs managed nonsurgically will demonstrate an increase in size, usually in the first few hours after injury. Some of these lesions may appear in a delayed manner after an initial CT scan failed to reveal their presence.

FIGURE 19-5

CT scan of acute subdural hematoma. Note that the crescentic hemorrhage crosses under the right coronal suture.

The classic clinical presentation of an EDH describes a brief post-traumatic loss of consciousness (LOC) followed by a lucid interval of varying duration, proceeding to obtundation, contralateral hemiparesis, and ipsilateral pupillary dilatation. In reality, however, this sequence of events occurs only rarely. LOC is seen in a small minority of cases. Overall mortality from a unilateral EDH has been reported as 5–12%,¹⁹ with rates increasing in cases of bilateral EDHs, posterior fossa location (25% mortality), and concurrent acute SDH.

Rapid diagnosis and timely intervention are paramount to optimize outcome. Surgical guidelines suggest that an EDH >30 cm³ in volume should be evacuated regardless of GCS score. EDH <30 cm³ in volume and <15 mm of thickness and <5 mm midline shift may be treated conservatively at a neurosurgical center with frequent neurological examinations and serial CT scanning.¹⁸ Relative indications for evacuation of EDHs include the presence of neurological symptoms or maximal hematoma thickness >1 cm. Acute EDH patients in coma (GCS score ≤8) and with anisocoria should undergo surgical evacuation as soon as possible.¹⁸

Posterior fossa injury is rare, comprising <3% of head injuries. However, a disproportionately large proportion of these lesions are EDHs. The limited volume of the posterior fossa and the potential compromise of the brainstem and CSF pathways underscore the importance of rapid evacuation via suboccipital craniectomy.¹⁸ Patients without signs of mass effect or neurological deterioration may be watched conservatively, with serial neurological examinations, CT scans, and a low threshold for surgical intervention.

Subdural Hematoma

SDH occurs when blood collects between the arachnoid and inner dural layers of the meninges. Thus, from a strict anatomic point of view, these are really intradural hematomas. A common cause is traumatic stretching and tearing of cortical bridging veins that cross the subdural space and drain into the dura or into a dural sinus. The force may be applied by direct impact or by indirect linear or rotational motion. Less common etiologies include coagulopathy, subdural dissection of parenchymal hematomas, and rupture of a vascular anomaly into the subdural space. Patients with cerebral atrophy, cranial CSF shunts, and large middle fossa arachnoid cysts are predisposed to SDH because of increased traction on cortical veins. Many patients with acute SDHs also have other significant intracranial lesions.

SDHs are commonly located over the hemispheric convexities and may cover part or all of a hemisphere. Classically, they are crescent-shaped, may cross calvarial suture lines, and layer along the falx or tentorium (Fig. 19-6). Patients may present with symptoms of mass effect or of more diffuse underlying brain injury. Chronic SDH may present more insidiously, with progressively worsening headaches and/or focal deficits.

FIGURE 19-6

CT scan with arrow pointing to a small traumatic subarachnoid hemorrhage in left central sulcus.

The appearance of SDHs evolves over time. On CT scanning, acute SDHs are usually hyperdense, but some may show areas of mixed density if ongoing active bleeding causes hyperacute (and not-yet-clotted blood) to continue to accumulate in the subdural space. Some acute SDHs may be isodense in the presence of coagulopathy, significant anemia, or admixing of blood and CSF. Subacute SDHs are isodense to brain, and chronic SDHs become hypodense. Inward displacement of the gray/white cortical ribbon and cortical vessels may be evident on contrast-enhanced CT scanning. The subdural membranes that often exist with chronic SDHs may appear within 4 days and enhance with contrast administration.²⁰ MRI may show evolving signal intensities that vary with the age of the SDH as blood breakdown products are converted to oxyhemoglobin, deoxyhemoglobin, methemoglobin, and hemosiderin (Table 19-2).

TABLE 19-2Appearance of SDH on CT and MRI

TABLE 19-2 Appearance of SDH on CT and MRI

CT density

MRI T1

MRI T2

Hyperacute (minutes)

Acute (hours to days)

Early subacute (4–7 days)

Late subacute (1–3 weeks)

Chronic (3 weeks to 3 months)

↓

↑/swirl/iso if coagulopathy

—

↓

—

↑

↓

↑

↓

↑

↓

↑/—/↓, hyperdense/isodense/hypodense to brain (CT) or hyperintense/isointense/hypointense (MRI).

SDHs often have worse outcomes when compared to EDHs of similar size. EDHs are frequently of arterial origin and thus present with symptoms quickly, facilitating prompt diagnosis and treatment. In contrast to EDHs, it has been postulated that many SDHs result from higher-magnitude forces, which cause greater damage to the brain and cortical vessels. Because of the venous origins of the bleeding, a SDH may require more time to grow and become symptomatic. The attribution of symptoms to diffuse brain injury has also been postulated to delay diagnosis in some cases until the signs of midline shift and brainstem compression become evident. Mortality associated with SDH can be high and may be related more to the underlying brain injury than to the SDH itself. Mortality rates increase in the elderly and in patients on anticoagulants.²¹

Guidelines propose that an acute SDH with thickness >1 cm or a midline shift >5 mm should be evacuated regardless of GCS score. Comatose patients (GCS score ≤8) with an acute SDH <1 cm in thickness and midline shift <5 mm should undergo SDH evacuation if the GCS decreases by 2 points between the time of injury and hospital admission, if they present with pupils that are asymmetric or fixed and dilated, or if intracranial pressure (ICP) reaches or exceeds 20 mm Hg.¹⁸ A craniotomy to evacuate an acute clot should be performed as soon as possible. Over time, as solid blood clots pass through subacute to chronic stages, they liquefy and may be amenable to drainage via burr holes.

Intracerebral Hematoma and Contusion

Traumatic intracerebral hematomas (TICHs) and contusions may expand rapidly. Worsening perilesional edema and rapid hematoma growth may produce increasing mass effect and neurological deterioration. If patients develop neurological decline referable to an expanding TICH, surgical intervention may be warranted. Surgical decompression is often necessary in patients when TICH volume exceeds 50 cm³ or when patients present with GCS scores of 6–8 with frontal or temporal contusions >20 cm³ in volume with midline shift ≥5 mm and/or cisternal compression on CT scan.¹⁸ Surgical procedures range from localized frontal or temporal craniotomy with resection of underlying focal clot to more extensive craniectomy with duraplasty, evacuation of severely contused brain, and temporal lobectomy.

Subarachnoid Hemorrhage

Subarachnoid blood occupies the space between the pial and arachnoid membranes. Traumatic subarachnoid hemorrhage (tSAH) results from venous tears in the subarachnoid space. The injured vessels are often quite small, and the resulting hemorrhage frequently appears as a thin, diffuse hyperdensity over the sulci and gyri of the cerebral convexity (Fig. 19-7) and as a thin hyperintensity on fluid-attenuated inversion recovery (FLAIR) MRI. It may be confused with FLAIR hyperintensities seen in patients with inflammatory conditions or those breathing 100% oxygen or receiving propofol. The usual convexity location of tSAH distinguishes it from SAH caused by spontaneous rupture of a cerebral aneurysm, in which the blood is usually most prominent in the basilar cisterns and appears thicker on CT scanning. Occasionally, tSAH can have a CT appearance similar to that of aneurysmal SAH, and if a detailed history cannot help distinguish between spontaneous and traumatic SAH, imaging of the vasculature via CT, MR, or catheter angiography may be required. In general, no specific treatment is needed for tSAH, and patient management is dictated by associated injuries.

