Mechanism

Head injury is classically categorized as “closed” or “penetrating” head injury. These categories are not necessarily mutually exclusive. For example, a depressed skull fracture with bone fragment extension into the brain may fit both descriptors. For practical purposes closed head injury is typically used to describe head injury after falls, automobile accidents, and assaults, and penetrating head injury is used to describe gunshot wounds and stabbings. More recently two new categories have been developed: crush and blast. Crush injury can best be described as the cranium being held between compressive forces that subject the skull and intracranial contents to increasing pressures. This force, if significant enough, can lead to failure of the calvarium as a protective shell to the intracranial contents. Blast injury has recently been added as a separate category after the experience with improvised explosive devices (IEDs) in the recent Afghanistan and Iraq conflicts.

Severity

Prior to 1974, different authors used various terms to describe patients with head injury, making it virtually impossible to compare groups of patients from different centers. In 1974, Teasdale and Jennett,¹³ by identifying the clinical signs that predicted outcome most reliably and that seemed to have the least interobserver variation, designed what has come to be known as the Glasgow Coma Scale (GCS). The introduction of the GCS (Table 20.1) brought some degree of uniformity into the head injury literature.¹³ This scale has gained widespread use for the description of patients with head injuries and has also been adopted for the description of patients with altered levels of consciousness due to other causes.

TABLE 20.1 Glasgow Coma Scale (GCS)

Jennett and Teasdale defined coma as the inability to obey commands, to utter words, and to open the eyes.¹⁴ A patient needs to meet all three aspects of this definition to be classified as comatose. In a series of 2000 patients with severe head injury, these authors observed 4% who did not speak but could obey commands and another 4% who uttered words but did not obey commands. Among patients who could neither obey nor speak, 16% opened their eyes and were therefore judged not to be in coma. Patients who open their eyes spontaneously, obey commands, and are oriented score a total of 15 points, whereas flaccid patients who do not open their eyes or talk score the minimum of 3 points. No single score within the range of 3 to 15 forms the cut-off point for coma. However, 90% of all patients with a score of 8 or less, and none of those with a score of 9 or more, are found to be in coma according to the preceding definition. Therefore, for all practical purposes, a GCS score of 8 or less has become the generally accepted definition of a comatose patient.

The distinction between patients with severe head injury and those with mild to moderate injury is thus fairly clear. However, distinguishing between mild and moderate head injury is more of a problem.¹⁵ Somewhat arbitrarily, head-injured patients with a GCS score of 9 to 13 have been categorized as “moderate,” and those with a GCS score of 14 or 15 have been designated “mild.” Authors have variably classified the GCS 13 patients with the mild or moderate TBI groups, but studies suggest that patients with a GCS of 13 at admission fit better into the moderate rather than mild TBI group. Eighty percent of head injuries are categorized as mild, 10% as moderate, and 10% as severe. Williams and colleagues reported that the neurobehavioral deficits in patients with mild head injury (GCS 14 or 15) and an intracranial lesion on initial computed tomography (CT) scan were similar to those in patients with moderate head injury (GCS 9 to 13), but patients with mild head injury uncomplicated by an intracranial lesion on CT scan did significantly better.¹⁶

Morphology

The advent and easy attainability of CT scans in most centers has revolutionized the evaluation and treatment of the head injury patient. It is rare in current practice for patients to receive exploratory bur holes/craniotomy as described historically. Frequent CT follow-up is essential as the morphology of the head injury patient evolves over hours, days, and even weeks. For a morphological description, head injury can be described into two broad categories as skull fractures and intracranial lesions.

Skull Fractures

In current practice in developed countries, CT scans are the imaging study of choice and plain skull films are rarely obtained. Skull fractures may be seen in the cranial vault or skull base, may be linear or stellate, and may be depressed or nondepressed (Fig. 20.3). Basal skull fractures are harder to document on plain x-ray films and usually require CT scanning with bone-window settings for identification. Another indication of covert skull fracture is the presence of pneumocephalus, which can be readily identified on CT scan.

FIGURE 20.3 A, Linear skull fracture; B, depressed skull fracture.

The clinical signs of a basal skull fracture include cerebrospinal fluid (CSF) leakage from the nose (rhinorrhea) or ear (otorrhea), blood behind the eardrum (hemotympanum), bruising behind the ear (postauricular ecchymoses or Battle’s sign), and bruising around the eyes (periorbital ecchymoses or raccoon eyes). The presence of these clinical signs should increase the index of suspicion and help in the identification of a basal skull fracture. Most require no treatment, but persistent CSF leakage may require operative repair.

A depressed skull fracture may cause pressure on the brain or a dural breach. As a general guideline, fragments depressed more than the thickness of the skull require elevation. Open or compound skull fractures have a direct communication between the scalp laceration and the cerebral surface because the dura is torn. They require early surgical repair and appropriate antibiotic coverage. Outcome after a depressed skull fracture is based on the degree and location of the underlying injury to the brain.

A linear vault fracture increases the risk of intracranial hematoma. For this reason, the detection of a skull fracture on plain skull radiograph always calls for a CT scan of the head and generally warrants admission to the hospital for observation.

Fractures can also involve the anterior or posterior tables of the frontal sinus. These fractures can lead to inadequate drainage and recurrent sinusitis if the communication between the sinus and nasal cavity (nasofrontal outflow tract) is obstructed. Furthermore, if the posterior table is violated with obstruction of the nasofrontal outflow tract, there is an increased risk of intracranial infections. Treatment of such fractures should be based on the fine cut CT bone window findings, patency of the nasofrontal outflow tract, and cosmetic deformity caused by the fracture.^17,18

Intracranial Lesions

Intracranially lesions may be broadly classified into focal or diffuse injuries. It is not uncommon to for these types of injuries to coexist. Focal lesions include epidural hematomas, subdural hematomas, and contusions/intracerebral hematomas. Diffuse brain injury, also referred to as diffuse axonal injury, may have a relatively benign-appearing CT scan (Fig. 20.4A); however, small punctate hemorrhages may be noted particularly at midline structures. Patients with diffuse axonal injury typically have a poor neurological examination with altered sensorium or even deep coma out of proportion to the findings on their imaging workup.

FIGURE 20.4 A, Diffuse brain injury; B, epidural hematoma; C, subdural hematoma; and D, intracerebral hematoma.

