Trauma to the Brain

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59 Trauma to the Brain

Carlos A. David, Jeffrey E. Arle

Traumatic brain injury (TBI), occurring worldwide in relation to various types of civilian and armed forces accidents, is one of the most common mechanisms for serious lifelong morbidity or mortality. Within the United States, one person sustains a head injury every 15 seconds. The societal loss is devastating as the majority of these injuries involve individuals entering adulthood with great promise only to be cut down, often with irretrievable injuries that leave them dependent for their remaining lives. For example, within the United States there are 2 million cases of traumatic head injury annually; 100,000 die within hours, 500,000 require hospital stays, and up to 100,000 have permanent disability. Whether it is a cycling, skiing, or relatively uncommon contact sports injury, or result of an impulsive acceleration while negotiating a challenging roadway to impress peers with one’s driving prowess, or on a battlefield such as currently occurs in Iraq or Afghanistan, the consequences are the same: a very promising or accomplished life has lost all its future potential. Various head injury classification systems exist. These include (1) severity (mild, moderate, severe), mechanism (closed vs. penetrating), (2) skull fractures (depressed vs. nondepressed), (3) presence of intracranial lesions (focal vs. diffuse), and (4) hemorrhages, that is, extra-axillary epidural or subdural, subarachnoid, or focal parenchymatous lobar, or brainstem Duret hemorrhage.

Clinical Vignette

An otolaryngologist requested an expeditious neurologic evaluation of a very vigorous octogenarian who was so fit that he downhill skied 3 weeks earlier; this patient reported recent-onset sense of “spinning vertigo” and cloudiness of vision, precipitated by sudden standing or neck extension. Additionally, he was experiencing new-onset headaches that were becoming increasingly severe and were awakening him from his sleep. Concomitantly he was having difficulty with mental concentration and hand coordination, as well as a feeling of “weak legs.” On further questioning, he recalled that 7 weeks earlier he had slipped on the ice, striking his occiput, while helping to push an auto out of a snow bank.

On examination, he had moderately severe difficulty performing tandem gait (something most healthy 70-year-olds often cannot perform, but this was probably abnormal in this athletic man). The remainder of his neurologic examination was normal. Head computed tomography (CT) demonstrated large biparietal subdural hematomas. Bilateral craniotomies were performed, draining both hematomas. Except for a few focal motor sensory seizures, occurring only in the immediate postoperative period and responding well to phenytoin, his recovery was otherwise excellent.

Comment: This gentleman presented a classic history for subdural hematoma. Initially he had disregarded a moderately significant closed head injury as there were no immediate sequelae other than for a modest scalp contusion. He was symptom-free for 5 weeks. This patient’s initial symptoms were not very impressive because his brain compensated well. Despite a careful neurologic examination, the tandem ataxia was his only neurologic abnormality. This could easily be dismissed as appropriate for age; however, the entire clinical picture was classic for a subdural hematoma until proven otherwise as defined by the CT scans.

General Principles of Head Injury Care

The initial management of severe head injuries, as for any serious trauma victim, includes the “ABC” evaluation for Airway, Breathing, and Circulation and a careful general and neurologic examination.

• A—airway: Suction to free pharynx from blood and other material; intubate after cervical spine evaluation.
• B—breathing: Evaluate rate, rhythm, and breath sounds; ventilate to raise PaO2 and reduce PaCO2 (to lower intracranial pressure [ICP]); monitor arterial blood gas levels.
• C—circulatory status: Start intravenous infusion of normal saline solution, followed by blood if indicated; obtain immediate laboratory work and x-rays; administer steroids and phenytoin, plus pressor agent if required (shock rarely due to head injury alone; search for cause).

Concomitantly, the patient’s general level of responsiveness must be assessed using the Glasgow Coma Scale (Fig. 59-1). The lowest possible score of 3 means that individuals have no ability to open the eyes, no motor response to verbal command or direct stimuli, and no verbal response to the physician’s questions, giving a score of 1 or nil for each of the three components. The highest possible score is 15. Soft tissue injuries are commonly associated with more severe head injuries. A complete examination of the exterior surface of the face and head is vital. Blood loss can be extensive given the location of blood vessels within the dense connective tissue of the scalp, which decreases retraction of cut vessels and promotes bleeding.

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Figure 59-1 Glasgow Coma Scale.