FIGURE 19-7

Intraoperative photograph of a penetrating intracerebral nail gun injury. The bone flap has been removed and the dura has been opened, showing the nail entering the brain parenchyma.

Vasospasm refers to narrowing or even closure of a vessel. Severe cases may lead to subsequent ischemia or infarction in the associated vascular territory. Although much more common after rupture of a cerebral aneurysm and associated spontaneous SAH, it has also been reported after tSAH, especially in association with blast injury. The classic time course of vasospasm after spontaneous SAH is onset as early as 2 or 3 days after injury, peak incidence from days three to 14, and duration of up to 3 weeks.

Vascular Injury

Post-traumatic stroke may result from injuries to the internal carotid artery (ICA), common carotid artery (CCA), or vertebral artery (VA) in the neck. Rarely, injury may be due to penetrating trauma with direct ICA, CCA, or VA injury. More often, vessel dissection is sustained in motor vehicle accidents, falls, extreme neck rotation, spine fracture, or iatrogenic injury, such as surgery or chiropractic maneuvers.

Traumatic dissection is more common in the ICA, occurs in 0.08–0.4% of blunt trauma patients, and can occur anywhere from a few centimeters above the carotid bifurcation to the skull base. Less frequent is VA dissection, which is seen most commonly at the C1–C2 level. Vessel dissection allows blood to collect between the adventitia and media (pseudoaneurysm formation) or between the intima and media of the vessel wall (luminal stenosis). This intramural hematoma may expand or may propagate, with distal propagation occurring more commonly than proximal.

Spontaneous dissections occur in younger to middle-aged adults; 70% occur between the ages of 35 and 50 years. A much lower proportion occurs in adolescents, and spontaneous dissection is rare in children. Most patients present with headache and neck pain that is often unrelenting. Symptoms and diagnosis may occur hours to weeks after the initial trauma and may include transient ischemic attack or stroke, Horner’s syndrome, and, less often, carotid bruits, pulsatile tinnitus, and lower cranial nerve palsies (CN IX–XII).

On CT scanning, dissection is seen as a linear lucency within an enhancing vessel. This represents the flap separating the true and false vessel lumens. MRI shows a crescentic band surrounding the native flow void. Ultrasound reveals an echogenic intimal flap.

Twenty percent of cases have an associated injury, such as cervical spine injury or silent dissection of another vessel. Treatment often consists of heparin anticoagulation (if not contraindicated by other injuries) followed by longer-term anticoagulation. Balloon angioplasty may be employed in select cases.

CLINICAL ASSESSMENT

Glasgow Coma Scale

The GCS has become the standard for clinical grading of TBI severity.² A patient is scored in three parameters: best motor function (M), best verbalization (V), and best eye opening (E). The sum of these individual scores represents the overall GCS score (Table 19-3). A neurologically intact patient can achieve a maximum score of 15. The most severely injured patients have a total score of 3. If a patient is intubated, the verbal score cannot be assessed. Instead of assigning an arbitrary verbal score in such cases, it is best to note that the verbal score cannot be determined reliably. Because the same GCS score can be derived from different combinations of motor, verbal, and eye opening scores, it is important that practitioners record each of the subscores and not just the overall number.

TABLE 19-3Glasgow Coma Scale (Recommended for Age ≥4)

TABLE 19-3 Glasgow Coma Scale (Recommended for Age ≥4)

Best motor

Best verbal

Best eye opening

6 Obeys

5 Localizes

4 Withdraws

3 Flexes

2 Extends

1 None

Oriented

Confused (fluent speech)

Inappropriate (words)

Incomprehensible (sounds/grunts)

None

Spontaneously

To speech

To pain

None

The GCS allows practitioners to communicate quickly and reliably about a patient’s neurological status. The postresuscitation GCS score is also effective for stratifying patients by injury severity. Patients with GCS scores between 13 and 15 are usually considered to have mild TBI. They are usually awake and have no focal deficits. Patients with GCS scores of 9 to 12 are often described as having moderate TBI. In general, they usually have alterations of sensorium and may have focal deficits. Those with the lowest GCS scores (3–8) have severe TBI. They usually will not follow commands and are often described as comatose.

Factors that may confound the neurological examination must be eliminated. Alcohol and other drugs may depress neurological function, as can hypotension, hypoxia, sepsis, hypothermia, and other systemic factors. Sedating agents and paralytics may also interfere with accurate assessment. Spinal cord injury and long bone fractures can affect the motor component score of the GCS and should be sought if suggested by the mechanism of injury. Hearing deficits, lack of hearing aids, or a language barrier should also be taken into consideration. The pediatric population represents a special group for whom a modified version of the GCS is often used (Table 19-4).²²

TABLE 19-4Glasgow Coma Scale for Children (Recommended for Age <4)

TABLE 19-4 Glasgow Coma Scale for Children (Recommended for Age <4)

Best motor

Best verbal

Best eye opening

6 Obeys

5 Localizes

Smiles, oriented to sound, follows objects, interacts

Crying

Interaction

4 Withdraws

3 Flexes

2 Extends

1 None

Consolable

Inconsistently consolable

Inconsolable

None

Inappropriate

Moaning

Restless

Spontaneously

To speech

To pain

None

Pupils

The pupillary light reflex can be easily and rapidly assessed in the unconscious patient. Damage or hypoperfusion affecting the Edinger–Westphal nucleus in the midbrain, or compression of the third cranial nerve as the uncus (located in the medial temporal lobe) herniates into the tentorial notch from displacement by a space-occupying mass lesion, may result in pupillary dilatation. If these pathological processes are sufficiently severe, the pupil will be fixed in the dilated position, with no constriction in response to bright light. Direct orbital trauma can also cause pupillary dilation and fixation in a sizable minority of cases. It should be considered (quickly) before automatically assuming that a dilated pupil is caused by intracranial hypertension.

To facilitate performance of fundoscopy in patients in coma or with orbital or periorbital trauma, facial fractures, abnormal eye movement, or other pathologies, it may be necessary to instill mydriatics. To avoid confusion, this should only be permitted after concerns regarding elevated ICP have been addressed. Clear notation should be made, in the chart and at the bedside, as to when and which mydriatics have been used and for how long their effect will persist.

Neurological Examination

An accurate neurological examination is essential to determine diagnosis, treatment, and prognosis in TBI patients. The examination may be limited due to a patient’s age, level of education, native language, presence of sedating or paralytic medication, illicit drugs, hypotension, hypoxia, hypothermia, hypoglycemia, or other factors. Examination of the pediatric patient may be further limited by other considerations, including inability to visualize the pupils or fundi of the premature or newborn infant, limited cooperation, inability to understand language, and others.