Epidural Hematoma (Fig. 20.4B)

This type of bleeding is located between the inner table of the skull and the dura. Most commonly these hemorrhages are located in the temporal or temporoparietal region and are classically associated with tearing of the middle meningeal artery secondary to calvarial fracture. Most epidural hematomas are related to arterial bleeding; however, in up to one third of the cases an epidural may be associated with bleeding from the bone. Epidural hematomas may also occur from tearing of the middle meningeal vein, diploic veins, or venous sinuses, particularly in the parieto-occipital area or the posterior fossa. Nonsurgical epidural hematomas are reported in 2.7% to 4% of TBI patients.^10,19–22 In patients presenting with coma up to 9% may harbor an epidural hematoma. Epidural hematomas tend to affect patients between 20 and 30 and are most commonly seen in traffic accidents (53%), falls (30%), and assaults (8%).¹⁰ The mortality rate in all age groups and GCS scores undergoing surgery for epidural hematoma is approximately 10%.¹⁰ More specifically in patients not in coma the mortality rate approximates 0%, for obtunded patients it is 9%, and for patients presenting in coma it approaches 20%.

Subdural Hematoma (Fig. 20.4C)

Subdural hematoma (SDH) is a much more common entity, with reports of 12% to 29% of patients with severe TBI having an associated SDH on initial imaging.¹⁰ The BTF review of surgical subdural hematomas showed that in 2870 patients 21% presented with SDH. They occur most frequently from a tearing of bridging veins between the cerebral cortex and the draining sinuses. However, they can also be associated with lacerations of the brain surface or substance. A skull fracture may or may not be present and the mechanism is often age dependent. Younger patients (18-40 years) presented with SDH after motor vehicle accident (MVA) (56%), with only 12% presenting after a fall.²³ In patients older than 65 the opposite is seen, with SDH seen in 22% of MVAs and 56% of falls, often seen in those on anticoagulants used in the management of other chronic disease processes.²³ The brain damage underlying acute SDHs results from direct pressure caused by the hematoma, brain swelling, increased intracranial pressure, or diffuse axonal injury as a result of mechanical distortion of the brain parenchyma. The injury in patients with SDH is usually much more severe, and the prognosis is much worse compared to epidural hematomas. MVA is described as the mechanism of injury in 53% to 75% of patients who are comatose with SDH. The mortality rate in a general series may be around 60% but can be lowered by very rapid surgical intervention and aggressive medical management.²⁴ Multiple studies show that the morbidity and mortality rates are increased if the surgery is performed after 3 to 4 hours, and the timing of acute SDH surgical intervention should be done within 2 to 4 hours of TBI if possible.¹⁰

Contusions/Intracerebral Hemorrhage (Fig. 20.4D)

Pure cerebral contusions are fairly common, found in 8% of all TBI^10,25 and 13% to 35% of severe injuries.¹⁰ The incidence is much more apparent as the quality and number of CT scans increase. Furthermore, contusions of the brain are often concomitant with SDH. The vast majority of contusions occurs in the frontal and temporal lobes, although they can occur at almost any site, including the cerebellum and brainstem. The distinction between contusions and traumatic intracerebral hematomas remains somewhat ill-defined. The classic “salt and pepper” lesion is clearly a contusion, but a large hematoma clearly is not. However, there is a gray zone, and contusions can, over a period of hours or days, evolve into intracerebral hematomas.

Management of the intracerebral hematoma is dependent on the neurological status of the patient. Rapid surgical evacuation decompression is recommended if there is a significant mass effect (generally, a 5-mm or greater actual midline shift). The current BTF guidelines state that patients with parenchymal mass lesions and signs of progressive neurological deterioration related to the lesion, refractory intracranial hypertension, or signs of significant mass effect on CT should be treated operatively. Also in patients with GCS scores of 6 to 8 with frontal or temporal contusion greater than 20 cm³ with midline shift greater than 5 mm or cisternal compression on CT scan, and patients with any lesion greater than 50 cm³ in volume should be surgically treated.¹⁰

Conservative management may be utilized in patients with no neurological compromise, no signs of elevated intracranial pressure, and no CT scan evidence of significant mass effect. These patients should be managed with intensive monitoring, serial imaging, and a constant vigilant neurological examination.

Diffuse Injuries

Diffuse brain injuries form a continuum of progressively severe brain damage caused by increasing amounts of acceleration-deceleration injury to the brain. In its purest form, diffuse brain injury is the most common type of head injury.

A mild concussion is an injury in which consciousness is preserved, but there is a noticeable degree of temporary neurological dysfunction. These injuries are exceedingly common and, because of their mild degree, are often not brought to medical attention. The mildest form of concussion results in transient confusion and disorientation without amnesia. This syndrome is usually completely reversible and is associated with no major sequelae. Slightly greater injury causes confusion with both retrograde and post-traumatic amnesia.

A classic cerebral concussion is that post-traumatic state that results in loss of consciousness. This condition is always accompanied by some degree of retrograde and post-traumatic amnesia, and the length of post-traumatic amnesia is a good measure of the severity of the injury. The loss of consciousness is transient and reversible. The patient has returned to full consciousness by 6 hours, although it is usually much sooner. Although the great majority of patients with classic cerebral concussion have no sequelae other than amnesia for the events relating to the injury, some patients may have more long-lasting and sometimes significant neurological deficits.

Diffuse axonal injury is the term used to describe a prolonged post-traumatic state in which there is loss of consciousness from the time of injury that continues beyond 6 hours. This phenomenon may further be broken down into mild, moderate, and severe categories.²⁶ Severe diffuse axonal injury usually occurs in vehicular accidents, comprising about 36% of all patients with diffuse axonal injury. These patients are rendered deeply comatose and remain so for prolonged periods of time. They often demonstrate evidence of decortication or decerebration (motor posturing) and often remain severely disabled, if they survive. These patients often exhibit autonomic dysfunctions such as hypertension, hyperhidrosis, and hyperpyrexia, and were previously thought to have primary brainstem injury. It is now believed that diffuse axonal injury throughout the brain is the more common pathological basis.

Mild Traumatic Brain Injury

Approximately 80% of patients presenting to the emergency room with head injury fall under the category of mild TBI. These patients are awake but may be amnesic for events surrounding the injury with a GCS score of 14 or 15. There may be a history of brief loss of consciousness, which is usually difficult to confirm. The issue is often confounded by alcohol or other intoxicants.

Most patients with mild head injury make “uneventful recoveries” but often suffer mild neurological sequelae that can be identified when given in-depth neuropsychological testing. Furthermore, about 3% of patients deteriorate unexpectedly, and can become neurologically devastated if the decline in mental status is not noticed early.²⁷ How can a physician guard against such an occurrence? Early CT scanning of all patients with a history of a TBI is generally advisable, although the classic struggle between “cost-effective” and the “best possible” management is clearly evident here, and practice varies in different centers.

In 1999, a Task Force on Mild Traumatic Brain Injury was devised under the support of the European Federation of Neurological Societies. The efforts of the task force produced the recommendations for the initial management of mild traumatic brain injury (Fig. 20.5).²⁸ Since their recommendations, further work has been done in the evaluation and treatment of mild TBI.