Skull Fractures

These can be located in the calvaria (vault) and/or the basal skull. Fractures of the cranial vault carry a 20 times greater incidence of intracranial hematoma in comatose patients and a 400 times greater incidence in conscious patients. Basal skull fractures, often difficult to identify on head CT, can present with pathognomonic signs, including raccoon or Panda bear eyes, battle signs (ecchymosis over the mastoid), and cerebrospinal fluid (CSF) leakage from the nose, throat, or ears (Fig. 59-2). Most leaks resolve spontaneously. Persistent leaks necessitate operative treatment (Fig. 59-3).

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Figure 59-2 Basilar Skull Fractures.

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Figure 59-3 Signs Suggesting Need for Operation.

Depressed fractures, and those along the temporal bone, are more commonly associated with injury to the brain or blood vessels. A fracture line across the middle meningeal artery may predispose to an epidural hematoma. Open fractures with their communication between the intracranial vault and the external environment are associated with higher risks of spinal fluid leaks and infection (Fig. 59-4).

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Figure 59-4 Compound Depressed Skull Fractures.

Extra-Axial Traumatic Brain Injuries

Traumatic Subarachnoid Hemorrhage

This is the most common sequela of TBI and is typically associated with other types of intracranial lesions. Subarachnoid hemorrhage (SAH) can range from clinically insignificant to fatal. These SAH blood products can obstruct CSF reabsorption, leading to increased intracranial pressure (ICP) with hydrocephalus. Treatment of SAH often involves placement of ventricular drains and shunting systems for secondary hydrocephalus.

Epidural Hematomas

These represent an acute blood collection contained between the dura and inner table of the skull. These occur in approximately 2% of TBIs (Fig. 59-5). Epidural hematomas (EHs) most commonly develop in the temporal and parietal regions; 90% of EH are associated with a skull fracture. Arterial lacerations, particularly of the middle meningeal artery (Fig. 59-6) or, less commonly, venous injuries, initiate the formation of hematomas. Contiguous lacerations of the dura mater allow this blood into the epidural space.

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Figure 59-5 Epidural Hematoma.

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Figure 59-6 Meningeal Arteries and Dura Mater.

Immediately after the closed head injury, the patient “typically” experiences an initial but relatively brief loss of consciousness secondary to the primary concussive injury. This is then followed by a lucid interval with return of wakefulness. Subsequently, as the torn vessels leak, an epidural hematoma develops and enlarges, leading to a rapid lapse into coma. Sometimes this entire process may transpire from injury, to transient loss of consciousness, and to a brief period of a “paradoxically reassuring alertness,” only to have a devastating, often irreversible, coma develop within just 1 hour after the blunt head injury (see Fig. 59-3). However, this classic presentation occurs in less than one third of affected individuals. The actual rate of symptom progression depends on the type of associated brain injuries, their etiology, and the subsequent precise rate of blood accumulation within the epidural space.

Cranial CT imaging usually demonstrates a hyperdense, biconvex collection between the skull and brain (Fig. 59-7). On occasion, the initial CT is normal as the hematoma has yet to develop to a size that is definable. Thus when the patient is “at risk,” it is essential to be prepared to repeat the CT scan at the slightest change in clinical status. Once the EH is identified, emergency surgical evacuation is indicated. Any failure to recognize an epidural hematoma has a most significant mortality depending on patient age, time of treatment, hematoma size, and associated injuries.

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Figure 59-7 CT and Angiogram of ICH.

Acute Subdural Hematoma

These blood collections are located between the brain parenchyma and the dural membranes and are classified by their temporal profile. Acute subdural hematomas (SDHs) occur in 15% of TBI patients; these are seven to eight times more common than epidural hematomas. Older individuals are at greater risk because as the brain ages, there is an innate atrophy of the cerebral cortex. Thus in seniors, as the brain “normally” lessens in volume, an increasing space develops within their subdural compartment. In turn this leads to increased stretch on the bridging veins between the skull and the cerebral surface (Fig. 59-8). When any individual sustains direct head trauma, the brain parenchyma accelerates and decelerates in relation to fixed dural structures. This leads to a tearing of the now anatomically stretched veins that form a “bridge” between the cerebral cortex and the skull. Similarly concomitant injury to cortical arteries can also lead to bleeding into the subdural space (Fig. 59-9).