Monitoring the overall trend of a neurological examination over time is critical. It must be understood that these examinations can and will fluctuate based on a patient’s improving or declining condition, the evolution of disease processes, and the ability of medical personnel to minimize or eliminate sedation and other factors that confound an accurate neurological assessment.

In the uncooperative patient or unconscious patient with severe TBI, the examination may be limited to the GCS, pupillary reactivity, and testing of various reflex actions (Table 19-5). As the patient becomes more alert and cooperative, a more complete neurological examination will provide greater sensitivity for assessment of neurological injury. The extent of the examination must be tailored to the patient’s ability to interact with an examiner.

TABLE 19-5Neurological Examination for Trauma

TABLE 19-5 Neurological Examination for Trauma

Uncooperative patient

Cooperative patient

Level of consciousness

Glasgow coma scale

Orientation

Comprehension, verbalization

Fluency of language

Cranial nerves

Pupil reactivity (ambient and bright light)

Afferent pupillary defect

Facial asymmetry

Visual acuity/visual fields

Funduscopic examination (papilledema, retinal hemorrhage)

Complete cranial nerve examination

Motor

Movement to central and peripheral noxious stimuli (differentiate from flexion-withdrawal spinal reflex)

Resting tone of anal sphincter

Strength assessment of muscle groups in four extremities

Tone of voluntary anal sphincter contraction

Sensory

Grimace/grunt/withdrawal to noxious stimulus

Detailed examination to light touch and pinprick in major dermatomes (C5, C6, C7, C8, T4, T10, L2, L4, L5, S1)

Joint position sense (posterior column function)

Reflexes

Deep tendon reflex

Plantar reflex (Babinski), clonus

Anal wink, bulbocavernosus reflex

Same as in uncooperative patient

Systemic Evaluation

Assessment and treatment of TBI patients often begin in the prehospital setting with input from family, bystanders, and off-duty medical personnel. Care continues with the primary care physician or emergency medical technician (EMT), transfers to the physician in the emergency department, and eventually involves the neurosurgeon and other members of the trauma team. Treatments may be started at any point along a patient’s journey as dictated by recognition of signs of neurological injury and by availability of appropriate medication, equipment, and personnel.

The nervous system does not function in isolation. Patients with TBI often have additional injuries. Treatment specific to TBI is often complementary or adjunctive to treatment of the trauma patient without neurological injury. The basic principles of trauma resuscitation should be followed. These include rapid assessment and maintenance of airway, breathing, and circulation.

A detailed medical and surgical history should be obtained, including the events preceding a trauma, a description of the accident scene, accurate description of the patient’s neurological baseline, and any subsequent changes in neurological status. Long-term medications as well as medications administered in the prehospital setting should be identified. Special attention should be paid to medications with the ability to alter the neurological examination, including sedatives or psychopharmacologics (to restrain a combative patient), paralytics (for intubation or transportation), atropine (for cardiac resuscitation), and other mydriatics (for evaluation of ocular trauma), in addition to the possible presence of alcohol and other recreational drugs.

Primary and secondary surveys should be undertaken to evaluate for systemic injuries. Open scalp lacerations with vigorous hemorrhage may lead to potentially fatal hemorrhagic shock. In the newborn or premature infant, cephalohematoma may allow enough displacement of blood to produce hemodynamic instability. Raccoon’s eyes (periorbital ecchymosis), Battle’s sign (postauricular ecchymosis), or otorrhea or rhinorrhea suggest the presence of a basilar skull fracture. Palpable fractures or depressions may indicate bony injury and a higher likelihood of underlying hemorrhage or parenchymal injury, but significant soft tissue edema is often mistaken for a bony step-off. Periorbital edema or proptosis may suggest local ocular or orbital trauma. Puncture wounds may suggest the existence of a serious penetrating injury to the brain, spinal cord, sympathetic plexus, or vasculature. Bruits of the carotid artery or globe of the eye may represent carotid dissection or carotid-cavernous fistula, respectively. Multiple areas of swelling or bruising may indicate prior seizure activity or repeated syncopal episodes, as well as serially inflicted injuries.

IMAGING

Computed Tomographic Scan and Skull Radiography

Advances in imaging technology have relegated plain x-rays to playing only a very limited role in the contemporary evaluation of trauma patients with potential head or spine injuries. Some clinicians still utilize skull films to identify pneumocephalus, skull fractures, and the tracts of penetrating objects. In the vast majority of cases, however, CT scanning provides more information. Also, it must be remembered that intracranial ricochets of projectiles may occur, and CT is far superior to plain films for characterizing such complex events.

Overwhelmingly, CT scanning has become the preferred initial imaging modality for patients presenting after head trauma. In a single rapid scanning session, and without patient repositioning, scans of the head, neck, chest, abdomen, and pelvis can be performed. From these, cervical, thoracic, and lumbar spine images can be reconstructed without additional radiation exposure. Administration of contrast allows for CT angiography and three-dimensional reconstruction to evaluate vasculature of the head and neck.

Magnetic Resonance Imaging

MRI scans provide higher-resolution images of the brain, spinal cord, and other soft tissues than CT scans. This superior visualization of neural parenchymal tissue is ideal for the evaluation of infarction, ischemia, edema, and DAI. MRI is also helpful for detecting ligamentous injury of the spine as well as spinal cord injury. It is generally performed after the initial trauma evaluation and resuscitation have been completed. Disadvantages of MRI compared to CT scanning include slower image acquisition time, increased cost, restricted access to patients during image acquisition, and the magnet’s incompatibility with ferromagnetic monitoring and supportive equipment that is commonly used in trauma patients. Use of MRI for the initial assessment of trauma is not routinely recommended since CT scanning permits detection of acute hemorrhage and fractures, which are the pathologies of greatest immediate concern in TBI patients.²³

Angiography

When the tract of a penetrating injury passes near known locations of major vessels, or when a delayed intracranial hemorrhage occurs, angiography may be used to look for pseudoaneurysms or other direct injuries to vessels. In prior decades, or even nowadays when CT or MRI scanning is unavailable, angiography could reveal midline shift or other types of vascular displacement indicative of compressive mass lesions that might require immediate intervention.

MANAGEMENT

General Measures

Numerous guidelines based on critical evaluation of the pertinent literature have been created and disseminated. Best-known among these is the Guidelines for the Management of Severe Traumatic Brain Injury.²⁴ Subsequent companion guidelines have been created for prehospital management of TBI,²⁵ pediatric TBI,²⁶ surgical management of TBI,¹⁸ penetrating TBI,²⁷ and field management of combat-related head trauma.²⁸ The reader is referred to these documents for further background about creation of treatment recommendations.

Interventions for TBI may be initiated in series or in parallel. Some treatments can be started in the field. Others may be added as more advanced equipment or qualified personnel become available in the emergency department, operating room, or intensive care unit.