FIGURE 20.5 Algorithm for management of mild head injury. ^∗Risk factors include ambiguous accident history, continued post-traumatic amnesia, retrograde amnesia more than 30 minutes, clinical signs of skull fracture, headache, vomiting, focal neurological deficit, seizure, age younger than 2 years and older than 60 years, coagulation disorder, or high-energy (speed) accident.

In the head-injured patient, skull x-ray films may be examined for the following features: linear or depressed skull fractures, position of the pineal gland if calcified, air-fluid levels in the sinuses, pneumocephalus, facial fractures, and foreign bodies. However, the routine ordering of skull films has in most instances become obsolete with the availability of CT scanners. Studies comparing skull radiography with CT have shown a low sensitivity and specificity of the presence of a skull fracture on skull radiographs for intracranial hemorrhage.²⁹ A meta-analysis confirmed that skull radiography is of little value in the clinical assessment of mild TBI.³⁰

Hence, CT is considered the gold standard for the detection of intracranial abnormalities after mild TBI. It is recommended for those with loss of consciousness or post-traumatic amnesia and is considered mandatory in all patients with GCS scores of 13 or 14, or in the presence of risk factors.

The cervical spine and other parts must undergo x-ray studies if there is any pain or tenderness. Non-narcotic analgesics are preferred, although codeine may be used if there is an associated painful injury. Tetanus toxoid must be administered if there are any associated open wounds. Routine blood tests are usually not necessary if there are no systemic injuries and the patient is not on anticoagulants. A blood alcohol level and urine toxic screen can be useful both for diagnostic and for medicolegal purposes.

Moderate Traumatic Brain Injury

Patients with moderate head injury constitute approximately 10% of head injury patients seen in the emergency room. They are still able to follow simple commands but are usually confused or somnolent and may have focal neurological deficits such as a hemiparesis. In patients with mild or moderate head injury, extracranial injuries play a significant role in the overall outcome. Approximately 10% of these patients will deteriorate and lapse into coma. Therefore, they should be managed as patients with severe head injuries, although they are not routinely intubated (Fig. 20.6).

FIGURE 20.6 Algorithm for management of moderate head injury.

On admission to the emergency room, a brief history is obtained and cardiopulmonary stability is ensured prior to neurological assessment. A CT scan of the head is obtained in all moderately head-injured patients. In a review of 341 patients with a GCS score of 9 to 12, 40% of cases had an abnormal initial CT scan and 8% required surgery.³¹ The patient is admitted for observation even if the CT scan is normal. If the patient improves neurologically and a follow-up CT scan of the head shows no surgical mass lesion, he or she may be discharged from the hospital over the next few days. On the other hand, if the patient lapses into coma, the management principles described for severe head injury are adopted.

Severe Traumatic Brain Injury

Severe TBI patients are those who are unable to follow simple commands even after cardiopulmonary stabilization. Although this definition includes a wide spectrum of brain injury, it identifies the patients who are at greatest risk of suffering significant morbidity and even death. We believe that in such patients a “wait and see” approach can be disastrous and that prompt diagnosis and treatment are of the utmost importance (Box 20.1).^24,32,33

Airway

A frequent concomitant of a severe TBI is transient respiratory arrest. Prolonged apnea may often be the cause of “immediate” death at the scene of an accident. If artificial respiration can be instituted immediately, a good outcome is possible.³⁴ Apnea, atelectasis, aspiration, and adult respiratory distress syndrome are frequently associated with severe head injury, and by far the most important aspect of the immediate management of these patients is the establishment of a reliable airway. Patients with severe TBI should be intubated early. One hundred percent oxygen is then used for ventilation until blood gases can be checked and appropriate adjustments of the FIO₂ made. There is little danger of oxygen toxicity even when 100% oxygen is used for less than 48 to 72 hours.

Blood Pressure

Hypotension and hypoxia are the principal enemies of the head-injured patient. It has been shown that the presence of hypotension (systolic blood pressure <90 mm Hg) in severe TBI patients increases the mortality rate from 27% to 50%.³⁵ Furthermore, it was found that 35% of patients arriving at major trauma centers are hypotensive. While the airway is being established, another group of emergency room personnel should be checking the patient’s pulse and blood pressure and taking steps to obtain venous access.

If the patient is hypotensive, it is vital to restore normal blood pressure as soon as possible. Hypotension is usually not the result of the brain injury itself, except in the terminal stages when medullary failure supervenes. Far more commonly, hypotension is a marker of severe blood loss, which may be either “overt” or “occult,” or possibly both. One must also consider associated spinal cord injury (with quadriplegia or paraplegia), cardiac contusion or tamponade, and tension pneumothorax as possible causes. While efforts are in progress to determine the cause of the hypotension, volume replacement should be initiated.

The importance of routine abdominal paracentesis in the hypotensive comatose patient has been demonstrated historically.³⁶ In most trauma centers today either high-resolution rapid CT scan or ultrasound (focused assessment with sonography for trauma, FAST) is an acceptable option to rule in or rule out intra-abdominal injury. It must be emphasized that a patient’s neurological examination is meaningless as long as he or she is hypotensive. Time after time, we have seen hypotensive patients who are unresponsive to any form of stimulation revert to a near-normal neurological examination soon after normal blood pressure has been restored.

Cardiopulmonary Stabilization

Brain injury is often adversely affected by secondary insults. In a study of 100 consecutive patients with severe brain injury evaluated on arrival in the emergency room, 30% were hypoxemic (PO₂ <65 mm Hg), 13% were hypotensive (systolic blood pressure <95 mm Hg), and 12% were anemic (hematocrit <30%).³⁷ It has subsequently been demonstrated that hypotension at admission (systolic blood pressure <90 mm Hg) is one of three factors in severe head injury with a normal CT scan (the other two being age over 40 years and motor posturing) that, when noted at admission, are associated with subsequent ICP elevation.³⁸ High ICP is in turn associated with poorer outcome. Subsequent analyses have also confirmed a strong association between hypotension and worse outcomes in patients with severe head injury.³⁹ Therefore, it is imperative that cardiopulmonary stabilization be achieved rapidly.

Catheters

A Foley catheter (16 to 18F for average adults) should be carefully inserted and a urine sample should be sent for urinalysis and toxic screen when appropriate. Gross hematuria, in the absence of local trauma, suggests renal injury and is an indication for an abdominal CT scan and an emergency intravenous pyelogram. Mild hematuria may be secondary to traumatic catheterization, renal contusion, or, rarely, a dissecting aortic aneurysm. Special attention must be paid to maintaining accurate records of fluid intake and output, especially in children and the elderly. In addition to ensuring fluid balance, such records help assess blood loss and monitor renal perfusion.

A nasogastric tube, preferably a Salem sump (double-lumen plastic catheter), should be inserted and connected to a wall suction unit. Potential, albeit rare, complications of this procedure, such as intracranial passage of the tube secondary to a basal skull fracture or those with a history of transnasal skull base surgery, must be kept in mind. In patients with anterior basal skull fractures it is probably wise to pass the tube under direct vision with a laryngoscope or to pass it through the mouth.

