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.