Basic measures should be implemented in all TBI patients undergoing monitoring. These patients often require a setting with the capability for careful assessment of vital signs, fluid balance, and neurological status. Initial goals are normothermia and euvolemia, with administration of isotonic fluids (ie, 0.9% NaCl + 20 mEq KCl/L). Many practitioners avoid dextrose-containing intravenous fluids because of concerns about exacerbating the deleterious effects of potential ischemia and cerebral edema. Patients usually receive prophylaxis against Cushing’s (stress) gastric ulcers, which are frequently seen in patients with severe TBI and elevated ICP. The head of bed is usually elevated to 30°C, the neck should be kept midline, and the fit of the patient’s cervical collar and endotracheal tube stabilizer should be assessed to prevent compression of the jugular veins. Most important is frequent assessment of the patient’s condition, evaluation of responses to therapies, and willingness of providers to modify care strategies in a timely manner to help ensure optimal patient outcome.

Another basic measure is maintenance of hemoglobin concentration (Hgb) above a specified minimum level. Historically, this level has been commonly set at 10 g/dL, which was felt to represent the optimal trade-off between blood viscosity and oxygen-carrying capacity. Numerous reports have questioned the benefit of such a high threshold, and most practitioners came to accept a Hgb as low as 7 g/dL. The question remained whether the exquisite sensitivity of the injured brain to hypoxia made TBI patients a special subgroup in which the traditional higher Hgb level was still required. A prospective trial failed to confirm this hypothesis,²⁹ leading many clinicians to accept the lower Hgb of 7 g/dL as the minimum acceptable value even in TBI patients—assuming, of course, that there exists no other indication to target a higher goal.

Over the past two decades, it has become common to advocate for systematic, evidence-based treatment of TBI patients by dedicated neurosurgeons, neurologists, intensivists, surgical trauma and critical care teams, nurses, and allied health care workers. Several publications claim to demonstrate improved outcomes as a direct result of the arrival of an intensivist to a specific ICU. More likely, however, is that the very process of standardizing care and eliminating unwarranted excessive variation in care was the real driver behind improvement in outcomes compared to historical controls. The exact background or specialty of the clinician driving that standardization is less important.

Blood Pressure and Oxygenation

Medical practitioners cannot undo the events surrounding a primary brain injury. However, every effort must be made to mitigate or eliminate secondary injuries, which may be even more devastating than the primary injury. Prior to, or during, transport to a hospital setting, a significant portion of patients may experience periods of hypoxemia or hypotension.³⁰ These are among the most common and most deleterious secondary insults. Occurrence of a single episode of hypoxemia or hypotension is an independent predictor of worse outcome after TBI.^31,32

Oxygen saturation and blood pressure monitoring should start in the field and continue in the hospital setting. The goal is to prevent hypoxemia and hypotension, or if they occur, to identify and treat them as rapidly as possible. Crystalloid, colloid, blood products, or even intravenous pressors may be required to avoid hypotension.²⁴ Empiric oxygen administration should start as early as possible. Endotracheal intubation may be required. Of interest, several studies have demonstrated worse outcomes in TBI patients who are intubated in the field. One possible reason is that the frequently chaotic prehospital environments surrounding TBI patients and the relative inexperience of some first responders in performing difficult intubations may combine to cause prolonged hypoxemia during attempts at endotracheal intubation. Another factor may be unintentional hyperventilation of intubated patients (and consequent cerebral vasoconstriction and reduction in cerebral blood flow [CBF]) from excessively rapid and forceful squeezing of the bag/valve system if patients are manually ventilated. Consequently, for many TBI patients, careful oxygenation and ventilation via a face mask may be preferred over prehospital endotracheal intubation.

Nutrition

TBI patients usually exhibit an increase in basal energy expenditure (BEE). Patients who are sedated and paralyzed may show BEE increases to 120–130% of baseline. Comatose patients (GCS score ≤8) with isolated TBI may have BEE approximately 140% of baseline (range 120–250%).³³ Mortality is reduced in patients who receive full caloric replacement by 1 week postinjury.³⁴ At least 15% of calories should be supplied as protein. Since it may take 2 or 3 days to ramp up feedings to desired levels, nutritional replacement should begin as soon after injury as possible.

Enteral feeding is preferred over parenteral nutrition because it enhances immunocompetence and reduces risk profile.³⁵ If a patient has diminished gastric motility, a jejunal feeding tube can be placed since patients with severe TBI can tolerate early jejunal feeding even in the presence of gastric dysfunction and limited small bowel activity. Total parenteral nutrition can be considered if enteral feeding is not possible or if higher nitrogen intake is required.

Prophylaxis

Seizures

Post-traumatic seizures (PTS) are potentially harmful in TBI patients for many reasons, including increased ICP and elevated metabolic demand that may exacerbate the effects of ischemia. TBI patients at increased risk for PTS include those with GCS score below 10 and those with depressed skull fractures, cortical contusions or intracranial hemorrhage, and penetrating injury or seizure within 24 hours of brain injury. Anticonvulsants have been shown to effectively reduce the risk of PTS during the first 8 days of injury, but not later.^24,36. Despite absence of high-quality studies showing equivalent efficacy for early PTS prevention, many centers are now using levetiracetam because of ease of administration and a perceived lower rate of adverse reactions.

Infection

Trauma patients may develop infections from grossly contaminated wounds, from immunosuppression following the stress of severe trauma or other causes, or from such necessary interventions as open surgical procedures, intubation for mechanical ventilation, and use of invasive monitoring equipment, as well as other causes. In general, antibiotic coverage should be targeted toward specific organisms and stopped as soon as possible to minimize the risk of development of drug-resistant strains of bacteria or alterations in normal floral patterns.

Perioperative antibiotics are generally recommended only for a single dose preoperatively or at most for the first 24 hours after surgery. This same principle applies to insertion of external ventricular drains (EVDs). Maintaining patients on prophylactic antibiotics for the entire period that an EVD is in place is not recommended. Routine flushing or exchange of ventricular catheters is also not recommended.²⁴ Use of antibiotic-impregnated or coated ventriculostomy catheters may result in an overall decrease in infection rate.³⁷

Hemorrhage

Most critically ill trauma patients have decreased levels of plasma antithrombin (AT) activity. TBI patients, however, tend to have increased rates of coagulopathy, with supranormal AT activity that can progress to disseminated intravascular coagulation and fibrinolysis (DICF), as well as expansion of existing cerebral contusions and delayed development of additional hemorrhages.³⁸ Coagulopathy may be especially severe after penetrating brain injury.

For all trauma patients, medical history and review of systems should specifically inquire about history of excessive bleeding or clot formation, use of specific antiplatelet or anticoagulant medication (such as aspirin, warfarin, or low-molecular-weight heparin), medications that have antiplatelet compounds as a component, and medical disorders that pose an increased risk of bleeding. Measurements of prothrombin time, activated partial thromboplastin time, international normalized ratio, platelet count, and possibly bleeding time, platelet function assay, or thromboelastography are often helpful in guiding the management of hemorrhage.

Effects of warfarin anticoagulation may be reversed by administration of vitamin K, fresh frozen plasma, or prothrombin complex concentrate; effects of heparin may be reversed with protamine sulfate; and thrombocytopenia or platelet dysfunction may be treated with donor platelet transfusion. Unfortunately, these interventions require time for preparation and administration, which may limit their usefulness in patients with life-threatening intracranial hemorrhage and rising ICP.