Diagnostic Radiographs

As soon as the preliminary steps toward cardiopulmonary stabilization have been taken, diagnostic radiographs should be obtained. Cervical spine films (cross-table lateral and anteroposterior) or a thin-cut cervical spine CT scan are the first to be taken in the severely traumatized patient and must be read by a knowledgeable reader before the patient’s neck can be moved. Features to look for in this study are loss of alignment of the vertebral bodies, bony fractures or compressions, loss of alignment of the facet joints, and prevertebral soft tissue swelling (more than 5 mm opposite the C3 vertebral body is significant). Every effort must be made to visualize the lower cervical levels (C6-T1); these are often obscured by the shoulders, especially in heavy-set patients. On plain films, fracture-subluxations at these levels may be overlooked if the films are not repeated with caudal traction on both arms and greater x-ray penetration (Fig. 20.7).⁴⁰ If these maneuvers also fail, a “swimmer’s view” lateral film can be obtained. If any of these films shows any of the abnormalities listed here, the neck must remain immobilized in a hard collar (Philadelphia, Aspen, or Miami J) pending further studies (high-resolution CT scan). In many centers, plain films of the cervical spine have been replaced by a thin-cut CT scan as the initial study.

FIGURE 20.7 A, The lower cervical spine is obscured by the shoulders. B, Traction on the shoulders reveals a fracture-subluxation at C6-C7.

Cervical spine CT is indicated for the unconscious patient with suspicious or inadequate cervical radiographs and with all cervical fractures or suspected fractures on initial plain films. Several studies have demonstrated the value of the full CT scan, with sagittal and coronal reconstructions, for the exclusion of significant spinal injury.⁴¹ Widening, slippage, or rotational abnormalities of the cervical vertebrae suggest soft tissue injury. An absence of such signs appears to exclude significant instability. Additional modalities, such as magnetic resonance imaging (MRI), can also be employed, although these studies are not generally used as initial studies.

If a cervical spine fracture does exist, either computed tomography angiography (CTA) or magnetic resonance angiography (MRA) may be ordered in specific cases in order to evaluate the carotid and vertebral artery to exclude vascular injury. It is important to rule out these injuries as arterial dissection or occlusion may to lead to ischemic stroke or cerebral hypoperfusion.

The chest film is useful in ruling out endotracheal tube malposition, pneumothorax, hemothorax, lung contusion, hemopericardium, rib fractures, thoracic spine fractures, and other thoracic injury that may have a bearing on patient management.

Although skull films (anteroposterior and lateral) have been overshadowed by CT scanning, they can be helpful in identifying maxillofacial injuries, depressed skull fractures, and penetrating injuries. The presence of pneumocephalus or an air-fluid level in one of the sinuses can alert the clinician to a basal skull fracture.

A single anteroposterior abdominal film (kidney, ureter, and bladder; KUB) may be taken in trauma patients. This film may help identify large retroperitoneal hematomas, lumbosacral spine fractures, distended viscera, and possibly subdiaphragmatic air.

Anteroposterior and lateral pelvic films may also be obtained, looking for pelvic injuries, which may be the site of significant blood loss. The extremities may be studied whenever indicated to rule out fractures or subluxations.

In most trauma centers today CT scanning is readily available and trauma patients meeting the indications for imaging workup will receive a CT scan of the head, neck, chest, abdomen, and pelvis as indicated, after being evaluated and stabilized by the trauma team.

General Examination

During the process of cardiopulmonary stabilization, the clinician conducts a rapid general examination looking for other injuries. In one series of severe TBI patients, more than 50% had additional major systemic injuries requiring care by other specialists (Table 20.2).³⁷ One must check for head and neck, thoracic, abdominal, pelvic, and spinal injuries, and injuries involving extremities.

TABLE 20.2 Frequency of Systemic Injuries in Patients with Severe Head Injury^∗

∗ N = 100.

Modified from Miller JD, Sweet RC, Narayan RK, Becker DP. Early insults to the injured brain. JAMA 1978;240:439-442.

Neurological Examination

As soon as the patient’s cardiopulmonary status has been stabilized, a rapid and directed neurological examination is performed (Box 20.2). Although various factors may confound an accurate evaluation of the patient’s neurological state (e.g., hypotension, hypoxia, intoxication, sedation or paralytic agents), valuable data can nevertheless be obtained. If a patient demonstrates variable responses to stimulation, or if the response on each side is different, the best response appears to be a more accurate prognostic indicator than the worst response. To follow trends in an individual patient’s progress, however, it is better to report both the best and the worst responses. In other words, the right-side and left-side motor responses should be recorded separately.

One should not limit the examination to the GCS. Other important data in the initial assessment of patients with impaired consciousness are the patient’s age, vital signs, pupillary response, and eye movements.⁴² The GCS score provides a simple grading of the arousal and functional capacity of the cerebral cortex, and the pupillary responses and eye movements serve as measures of brainstem function. Advanced age, hypotension, and hypoxia all adversely affect outcome. Indeed, there is considerable interplay between all these factors in determining the ultimate outcome in the severe TBI patient.

Diagnostic Procedures

As soon as a patient’s cardiorespiratory condition has been stabilized and a preliminary neurological examination completed, it behooves the physician to rule out the presence of an intracranial mass lesion. The patient is by this time intubated, often paralyzed with a paralytic agent, and on mechanical ventilation. This prevents the patient from straining and moving around, thus avoiding intracranial pressure surges and greatly enhancing the quality of the diagnostic studies. Needless to say, CT scanning has rendered all other diagnostic tests virtually obsolete. However, other tests have to be used in certain instances either to substitute for CT scanning or, as in the case of angiography, to obtain certain supplemental data.

Intracranial Pressure

Since the early 1970s, there has been an increasing interest in ICP monitoring and control This has been associated with progressive evolution of related technology. However, the intraventricular catheter (or ventriculostomy) remains the most widely used and most useful device for measuring ICP and helping in its control and for maintaining cerebral perfusion pressure.^57,58

Cerebral perfusion pressure (CPP) is the mean arterial blood pressure minus ICP. Because cerebral ischemia may be the single most important secondary effect affecting outcome following severe TBI, it is useful to follow CPP rather than ICP alone.⁵⁹ The guidelines have recommended maintaining CPP at a minimum of 60 mm Hg to possibly help in the avoidance of both global and regional ischemia. Conversely, too great a CPP may also have a deleterious effect, particularly with respiratory complications.