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Figure 59-8 Superficial Cerebral Veins and Diploic Veins.

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Figure 59-9 Acute Subdural Hematoma.

Clinical Presentation and Diagnosis

The initial severity of the injury determines the patient’s clinical presentation; this varies from neurologically intact, to altered mental states, subsequently associated with pupillary inequality and motor weakness, and eventually becoming comatose with signs of decorticate or decerebrate posturing. The lucid interval, a classical finding with epidural hematoma, is also commonly seen with acute SDH. Brain CT is the initial test of choice for detecting SDH and concomitant brain injuries. An acute SDH is recognized by its hyperdense crescent-shaped image between the brain and skull (see Fig. 59-7). Unlike epidural hematomas, SDHs typically cross skull suture lines, and sometimes extend along the falx cerebri. Head CT sometimes underestimates the size of the SDH given the similar imaging density of the nearby bone.

Treatment and Prognosis

If the patient has mental status changes or signs of focal cerebral compromise, beginning treatment of acute SDH as rapidly as possible with medical management for increased ICP and the associated cerebral edema using mannitol is very useful. Surgical intervention with a craniotomy is appropriate for individuals whose SDHs have mass effect, leading to focal neurologic deficits. Once a significant SDH is defined, surgical evacuation of the clot must be expeditiously performed. A burr-hole trephine evacuation is inadequate because the clot is often already more viscous than normal blood. Increased postoperative ICP occurs in almost 50% of SDH patients, and thus the initial medical management must be continued (Fig. 59-10). Residual and recurrent hematomas are also postoperative concerns.

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Figure 59-10 Intensive Medical Management of Severe Head Injury.

An acute SDH is often associated with a poor outcome. The combination of the hematoma with other injuries, particularly those affecting the brain parenchyma, is associated with a 50% mortality rate. Of those patients who do survive a significant number have permanent mental and physical disabilities. Outcomes are strongly predicted by patient age and initial presentation. Mortalities of 20% are recorded for individuals younger than 40 years, but this number increases to 65% for those older than this. This is a devastating lesion in senior citizens as there is an 88% mortality for octogenarians. The initial consciousness level also provides a prognostic guide. Conscious patients have a mortality rate of less than 10%, whereas unconscious patients have 45–60% mortality.

Chronic Subdural Hematoma

These subdural blood collections commonly appear 2–3 weeks after an often seemingly innocuous injury, as illustrated in the initial vignette. Their incidence is 1–2 per 100,000 persons each year. Most chronic SDH patients are older than 50 years. Chronic alcoholics or patients with coagulopathies, particularly from iatrogenic sources such as anticoagulants, are more prone to bleeding with relatively minor trauma such as striking one’s head on the door frame on entering an automobile.

Initially, relatively minor amounts of blood enter the subdural space after trauma or spontaneous hemorrhages. Subsequently, over a few weeks’ interval these blood products lead to a membrane formation at both the inner and outer aspects of the hematoma. Eventually, these membranes are prone to low-grade bleeding and thus lead to slow enlargement of the SDH. Concomitantly a higher osmotic pressure develops within the subdural hematoma leading to an osmotic gradient that promotes passage of CSF into the initial SDH and consequently this mass lesion gradually enlarges. The clinical course is variable and not predictable. If the SDH reaches a critical size to compromise brain function, symptoms will develop. In contrast, a number of SDHs will slowly reabsorb without ever becoming symptomatic.

Clinical Presentation and Diagnosis

The presentation may range from subtle focal signs of cerebral compromise as determined by the site of injury such as aphasia, focal weakness or sensory loss, confusion, or seeming early dementia with bifrontal lesions, to those symptoms of the various herniation syndromes. A high clinical suspicion of SDH must always occur especially with the at-risk individual whenever there is remote history of head trauma. CT is the study of choice (see Fig. 59-7). Occasionally, a brain MRI serendipitously leads to a diagnosis of SDH in patients presenting with stroke-like or seizure-type symptoms.

Treatment and Prognosis

Medical management and observation is recommended for individuals with subtle clinical symptoms and signs: discontinuation of anticoagulant medications, close observation in a hospital or by a reliable adult, and serial CT. Surgical therapy is advisable for any chronic SDH that is causing significant mass effect or is associated with significant clinical morbidity. Up to 45% of chronic SDHs reaccumulate. Postsurgical mortality is approximately 10%. Unlike acute SDH, most chronic subdural patients are able to return to their previous levels of functioning although about 10% may develop seizures.