Recombinant activated coagulation factor VII (rFVIIa) rapidly forms a complex with tissue factor to produce thrombin and, separately, converts factor X to its active form, factor Xa, resulting in a “thrombin burst” at the site of tissue damage. It is FDA-approved for use in hemophiliacs and in patients with antibodies to factor VIII or IX, and it has been studied off-label in intracerebral hemorrhage and TBI patients requiring rapid craniotomy in the face of coagulopathy. Its effects on neurological outcome and mortality, as well as its cost burden, are currently under investigation and have not been fully defined.³⁹

Deep Venous Thrombosis

Trauma patients in general, and TBI patients in particular, are at risk for venous thromboembolic complications like deep venous thrombosis (DVT) and pulmonary embolus (PE). Risk factors for DVT and PE include stroke or spinal cord injury, prolonged surgery or prolonged bed rest, SAH or TBI causing altered coagulation or dehydration, and increased blood viscosity from cerebral salt wasting and treatment of cerebral edema.⁴⁰ Low-risk, prophylactic measures against DVT include passive range of motion, early ambulation, rotating beds, and electrical stimulation of calf muscles. If DVTs are not already present, pneumatic compression boots (PCBs) and sequential compression devices may be safely used and can reduce the incidence of DVT and PE.

Pharmacologic anticoagulation can increase the effectiveness of DVT prophylaxis, but with the risk of additional hemorrhagic complications. Low-molecular-weight heparins have a higher ratio of anti-factor Xa to anti-factor IIa activity versus unfractionated heparin, have greater bioavailability after subcutaneous injection, and have more predictability in terms of plasma levels. They can be added to use of PCBs without significantly increased risk of hemorrhage,⁴¹ and their use has been recommended in postoperative neurosurgery patients.²⁴ Because there are no universally accepted recommendations for the method and timing of postoperative anticoagulation, this decision should be tailored individually to each patient. One study reported no increased incidence of hemorrhagic complications if full anticoagulation was resumed 3 days after craniotomy.²¹

Cerebral Metabolism and Pathophysiology

Intracranial Pressure

To understand the rationale behind ICP management, one must start with understanding how pressure in the intracranial space differs from that in other body compartments. If a patient sustains an injury to an arm or leg, the surrounding soft tissue may expand outwards from the humerus or femur. By contrast, in cases of TBI, the brain is unable to expand because it is confined within the rigid skull.

The modified Monro–Kellie hypothesis assumes that the skull is completely inelastic, that the ventricular space is confluent, and that pressures are equally and readily transmitted throughout the intracranial space. This hypothesis states that there is a balance between the brain, intravascular blood, and CSF contained in the intracranial space. Increases in the volume of one constituent (eg, cerebral edema, hyperemia) or addition of new components (eg, tumor, hemorrhage) mandate compensatory decreases in other constituents in order to maintain constant ICP.

Mildly increased localized pressure in part of the brain may cause neurological dysfunction confined to the affected area. More severe increases in pressure may cause local tissue compression as well as shift of intracranial structures, subfalcine and transtentorial herniation, and both local and distant neurological dysfunction. In the most severe cases, transtentorial herniation causes compression at the level of the brainstem, with direct tissue damage to the midbrain, occlusion of arteries, infarction, and death.

Normal ICP varies by age. Normal values probably lie below 10–15 mm Hg in adults and older children and in the range of 3–7 mm Hg in younger children, 1.5–6 mm Hg in infants, and possibly even at subatmospheric levels in neonates. Intracranial hypertension (IC-HTN) has been reported in 13% of trauma patients with a normal head CT, 60% of patients with an abnormal head CT (demonstrating hemorrhage, contusion, edema, herniation, or compressed basal cisterns), and ~60% of patients with a normal head CT plus two or more of the following criteria: age > 40 years, SBP > 90 mm Hg, and unilateral or bilateral abnormal motor posturing (flexing or extending to a noxious stimulus).⁴² Therefore, ICP monitoring is often recommended in patients with severe TBI (GCS score of 3–8) and an abnormal CT scan or with severe TBI, a normal CT scan, and two or more of the select criteria listed earlier. ICP monitoring may also be considered in patients in whom a reliable neurological examination cannot be performed because of sedatives, paralytics, or general anesthesia required for other reasons, such as difficult ventilator management, extreme agitation, or need for non-neurological surgery.

Higher mortality and worse outcomes have been described in patients with ICP persistently above 20 mm Hg.⁴³ Therefore, most centers consider ICP to be elevated when it exceeds 20–25 mm Hg, and ICP reduction measures are often recommended to bring values below this range.²⁴

Monitoring of ICP

The most accurate, reliable, and lowest-cost ICP monitoring technology is the fluid-coupled ventriculostomy catheter, or EVD, connected to an external strain gauge.²⁴ Another advantage of EVDs is that CSF drainage can be performed as a therapeutic measure to control ICP. Parenchymal ICP monitors based on fiberoptics or miniaturized strain gauge transduction require less tissue penetration and do not require the ability to localize the ventricle. They are roughly as accurate as EVDs but carry a higher cost. They cannot be recalibrated in situ and may be subject to measurement drift, although this is currently not as significant a concern as it was with earlier versions of these monitors. Parenchymal monitors do not allow for therapeutic drainage of CSF. Placement of these devices in the subdural or epidural spaces renders their data less accurate.

Of interest, a recent prospective trial found no difference in outcome between severe TBI patients managed with ICP monitoring and patients in whom elevated ICP was inferred and treated based on clinical and imaging findings.⁴⁴ This trial is often incorrectly interpreted as indicating that ICP monitoring is of no benefit in severe TBI patients. A more appropriate interpretation is that ICP was monitored, and elevated ICP was treated, in both groups, with the difference being invasive monitoring versus noninvasive monitoring based on examination and imaging. This trial did not compare a monitored to an unmonitored group.

Cerebral Perfusion Pressure

The recently injured brain is highly vulnerable to ischemia both regionally, near contused or otherwise damaged tissue, and also globally, from more diffuse impairment of CBF regulation. In addition, brief periods of hypotension or hypoxia that might be well-tolerated by an uninjured brain may have significant deleterious consequences in a brain that has just received a traumatic insult. Neurological dysfunction may result from direct disruption of tissue or from impaired metabolism of a structurally intact brain. For neural tissue to function normally, CBF must be adequate to meet metabolic demand. CBF depends on cerebral perfusion pressure (CPP), calculated by subtracting ICP from mean arterial pressure (MAP – ICP). Studies have shown that the injured adult brain is more susceptible to ischemia if the CPP trends below 50 mm Hg.⁴⁵ Children have been demonstrated to show improved survival when CPP is sustained above 40 mm Hg.⁴⁶ In adults, artificially maintaining CPP above 70 mm Hg results in unacceptably higher rates of adult respiratory distress syndrome without significant improvement in functional outcome.^47,48 Collectively, these data suggest that there exists a “floor” below which CPP should not drop (the exact value varies with age), but above this floor, there is no benefit from driving CPP to higher levels. There is likely an age-dependent continuum of optimal CPP values. Current recommendations support avoidance of CPP <40 mm Hg in children, <50 mm Hg in adults, and artificial elevation >70 mm Hg in either population.²⁴

Monitoring of Cerebral Blood Flow and Metabolism

CT perfusion scanning can measure relative cerebral blood volume, CBF, and mean transit time after injection of iodinated contrast. It has been used extensively in stroke patients and has been investigated in TBI patients to determine the potential viability of contusional and pericontusional tissue, and also to help guide judicious use of other therapeutic strategies, such as hyperventilation (HV).