Head injury is the most common indication for ICP monitoring. As a general rule, patients who can follow simple commands need not be monitored and may satisfactorily be followed clinically. In patients who are unable to follow simple commands and have an abnormal CT scan, the incidence of intracranial hypertension is high (53-63%), and monitoring is warranted.³⁸ Severe TBI patients with normal CT scans generally have a lower incidence of elevated ICP (approximately 13%) unless they have two or more of the following adverse features at admission: systolic blood pressure less than 90 mm Hg, unilateral or bilateral motor posturing, or age over 40 years. In the presence of these adverse features, the incidence of intracranial hypertension (even in patients with normal CT scans) is as high as in those with abnormal CT scans on admission.³⁸ Compression or absence of basal cisterns has also been associated with elevated ICP.⁶⁰

Normal ICP in a relaxed or paralyzed patient who is neither hypotensive nor hypercarbic is 10 mm Hg (136 mm H₂O) or less (1 mm Hg = 13.6 mm H₂O = 1.36 cm H₂O). Pressures in the range of 10 to 20 mm Hg (136-272 mm H₂O) may occur with moderate disturbances of intracranial volumes; pressures greater than these herald an intracranial hematoma, diffuse brain swelling, or both.

Most dangerous traumatic intracranial mass lesions shift the midline 5 mm or greater. This is invariably associated with an elevated ICP unless a CSF leak is present. Significant temporal lobe lesions may cause only a minimal shift of the midline, but the ICP may be elevated and the third ventricle, if seen, will often be shifted more than the lateral ventricles. If there is little or no midline shift, the ICP is elevated, and the patient is not hypercarbic, then either there are bilateral mass lesions or there is significant diffuse brain swelling.

When intracranial pressure demonstrates an upward trend, certain basic items should be checked. The neck should be in a neutral position to facilitate venous drainage. In most cases, having the head end of the bed elevated approximately 30 degrees is useful.⁶¹ The calibration of the system must be checked, and one should confirm that the transducer is level with the foramen of Monro. If the patient is fighting the ventilator, he or she should be sedated or chemically paralyzed. If these measures are not adequate, various methods exist to reduce the ICP, including ventricular drainage, mannitol, and hyperventilation.

New technology now allows one to monitor cerebral oxygenation, via the LICOX CMP System. The purpose of this triple-lumen bolt system is to provide additional data including brain tissue oxygenation (PBTO₂) and temperature as well as ICP in patients in whom cerebral hypoxia and ischemia are a concern. Mean normal brain tissue oxygen pressure is greater than 30 mm Hg (range 25-50 mm Hg) with ischemia reported at ranges less than 8 to 12 mm Hg and cell death at less than 5 mm Hg.⁶²

Because the duration and severity of cerebral tissue hypoxia correlates with unfavorable outcomes in severe TBI, this could prove a valuable tool in management and possibly in predicting outcome. The monitor is able to indicate cerebral tissue perfusion status local to the sensor placement, although local brain oxygen levels may not reflect what is happening in the rest of the brain. In the recent literature brain tissue oxygenation monitoring and treatment have shown promise in decreasing morbidity and fatality associated with traumatic brain injury.^63–65

Blood Pressure and Oxygenation

A significant portion of brain injury patients have hypotension and hypoxia in the prehospital and hospital setting. These confounding factors increase the resultant secondary brain injury. Presently the exact level of hypotension that is detrimental to outcome is unknown; however, systolic blood pressure (SBP) less than 90 mm Hg is the currently used definition of hypotension. The level of hypoxia is similarly unknown; however, the definition is apnea cyanosis in the field or a PaO₂ less than 60 mm Hg. Clinical studies have yet to show a decrease in morbidity and mortality rates in TBI patients when these factors are corrected. Currently there are insufficient data to support level I recommendations. There is level II evidence for monitoring blood pressure and avoiding hypotension defined as SBP less than 90 mm Hg.⁹ Level III evidence exists for oxygenation monitoring and avoidance of hypoxia (PaO₂ <60 mm Hg or O₂ saturation <90%).⁹

Hyperosmolar Therapy

Classically the hyperosmolar therapy for elevated intracranial pressure consisted of mannitol. Recent literature has supported the use of hypertonic saline as a trauma resuscitation fluid, as well as a therapy for treating elevated ICP.

The indications for mannitol are as a one-time dose to lower ICP while obtaining further diagnostic studies or while waiting for definitive treatment. Mannitol has been used on an intermittent basis on a more prolonged timeline for the treatment of elevated ICP. There are few human trials that validate the currently used regimens of mannitol in most centers.

Mannitol’s physiological effect relies on its ability to expand plasma, reduce hematocrit, and increase deformability of erythrocytes, reducing blood viscosity and increasing cerebral oxygenation delivery. Mannitol’s effect takes place between 15 and 30 minutes while plasma gradients are established. Mannitol should be used with caution in patients with renal issues or on nephrotoxic drugs as serum osmolality rises and patients are at risk for acute tubular necrosis. Serum osmolality should not generally be allowed to go much above 320 mOsm/L, if possible, to avoid systemic acidosis and renal failure. There is clinical and laboratory evidence to suggest that long-term, repeated use of mannitol can worsen brain edema and hence reverse the initial beneficial effect.²⁷ Mannitol has been shown to have an effect on ICP lasting from 90 minutes to 6 hours or more.

Recently studies on small volume resuscitations have shown the therapeutic effectiveness of hypertonic saline (HS) administration. Hypertonic saline solutions were administered in poly-trauma patients with hemorrhagic shock, and the subset of patients in the group with TBI showed an increase in survival and stabilization of hemodynamic properties.⁹ As a result of this finding, other studies have been conducted showing its utility in the treatment of elevated ICP in trauma, subarachnoid hemorrhage, stroke, and other pathological insults.

The effect of HS on ICP is theorized to come from mobilization of water across the blood-brain barrier, decreasing cerebral water content. HS also increases plasma volume and cerebral blood flow. HS must be used with caution in patients with underlying cardiac or pulmonary issues as they are at risk for pulmonary edema. It must also be used with caution in patients with hyponatremia because rapid correction may lead to central pontine myelinolysis.

The theoretic advantage of using HS therapy over mannitol lies in the fact the HS pulls water intravascularly, increasing blood pressure and maintaining cerebral perfusion. Mannitol has the unfortunate result of diuresis and potential decrease in blood pressure, decreasing cerebral perfusion pressure.

Current Brain Trauma Foundation guidelines show level II evidence for mannitol’s effective control of raised ICP at doses between 0.25 mg/kg to 1 g/kg of body weight.⁹ Level II evidence exists to avoid hypotension (SBP <90 mm Hg).⁹ Recent studies of HS show its utility in a continuous infusion form or as bolus treatment form equivalent to or superior to mannitol for refractory elevated ICP.^66–69 More studies need to be performed to evaluate mannitol versus HS with respect to clinical outcome after TBI.