Intermittent measurements of cerebral arteriovenous difference in oxygen content or of oxygen saturation in the jugular bulb (S_jvO₂) can also be used to assess global cerebral perfusion. Normal venous saturation of oxygen is approximately 50–69%. The occurrence of multiple episodes of venous desaturation (<50%) or of a sustained and profound single such episode is associated with poor outcome.⁴⁹ In addition, excessively high S_jvO₂ (>75%) is associated with poor outcome, perhaps because such measurements reflect cerebral hyperemia or possibly the existence of significant areas of infarcted tissue which will not extract oxygen.

More focal techniques to measure CBF include transcranial Doppler ultrasonography and parenchymal CBF monitoring. Thermal diffusion probes provide local CBF measurements based on the temperature difference between two points on a probe, the relative conductive properties of cerebral tissue, and convective properties of blood flow.

Cerebral microdialysis requires intraparenchymal placement of a fine catheter. Specific chemicals diffuse into dialysate through a semipermeable membrane at or near the tip of these catheters. The dialysate is collected and subsequently analyzed. Neurochemical changes indicative of primary and secondary brain injury may be detected. TBI patients with poor clinical outcome have been shown to have elevated levels of specific neurotransmitters, as well as elevated lactate/pyruvate ratios and abnormal lactate and glutamate levels.

Brain tissue oxygen tension (P_btO₂) monitoring allows direct measurement of oxygen level in a specific region of the brain. In most cases, P_btO₂ mirrors oxygen delivery, but it may also increase if the tissue surrounding the catheter is infarcted and incapable of metabolizing oxygen. Normal P_btO₂ has been reported as approximately 32 mm Hg. Patients with multiple or prolonged episodes of P_btO₂ below 10–15 mm Hg have been shown to have increased morbidity and mortality.⁵⁰ Probes are often placed in penumbral tissue that is thought to be “at risk” but still salvageable. Others prefer to place such probes in brain that appears “normal,” with the thought that monitors in this area provide data about global cerebral metabolism, as opposed to the local metabolic environment near a contusion or other visible lesion.

Therapies are commonly targeted to keep S_jvO₂ above 50% and P_btO₂ above 15 mm Hg or higher.²⁴ A multicenter trial is currently testing the value of this approach. At the present time, S_jvO₂ and P_btO₂ monitoring are best viewed as adjuncts to ICP and CPP monitoring.

Management of Elevated ICP

Analgesics and Sedatives

TBI patients will likely have increased levels of stress, agitation, and discomfort. These may cause increases in sympathetic tone, temperature, and blood pressure and produced increased ICP, metabolic demand, and resistance to controlled ventilation.

The medications used to treat pain and agitation and their doses must be carefully monitored and administered to achieve a balance between their beneficial effects in reducing pain and anxiety and their potentially adverse effects of hypotension, alteration or masking of the neurological examination, and rebound ICP elevation when they are discontinued. If heavy sedation or pharmacological paralysis is needed and a neurological examination becomes unobtainable, consideration should be given to placement of an ICP monitor.

Short-acting agents are preferred in order to facilitate frequent neurological examinations. Continuous infusion is often used instead of bolus administration to avoid potential transient ICP increases between doses. Fentanyl and its derivatives (remifentanil and sufentanil) are used increasingly for both acute and longer-term analgesia. They are short-acting, reversible, and suitable for administration by continuous infusion.

Midazolam and propofol are two commonly used sedatives. Midazolam is a short-acting benzodiazepine that is effective for sedation of the ventilated TBI patient. Propofol is a hypnotic anesthetic with rapid onset and a very short half-life that facilitates rapid neurological assessment. It should be limited in both concentration and duration to avoid propofol infusion syndrome.⁵¹ First described in children, and later in adults, this syndrome has generally been reported after use of excessively high doses or extensive durations of use of propofol. Features can include hyperkalemia, hepatomegaly, metabolic acidosis, rhabdomyolysis, renal failure, and death. Caution should be exercised if doses exceed 5 mg/kg/h or if duration of treatment exceeds 48 hours.

Hyperosmolar Therapy

While the exact mechanism of mannitol’s beneficial effects is unclear, two primary actions have been postulated. In the first few minutes, it produces immediate plasma expansion with reduced hematocrit and blood viscosity, improved rheology, and increased CBF and O₂ delivery. This reduces ICP and is most notable in patients with CPP below 70 mm Hg.^52,53 Over the next 15–30 minutes, and perhaps lasting 90 minutes to 6 hours, mannitol creates an osmotic gradient, with increased serum tonicity and withdrawal of edema fluid from the cerebral parenchyma.

When given as a bolus, mannitol begins to reduce ICP after 1–5 minutes. This effect peaks at 20–60 minutes. For acute ICP reduction in cases of neurological worsening or herniation, an initial bolus of mannitol is often given at 1 g/kg, with subsequent administration at smaller doses and longer intervals, such as 0.25–0.5 g/kg every 6 hours. Mannitol opens the blood–brain barrier (BBB). It may cross the BBB itself, drawing water into the brain and transiently exacerbating vasogenic cerebral edema. Furosemide may also be used synergistically with mannitol to reduce cerebral edema through increased serum tonicity and reduced production of CSF.

There has been concern that continuous mannitol infusions lead to elevated serum levels of mannitol, sequestering of mannitol within brain tissue, rebound shifts of water back into the brain, and worsening outcomes. It was thought that bolus administration reduced this effect and was more effective than continuous mannitol infusion for ICP reduction, with the added benefit of maximized rheologic increase in CBF. More recent investigations suggest that there are no good data to support this.⁵⁴ The significant water shifts caused by mannitol suggest that it may be wise to replace fluids to maintain euvolemia.

Acute renal tubular necrosis may be seen when mannitol is used in high doses in patients with preexisting renal disease or when other potentially nephrotoxic drugs are administered. Use of mannitol is often restricted when serum osmolality exceeds 320 mOsm/L.⁵⁵ Urine output should be followed to help minimize the likelihood of hypotension and hypovolemia.

Although TBI patients usually receive mannitol in conjunction with ICP monitoring, some clinicians employ high-level empiric dosing.²⁵ No strong evidence supports empiric prehospital administration of mannitol to TBI patients,⁵⁶ but in principle, mannitol may be of benefit in patients with signs of rapidly expanding mass lesions, such as decreasing level of consciousness with unilateral pupillary dilatation and contralateral hemiparesis. In such cases, mannitol may be used as a bridge toward definitive therapy, such as operative evacuation of mass lesions.

As with mannitol, hypertonic saline (HTS) is thought to lower ICP through two mechanisms. First, hypernatremia produces an oncotic pressure gradient across the BBB and mobilizes water from brain tissue. Second, rapid plasma dilution and volume expansion, endothelial cell and erythrocyte dehydration, and increased erythrocyte deformability lead to improvements in rheology, CBF, and oxygen delivery. HTS is often administered as a continuous infusion of 25–50 mL/h of 3% saline (replacing the patient’s isotonic IV fluid) or bolus infusions of 10–30 mL of 7.2%, 10%, or 23.4% saline solution. Clinical response can begin within minutes and may last for hours, making HTS a potentially useful intervention in cases of severe ICP elevation or acute herniation syndrome.

A common target for serum sodium concentration is 145–160 mEq/L, and even higher serum sodium levels may be chosen. However, it is unclear if deliberately driving up the serum sodium concentration to supranormal levels can prevent IC-HTN. Instead, high sodium levels are better viewed as a reason to stop administering HTS, rather than as a desired goal. Serum sodium and osmolality levels are often followed serially because excessively rapid increases in sodium, which may occur during HTS administration, may result in central pontine myelinolysis. This occurs most commonly in patients with preexisting chronic hyponatremia and is rarely seen in the chronically normonatremic patient who receives HTS. HTS may also induce or exacerbate pulmonary edema in patients with underlying cardiac or pulmonary deficits.

Hyperventilation

By lowering PCO₂, HV induces vasoconstriction, reduction of cerebral blood volume, and reduction in ICP. Time of onset of effect ranges from 30 seconds to 1 hour. Peak effect may be seen at 8 minutes and may last up to 15–20 minutes. This rapid onset of action makes HV particularly effective in the treatment of an IC-HTN crisis and as a bridge to more definitive therapy, such as surgical decompression, or as a temporizing measure while other ICP-lowering therapies take effect.

Although HV was once used as a first-line therapy, concerns subsequently grew regarding prophylactic or prolonged use in TBI patients. During the first 24 hours after injury, perhaps as many as 50% of patients with severe TBI exhibit cerebral ischemia.⁵⁷ Induced vasoconstriction from HV may lower CBF even further. Depending on the degree of functional autoregulation, the brain may undergo increases in the oxygen extraction fraction or shunting of blood to ischemic areas, with the net result being an increase in the total ischemic volume.

Severe TBI patients should be kept normocarbic (PCO₂ = 35–45 mm Hg). If HV becomes necessary, brief periods of mild HV (PCO₂ = 30–35 mm Hg) may be effective for bringing ICP down while other treatment strategies are initiated. Prophylactic HV is contraindicated because it has been associated with worse outcomes.⁵⁸ If HV is used, consideration should be given to tracking cerebral oxygenation via monitoring of jugular venous oxygen saturation or brain tissue oxygen tension.

Decompressive Craniectomy

If the above therapies fail to provide adequate control of ICP, additional therapies that may be considered include decompressive craniectomy (DC), barbiturate coma, and hypothermia.

Some patients with TBI require emergency craniotomies to evacuate focal hemorrhagic lesions. The bone is removed, the lesion resected, dura closed, and bone replaced. More severe cases of TBI may develop diffuse cerebral edema, contusions of large size in eloquent areas, or multiple, coalesced contusions. In these cases, it may be preferable to leave the bone flap off. Additionally, when ICP is refractory to the previously mentioned management techniques, DC effectively expands the intracranial space to lower the ICP.

The most common DC technique is a unilateral hemispheric decompression. Bifrontal and bilateral hemispheric craniectomies (Fig. 19-8) have also been described and may be more appropriate in some cases. The dura is opened widely, and areas of noneloquent contused or devitalized brain can be removed if required. The larger the size of the decompression, the better. The brain is then contained only by the augmented dural covering and the more compliant scalp.

FIGURE 19-8

CT scan showing bilateral hemispheric decompressive craniectomies performed in a patient with severe cerebral edema.

DC is most commonly used in patients with IC-HTN refractory to maximal medical management. Ideally, operative intervention should occur before ICP has been dangerously elevated for sustained periods of time. Success depends largely on patient selection. Regardless of the preoperative indications or patient profile, continuing postoperative IC-HTN greater than 35 mm Hg has been associated with very high mortality rates.⁵⁹

Early surgical intervention may be an option for potentially salvageable patients presenting with severe unilateral or bilateral cerebral edema, parenchymal lesions resistant to initial medical management of ICP, or other injuries whose management conflicts with standard ICP control measures (eg, patients with acute respiratory distress syndrome requiring elevated ventilatory pressures).

DC can be effective for reducing ICP, but improvement in outcome has been difficult to demonstrate because most reports describing this practice consist only of case series, lack appropriate control subjects, and/or do not achieve statistical significance with regard to all end points.⁶⁰ The prospective, randomized, controlled DECRA trial of bifrontal DC in patients with diffuse TBI who exhibited increasing ICP found that DC not only failed to improve outcome, but was actually associated with worse outcomes.⁶¹ RESCUE-ICP is another trial investigating the role of DC as a salvage procedure after other interventions have failed to control elevated ICP.⁶² Results are not available at the time of this writing.

DC is not a benign procedure. Complications are common. These include infection, subdural hygroma, hydrocephalus, syndrome of the trephined, CPP breakthrough, and cerebral infarction.

Barbiturates

Barbiturates benefit TBI patients by decreasing the cerebral metabolic rate of oxygen (CMRO₂), decreasing formation of free radicals and intracellular calcium influx, and lowering ICP. Side effects such as immunosuppression and hypotension from reduced sympathetic tone and mild myocardial depression often limit their use. TBI patients in coma (GCS score ≤8) receiving barbiturate therapy demonstrate infectious and respiratory complication rates in excess of 50%,⁵⁹ and significant systemic hypotension may occur in 25% of patients⁶³ despite adequate intravascular volume and pressor therapy. Barbiturates clearly reduce ICP, but studies have shown both improved and worsened outcomes for TBI patients receiving barbiturate therapy.

Patients with hemodynamic instability, sepsis, respiratory infection, or cardiac risk factors are excluded from barbiturate therapy. Those receiving barbiturates should be closely monitored for signs of cardiac compromise or infection, with cessation of therapy if systemic effects of the treatment become significant and unmanageable. A pretherapy echocardiogram and intratherapy use of a pulmonary artery catheter should be considered.

There is no role for prophylactic barbiturate therapy in TBI patients because it increases hypotension without significantly improving outcome.⁶⁴ It should be reserved for use in controlling ICP only after other treatments have failed.

A typical pentobarbital regimen is a loading dose of 10 mg/kg over 30 minutes, followed by a 5 mg/kg/h infusion for 3 hours. A maintenance dose of 1 mg/kg/h should then be started.²⁴ Serum barbiturate levels of 3–4 mg% should be maintained, although poor correlation exists between serum level, therapeutic benefit, and systemic complications. Titration to clinical effect is commonly done. Continuous electroencephalographic evaluation is preferred by some, with dosing to the point of burst suppression producing near-maximal reductions of CMRO₂ and CBF.