Furosemide

Furosemide (Lasix) has been used alone and in conjunction with mannitol in the treatment of raised ICP. It has been shown that diuresis can be enhanced by the combined use of these agents with more pronounced and consistent brain shrinkage. A dose of 0.3 to 0.5 mg/kg of furosemide given intravenously is reasonable. When using diuretics the blood pressure must be monitored closely to prevent hypotension. This drug is not commonly used in TBI management at present.

Prophylactic Hypothermia

The utility of hypothermia in TBI has inconsistent results in the medical literature. During the BTF review of the literature mortality rate was affected only by the duration of cooling, which meant a decrease in mortality rate if cooling was for more than 48 hours.⁹ Target cooling temperatures or rate of rewarming had no effect on outcome. The pathophysiological theory behind this treatment is that ICP can be decreased by decreasing brain metabolic demand.

Interpretation of trials involving hypothermia is difficult secondary to confounding factors affecting outcome. It appears that patients who are treated with hypothermia have a trend to more favorable outcome, Glasgow Outcome Scale scores of 4 to 5. Currently there are no level I or level II recommendations for this treatment. A Cochrane Database review in 2009 found no evidence that hypothermia is beneficial in the treatment of head injury. Hypothermia may be effective in reducing death and unfavorable outcomes for traumatic head-injured patients, but significant benefit was only found in low-quality trials.⁹ High-quality trials found no decrease in the likelihood of death with hypothermia, but this finding was not statistically significant and could be due to the play of chance.⁹ Hypothermia should not be used except in the context of a high-quality randomized controlled trial with good allocation concealment.⁹

Infection Prophylaxis

In polytrauma patients the risk of infection can be increased significantly secondary to intubation, invasive lines, and placement of intracranial monitors. Infections can be broken down into infection/colonization of ICP monitors and infection/colonization of peripheral lines/pneumonia. Most trials of prophylactic antibiotics have shown selection of more virulent gram-negative organisms. Currently BTF guidelines recommend at a level II the use of periprocedural antibiotics for intubation to reduce the incidence of pneumonia.⁹ This does not change length of stay or mortality rates. Early tracheostomy reduces mechanical ventilation days, but it does not alter mortality rate or nosocomial pneumonia rate. There is level III evidence against the routine use of prophylactic antibiotics for ventricular catheter placement.⁹ There is currently level III evidence against the routine use of ventricular catheter exchange to prevent infection.⁹

Deep Venous Thrombosis Prophylaxis

The risk of developing deep venous thrombosis (DVT) in the absence of prophylaxis was found to be 20% after severe TBI in a study by Kaufman and associates.⁷⁰ This risk is related to systemic trauma as well as the relative period of immobility these patients face. DVTs of the distal lower extremity veins tend to be clinically silent and tend to stay that. Proximal lower extremity DVTs are more likely to produce symptoms clinically and result in pulmonary embolism (PE). The treatment of DVT and PE in the TBI patient is complicated by the uncertainty of the safety of anticoagulation, specifically in postcraniotomy patients or those with intracerebral hemorrhage from their trauma.

Prophylaxis options can be considered in two categories: mechanical versus pharmacological. These can be thought of in a graduated fashion ranging from graduated compression stockings, intermittent pneumatic compression stockings, and finally anticoagulant medications (low-dose heparin and low-molecular-weight heparin).

In studies comparing pharmacological versus mechanical treatment for the prevention of DVT, pharmacological treatment is more efficacious in preventing DVT but there is a trend toward increased risk of intracranial bleeding.⁹ There are no current recommendations as to the timing or optimal dosing of pharmacological prophylaxis in neurosurgical patients with the current evidence.

Current BTF guidelines show level III evidence for graduated compression stockings or intermittent pneumatic compression stockings unless lower extremity injury prevents their use.⁹ Low-molecular-weight heparin or low-dose unfractionated heparin should be used in combination with mechanical prophylaxis, but there is an increased risk for expansion of intracranial hemorrhage. There are currently no timing recommendations for the initiation of pharmacological DVT prophylaxis.

Intracranial Pressure Monitoring

With the relatively recent understanding of the evolution of brain injury starting at impact and continuing through as secondary insults in the following hours and days the management has taken shape in attempts to prevent these secondary injuries. This understanding has led to protocols to prevent hypotension, hypoxia, and anemia as discussed earlier and maintaining CPP. As discussed earlier the mean arterial pressure minus the ICP equals the CPP. The main way to ensure adequate CPP is to monitor arterial pressure and ICP.

Monitoring ICP can be used to monitor patients for worsening intracranial injury, help predict outcome, calculate CPP, and if ventriculostomy is used, therapeutic CSF drainage. When comparing patients with ICP monitoring to prior reports of patients without monitoring, monitored patients have improved outcome.⁹

Monitoring options include intraparenchymal monitors (Camino monitor), ventriculostomy catheter, and brain oxygen tension monitor (Licox). Ventriculostomy remains the gold standard, as it can monitor ICP as well as drain fluid as a therapeutic treatment to lower elevated ICP. The Licox monitor has the ability to measure ICP as well as brain oxygenation. The utility of these measurements has shown decreased morbidity and mortality rates in the recent literature, as discussed earlier.

Currently BTF guidelines show level II evidence for placing an ICP monitor in all salvageable patients with severe TBI defined by a postresuscitation GCS score of 3 to 8 and an abnormal CT scan of the head.⁹ An abnormal CT of the head is defined as one showing hematomas, contusions, swelling, herniation, or compressed basal cisterns.⁹ Current level III evidence exists for ICP monitoring in patients with severe TBI with a normal CT and two or more of the following: (1) age over 40 years, (2) unilateral or bilateral motor posturing, or (3) systolic blood pressure less than 90 mm Hg.³⁸ These three factors were found to have higher incidence of elevated ICP in patients with normal admission CT scan.

Brain Oxygenation Monitoring and Threshold for Treatment

In recent years the monitoring of cerebral oxygenation has taken form in two different ways: (1) brain oxygenation monitoring probes, and (2) jugular venous oxygen monitoring. Other novel monitoring techniques have been developed but have yet to be substantiated in clinical studies. Abnormal venous jugular oxygen levels have been correlated with poor outcomes. High and low values have been associated with poor outcomes, which is believed to be related to brain metabolism. Venous jugular oxygenation is more helpful when arteriojugular difference in oxygenation is measured, most likely giving a more accurate picture of cerebral metabolism.

Multiple studies have shown that a diminished oxygenation of brain tissue (as measured by the partial pressure of oxygen in brain tissue, PBTO₂) is correlated with poorer outcomes and death.^63–65 Treatments to keep PBTO₂ greater than 25 mm Hg along with CPP and ICP management have shown decreased mortality rates when compared to outcomes of treating CPP and ICP alone.^63–65

Even though treatments to maintain cerebral oxygenation seem promising there is only level III evidence for jugular venous monitoring and brain tissue oxygen tension monitoring.⁹ Treatment thresholds are less than 50% for jugular venous saturation and more than 15 mm Hg for brain tissue oxygenation.⁹

Anesthesia, Analgesics, and Sedatives

It has been long understood that pain and agitation may raise ICP in the TBI patient. Pain medications and sedatives have often been used to calm patients to prevent a dangerous rise in ICP that may be associated with severe agitation. Barbiturates have been used since the 1930s with the knowledge of their ability to lower ICP.⁷¹ Barbiturates are also known to decrease cerebral metabolism having a cerebral protective effect.^72,73 The use of barbiturates couples blood flow to cerebral metabolism, decreasing blood flow where metabolism is low and shunting blood flow to areas where metabolism is high.

Prophylactic administration has not proved to be effective in preventing elevated ICP. The Cochrane group reviewed two randomized controlled trials of barbiturate use showing no evidence of improved outcomes in severe TBI. They also found that there was a 25% chance of hypotension when receiving barbiturates, offsetting any effect of ICP lowering. To monitor for appropriate sedation patients are placed on electroencephalograph (EEG) monitoring. Dosing to burst suppression reduces cerebral metabolism to maximal reduction.

Propofol has more recently been studied because of its quick onset of action, and its short duration of action allows quick neurological assessment. Studies have shown that propofol does have a minimal effect at lowering ICP, and one study reported high-dose propofol showing a favorable neurological outcome when compared to a low-dose propofol.⁷⁴ Propofol must be used with caution, especially in high doses, as some patients develop propofol infusion syndrome, which may lead to death.

BTF guidelines currently have level II evidence that prophylactic administration of barbiturates to burst suppression is not recommended. High-dose barbiturate treatment is recommended for refractory ICP control; however, hemodynamic stability must be maintained and improved outcomes have never been proved.⁹ Propofol is recommended for the control of ICP, but not for improvement of 6-month outcomes.⁹

Nutrition

It is known that patients with TBI have dysfunction of metabolism. These patients require a higher nitrogen intake as their nitrogen balance becomes negative. Studies show that TBI patients’ caloric intake had a mean increase of 140%. Studies have shown a decreased mortality rate when full caloric replacement is achieved by 7 days. Typically to reach this goal caloric replacement begins around 72 hours after injury.

There are three ways to initiate early feeding: gastric, jejunal, and parenteral. It is important to maintain normoglycemia in head injury patients as hyperglycemia has been associated with worse outcomes.

Current level II evidence recommends that patients should be fed full caloric replacement by 7 days after injury.⁹

Antiseizure Prophylaxis

The role of prophylactic anticonvulsants in patients with severe head injury has been more clearly defined with the advent of the published guidelines. Post-traumatic seizures are classified as “early,” occurring within 7 days of injury, or “late,” occurring more than 7 days after the injury.^75,76 It is desirable to prevent early and late seizure activity, although these medications have been associated with adverse and neurobehavioral ill effects. The classic study by Jennett⁷⁷ found post-traumatic epilepsy to occur in about 5% of all patients admitted to the hospital with closed head injuries and in 15% of those with severe head injuries. Three main factors were found to be linked to a high incidence of late epilepsy: early seizures occurring within the first week, an intracranial hematoma, or a depressed skull fracture. Recent updates show that post-traumatic seizures are also associated with GCS scores less than 10, penetrating head wound, or a seizure within the first 24 hours. Although certain earlier studies were unable to show significant benefit of prophylactically administered anticonvulsants, a double-blind study of 404 patients with severe head injury, who were randomized to receive phenytoin or placebo beginning within 24 hours of injury and continuing for 1 year, found that phenytoin reduced the incidence of seizures in the first week after injury but not thereafter.⁷⁸ This study appears to justify stopping prophylactic convulsants after the first week in most cases. In patients who have had a seizure, anticonvulsants are continued for at least a year.

With the recent use of Keppra (levetiracetam) as an antiepileptic, with its relatively low side effect profile, studies have been done to evaluate its efficacy compared to the gold standard Dilantin (phenytoin). It does appear to be as effective as Dilantin at preventing early seizures with a lower side effect profile.^79,80 Larger scale studies will need to be done to confirm this finding. It should also be noted the Keppra had a tendency to show more seizure activity on EEG analysis in one study.⁷⁹

Current BTF recommendations show level II evidence that Dilantin and valproate are not indicated to prevent late onset seizure activity.⁹ Level II evidence shows that antiepileptic medication is indicated to prevent early onset seizure (within 7 days); however, early onset post-traumatic seizure have not been proved to be associated with worse outcomes.⁹

Hyperventilation

Hyperventilation has been used in the treatment of severe TBI for the past 20 years. Recent pathophysiological understanding of TBI and the mechanism of ICP lowering of hyperventilation have put it under recent scrutiny. Hyperventilation decreases ICP by decreasing CO₂ leading to cerebral vasoconstriction. This in turn leads to decreased cerebral blood flow (CBF). Aggressive sustained hyperventilation may lead to cerebral ischemia and stroke, especially in the severe TBI patient who may already have alterations in CBF and autoregulation.

Hyperventilation does have utility in the deteriorating TBI patient as a temporizing measure until more definitive treatment of elevated ICP may be implemented.

Current BTF recommendations show level II evidence against the routine use of prophylactic hyperventilation to PaCO₂ less than 25 mm Hg.⁹ Level III evidence exists that hyperventilation may be used as a temporizing measure in the acutely deteriorating patient.⁹ Hyperventilation should be avoided in the first 24 hours after TBI when CBF may be critically reduced. If hyperventilation is used, there is level III evidence for jugular venous oxygen monitoring or brain tissue oxygen tension monitoring.⁹

Steroids

While steroids are clearly useful in reducing the edema associated with brain tumors, their value in head injury is not clear. In fact, most studies to date have not demonstrated any beneficial effect associated with steroids in terms of either ICP control or improved outcome from severe head injury. Furthermore, there is some evidence that steroids may have a deleterious effect on metabolism in these patients. It is possible that very high doses of particular steroids may have a beneficial effect in certain subsets of head-injured patients. However, currently available steroids in standard dose regimens have not proved to be valuable in severe head injury.

Level I evidence currently recommends against the routine use of steroids for improving outcome or reducing ICP.⁹ It has been shown in patients with moderate to severe TBI on high-dose methylprednisolone that mortality rate is increased.⁹

Indications for Surgery

An important reason for operating on a mass lesion is a midline shift of 5 mm or more. Such a shift may be demonstrated by CT scan, occasionally by angiography or ventriculography. Most epidural, subdural, or intracerebral hematomas associated with a midline shift of 5 mm or more are surgically evacuated. In a patient who has a small hematoma causing less than 5 mm shift and is alert and neurologically intact, a conservative approach is justified. However, the patient may deteriorate, and very close observation is vital. Should there be any change in mental status, a repeat CT scan should be obtained immediately.