Hypothermia

Induced therapeutic hypothermia in TBI patients may reduce cerebral metabolism, ICP, inflammation, lipid peroxidation, excitotoxicity, cell death, and seizures. Adverse effects of hypothermia include decreased cardiac function, thrombocytopenia, elevated creatinine clearance, pancreatitis, and shivering with associated elevations in ICP. Initial interest in induced hypothermia stemmed from a large body of preclinical evidence, anecdotal observations (such as children trapped under the ice in frozen lakes), single-center clinical trials, and several meta-analyses.^{65,66,67,68,69} Although its use in TBI patients has been adopted by some trauma centers, and level 1 evidence supports its use in patients with cardiac arrest from ventricular fibrillation or ventricular tachycardia, clinical trials to date have not shown significant improvements in outcome from induction of hypothermia in TBI patients.

Meta-analyses of more recent data and subsequent guidelines²⁴ note a nonsignificant trend toward mortality reduction (compared to normothermic controls) when target temperatures are maintained for greater than 48 hours. Hypothermia-treated patients have been reported to reach significantly better outcomes. Additionally, patients who were hypothermic on admission seem to have improved outcomes if hypothermia is maintained, as opposed to rapidly warming them to normothermia. Interpretation of these results is limited, however, by small sample sizes and potential confounding factors in each study.

Hypothermia is an option (ie, supported by only weak evidence) for treatment of patients with severe TBI. Patients who are hypothermic on arrival should be maintained in a cooled state or rewarmed only very slowly. An initial target temperature of 33°C may be targeted and, if possible, maintained for greater than 48 hours. This temperature may be carefully titrated upward to 34°C or 35°C while ICP is monitored because some patients may still demonstrate the ICP-lowering benefit of hypothermia at these temperatures, with perhaps less risk of adverse events from lower temperatures. Monitoring for untoward effects of hypothermia should include attention to potential electrolyte abnormalities and cardiac rhythm disturbances. Rewarming of these patients should take place very slowly, not exceeding 1°C per 4–6 hours or even more slowly (or even returning to a lower temperature) if ICP begins to rise precipitously.

Steroids

Glucocorticoids are not recommended for treatment of TBI.^24,70,71 Increased mortality has been reported in trials investigating the effect of steroids on outcome after TBI. Of course, this restriction does not apply in cases when patients require steroids for treatment of other medical problems.

Progesterone is another steroid that has been investigated as a potential therapy for TBI. Despite supportive preclinical and early-phase clinical data, progesterone failed to confer benefit to TBI patients in two large multicenter trials.^72,73

OUTCOME

Prognostic Data

To interpret and compare the effectiveness of various treatments, common end points are necessary for communication between practitioners or comparison of studies. The Glasgow outcome scale (GOS)⁷⁴ (Table 19-6) is a widely used outcome grading scale, with many studies separating patients into those with good outcome (GOS = 4 or 5) and those with poor outcome (GOS = 1–3). Although its separation of patient categories is relatively coarse and may not identify the subtleties of recovery in many TBI patients, it remains a useful tool for describing patient outcome, just as the GCS is a useful tool for tracking a patient’s neurological examination. A patient’s ultimate neurological outcome may not be fully evident until weeks or months of treatment have taken place in hospitals, rehabilitation centers, and at home.

TABLE 19-6Glasgow Outcome Scale

TABLE 19-6 Glasgow Outcome Scale

Score

Meaning

Notes

5—good recovery

Resumption of normal life

May have minor deficits, ± return to work

4—moderate disability

Disabled but independent

Can use public transportation and work in sheltered environment

3—severe disability

Conscious but disabled

Dependent for daily support, ± needs institutionalization

2—persistent vegetative state

Unresponsive, speechless

May open eyes spontaneously after several weeks and achieve sleep/wake cycles

1—death

Dead

The medical practitioner is often called upon early in a patient’s course to make predictions of outcome based on limited information. Various studies and meta-analyses^75,76,77 show that worse prognosis is seen in patients with bilaterally dilated pupils or absent pupillary light reflexes, absent oculocephalic or oculovestibular reflexes, increased injury severity scale score (>40), extremes of age (>60 years and possibly <2 years), hypotension (SBP <90 mm Hg, worse with concomitant hypoxemia), abnormal CT scan (extensive tSAH, compression or obliteration of basal cisterns), persistent ICP >20 mm Hg, elevated ICP during the first 24 hours, or presence of apolipoprotein E4 allele. Probability of poor outcome increases with worsening initial total GCS score (especially GCS < 9), and some studies show worse prognosis based on lower GCS subscores (motor ≤3, eye opening ≤2, verbal response ≤2).

Brain Death

“Brain death” refers to the irreversible absence of any brain function. Ancillary tests are sometimes used to support the clinical diagnosis, but they should not supplant the clinical examination as the primary means of making this diagnosis. Many people, including some in health care fields, think that brain death is somehow not “real” death. Discussion of this condition by popular media often contributes to this misunderstanding. It must be emphasized that brain death is a legally binding death, with the same degree of finality and certitude as cessation of cardiopulmonary function. The required components of diagnosing brain death may vary between states and between different hospitals, but the core elements are comparable.

No confounding factors may be present if brain death is to be diagnosed. Examples include hypothermia, hypotension, sedatives, paralytics, alcohol or other dugs of abuse, hepatic encephalopathy, hyperosmolar coma, atropine, recent CPR/shock/anoxia, and similar factors. Patients have nonreactive and usually dilated pupils and no observable corneal, oculocephalic, oculovestibular, gag, cough, or other brainstem-mediated reflexes. No spontaneous breathing is present. Patients demonstrate no movement or other response to pain.

If the clinician chooses to forgo apnea testing because of a patient’s inability to tolerate it or because of institutional protocols, other types of ancillary testing may be used. These include cerebral radionuclide testing to confirm lack of uptake in brain parenchyma, cerebral angiography to verify absence of intracranial blood flow, and specialized electroencephalography techniques to verify electrocerebral silence, among other methods.

TBI patients who progress to brain death may be candidates for organ donation. Specialized organ procurement organizations are present in most states and represent a party separate from the treating team, with no conflict of interest regarding the patient’s care. In many of these tragic cases, a patient’s family members may receive a small measure of comfort from the knowledge that their decision to donate has helped other suffering patients.

FUTURE DIRECTIONS

Although much has been learned about the pathophysiology and treatment of TBI, translation of this knowledge to effective treatments has been challenging. One major change in the conceptualization of TBI has been the realization that TBI is actually a heterogeneous category composed of different subtypes of diseases, such as nonoperative diffuse injury versus large focal hematoma requiring immediate surgery. Future trials will likely be more focused in terms of the subtypes of TBI patients that are enrolled.

Another change in approach to clinical research is the growing recognition of the value of high-quality patient registries. There are far too many questions and far too few patients, investigators, and funds to subject every research question to a randomized, prospective, blinded, controlled trial. Conducting such trials for surgical interventions in emergency and critical care patients is especially problematic. Despite these challenges, the traditional approach to clinical trials will continue to predominate. But the awareness that registries can supplement such trials and even represent a better method of investigation in some cases will allow many important questions to be addressed in a more expeditious manner than in the past.

REFERENCES