Our policy is to operate on all comatose patients with an intracranial mass lesion and 5 mm or more of midline shift unless they are brain-dead. This policy is based on evidence that some patients with bilaterally nonreactive pupils, impaired oculocephalic responses, and decerebrate posturing can nevertheless make a good recovery. In one series, 3 of 19 such patients who were treated maximally ended up in the “good” or “moderately disabled” category, despite the foreboding constellation of signs.⁸¹

The management of brain contusions is somewhat less clear-cut. Galbraith and Teasdale,⁸² in their series of 26 patients with acute traumatic intracranial hematomas who were managed without surgery, found that all patients with ICP greater than 30 mm Hg eventually deteriorated and required surgery. In contrast, only one patient with ICP less than 20 mm Hg deteriorated. Patients in the 20 to 30 mm Hg range were about evenly divided between the surgical and nonsurgical groups.

We have recently analyzed our experience with 130 head-injured patients with pure contusions who were managed with CT scanning and ICP monitoring as needed.⁸³ This study showed that patients with brain contusions who could follow commands at admission did not require ICP monitoring and, as a rule, did well with simple observation. However, those who could not follow commands (in the absence of a focal lesion in the speech area) often had intracranial hypertension and needed to have their ICP monitored. The majority of these patients who had a midline shift of 5 mm or more required surgery.

It has been demonstrated conclusively that patients with a large (over 30 mL) temporal lobe hematoma have a much greater risk of developing tentorial herniation than those with a frontal or parieto-occipital lesion.⁸⁴ The bias should therefore tilt toward early surgery in such cases.

Once a decision has been made as to whether the patient is a surgical candidate or not, he or she is promptly moved to the operating room or to the neurosurgical intensive care unit (NICU), respectively. If the patient is harboring a mass lesion, mannitol (1-2 g/kg) should be administered en route to the operating room. In addition, the patient can be hyperventilated briefly to achieve an arterial PCO₂ of 25 to 30 mm Hg. As in all the maneuvers undertaken thus far, time is of the essence. The sooner the mass lesion is evacuated, the better the possibility of a good recovery.²⁴ If, on the other hand, no surgical lesion is found, the patient is carefully monitored in the NICU, both clinically and with various physiological parameters, notably ICP recordings and serial CT scans. Any rise in ICP above 20 mm Hg that cannot be readily explained and reversed or any deterioration in neurological status warrants prompt repetition of the CT scan followed by appropriate corrective measures.

Because there is great concern about increased ICP as a result of a mass lesion, the anesthetic agents that are used in head-injured patients preferably should not increase the ICP. Nitrous oxide has only a slight vasodilatory effect and generally does not cause a significant ICP increase. It is therefore considered a good agent for use in the head-injured patient. A commonly used combination is nitrous oxide with oxygen, intravenous muscle relaxant, and propofol. Hyperventilation and mannitol prior to and during induction can blunt the vasodilatory effect and limit intracranial hypertension to some degree while the cranium is being opened. If, during surgery, malignant brain swelling occurs that is refractory to hyperventilation and mannitol, pentobarbital in large doses (5-10 mg/kg) should be used. This agent can cause hypotension, especially in hypovolemic patients, and should therefore be used with caution.

Subdural Hematomas

Acute subdural hematomas may result from bleeding from lacerated brain, ruptured cortical vessels, or an avulsed bridging vein. The most common sites for brain injury are the inferior frontal lobes and the anterior temporal lobes. In the surgical management of subdural hematomas, a large fronto-temporoparietal question mark–shaped incision is recommended. This allows the surgeon to deal with bleeding near the midline as well as to débride effectively parts of the frontal, temporal, and parietal lobes as needed. If the patient is deteriorating rapidly, a quick temporal decompression can be performed via a small craniectomy before opening up the rest of the flap. This maneuver could reduce the probability of tentorial herniation. A generous subtemporal craniectomy may be useful in postoperative ICP control. The role of decompressive craniotomy with removal of the bone flap and creation of a dural pouch to allow brain swelling is currently being examined.

Epidural Hematomas

Epidural hematomas are most often located in the temporal region and often result from tearing of the middle meningeal vessels due to a temporal bone fracture. Venous epidural hematomas may occur as a result of a skull fracture or an associated venous sinus injury. These tend to be smaller and usually have a more benign course. Such hematomas often present several hours or days after the initial injury and can be managed nonsurgically. However, usually an epidural hematoma represents a surgical emergency and should be evacuated as rapidly as possible. Every effort should be made to relieve the pressure as soon as possible. A more localized craniotomy flap is warranted for epidural hematomas.

Contusions/Intracerebral Hematomas

Contusions are most often located in the anterior and inferior frontal lobes as well as the anterior temporal lobes. Quite commonly, the CT appearance of a contusion evolves over several days so that what are initially small “salt and pepper” lesions coalesce to form hematomas. This phenomenon is also termed delayed traumatic intracerebral hematoma. Patients who are awake and alert but demonstrate cerebral contusions can be managed without surgery in the vast majority of cases.⁸³ However, patients who are comatose and have a significant midline shift usually need surgery. Between these two extremes, there are patients who demonstrate alterations in levels of consciousness or focal neurological deficits; in these, the decision to undertake surgical débridement is not always easy. As a general rule, débridement of the left frontal and temporal lobes is undertaken more reluctantly because the speech area is on this side.

Depressed Skull Fractures

A skull fracture is considered significantly depressed if the outer table of the skull lies below the level of the inner table of the surrounding bone. Sometimes such depression may not be evident on plain radiographs, but it is usually seen clearly on the CT scan. Most closed depressed fractures occur in young children and may be of the ping-pong ball variety. Surgery may be undertaken in such cases for cosmetic reasons or because of brain compression. In compound depressed fractures, the wounds are often dirty and contaminated. Hair, skin, or other foreign debris may be insinuated between the depressed bone fragments. Therefore, except in the simplest of injuries, the use of the operating room for the closure of such wounds is recommended.

Venous Sinus Injuries

Injuries of the major venous sinuses are among the most difficult problems a neurosurgeon has to face. As a general rule, ligation of the anterior third of the superior sagittal sinus is tolerated well; ligation of the posterior third is most likely to produce massive venous infarction of the brain. Ligation of the middle third of the superior sagittal sinus has somewhat unpredictable effects. A dominant transverse sinus usually cannot be safely ligated. Although the use of shunts in the repair of these major sinuses has been often described, in our experience simple pressure with the use of hemostatic agents is much more practical in the majority of cases.

Posterior Fossa Hematomas

Posterior fossa hematomas, fortunately, are less common than supratentorial hematomas. In general, an aggressive surgical approach is recommended for most of these lesions because the patient can deteriorate very rapidly. Because it generally takes longer to expose the posterior fossa and because the brainstem structures are likely to suffer irreversible damage from a shorter period of compression, the surgeon does not have much leeway in terms of time.