Intra-Axial Traumatic Injuries

Cerebral Contusions

These are the second most common of the TBI lesions. Usually the frontal and temporal lobes are affected. Basically a contusion is a bruise to the brain tissue per se. These lesions are composed of hemorrhage, infarcted tissue, and necrosis. Coup lesions are those found under the sites of direct injury; contrecoup lesions are located at sides opposite to impact secondary to brain tissue necrosis and edema sites, where the brain decelerates against the skull (often the frontal and temporal poles). Cortical contusions are most common, but they also will occur within the deep white matter.

Clinical presentation varies widely and is predicated on the location and size of the lesion. Many brain contusions enlarge during the first few days after injury. This can become very significant in patients who sustain high-impact trauma. Surgical intervention is usually not required for intracerebral contusions, especially for small, deep subcortical contusions; these are generally managed medically. However, larger lobar contusions with significant signs of mass effect sometimes require craniotomy and evacuation. Temporal lobe contusions are potentially the most dangerous given their location near the brainstem. Repeat CT scanning is essential to follow these lesions. Mortality rates for cerebral contusions range from 25% to 60%.

Intraparenchymal Hematomas

About a quarter of head injury patients develop intraparenchymal hematomas: these are well demarcated areas of acute hemorrhage. The basic pathophysiology is similar to contusions. Most (90%) occur within the frontal and temporal lobes. Shear injury leads to deep cerebral white matter hematomas. Two thirds of intraparenchymal hematomas are also associated with concomitant subdural or epidural hematomas (see Fig. 59-9). An intraventricular hemorrhage, often complicated by hydrocephalus, may also commonly develop.

Depending on the severity of the injury, almost half of these patients present with a loss of consciousness. Other signs and symptoms relate to the size and location of the hemorrhage.

Medical management is the treatment of choice for deep or small hemorrhages and for unstable patients. Surgical resection is indicated for large superficial lobar hematomas associated with clinical signs of mass effect. Ventricular CSF drains also serve to monitor their ICP. These provide a means to follow neurologically severely compromised patients.

Mortality rates vary from 25% to 75% in patients with an intraparenchymal hemorrhage. The eventual outcome of those who survive depends on their level of consciousness at presentation, size and location of hematoma, and severity of concomitant injuries. Lastly, age is a very important determiner of morbidity. The teenager may eventually have his or her posttraumatic parenchymal hemorrhage reabsorbed without significant residual neuronal damage. In contrast, the senior citizen may already have sustained age-related neuronal compromise and thus have a much diminished prognosis for reasonable return to a productive life.

Diffuse Axonal Shear Injury

The combination of rotational acceleration and deceleration of the brain during traumatic impact results in shearing of both diffuse axonal pathways and small capillaries. High-speed motor vehicle accidents are the most common etiology in the civilian population. Very microscopic, penetrating blood vessels are damaged at multiple levels including the corticomedullary junction, corpus callosum, internal capsule, deep gray matter, and upper brainstem, leading to numerous small hemorrhagic foci. Early on, conventional CT scanning will not demonstrate any abnormality related to this type of lesion. The micro-hemorrhages may be best seen on gradient echoT2-weighted sequences (Fig. 59-11). Later there may be nonspecific white matter hyperintense lesions with atrophic changes. Shear injury is very commonly associated with other intraaxial and extraaxial traumatic insults, including focal hematomas. Shear injury is a major prognostic contributor to overall head injury morbidity.

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Figure 59-11 Shear Injury.

Often the initial brain CT is unremarkable, especially when there is no concomitant hematoma, as there are no specific findings associated with shear injury. However, during the first 48–72 hours after the injury, cerebral edema may become obvious. Small areas of punctate contusions can also be found in areas of diffuse axonal injury. The most common MRI finding is the presence of multifocal areas of abnormal signal (bright on T2-weighted images) at the white matter in the temporal or parietal corticomedullary junction or in the splenium of the corpus callosum.

Patients with diffuse axonal injury often develop cerebral edema, with resulting increased ICP. Pressure monitors are required in patients whose clinical examination results are not reliable. Intraparenchymal monitors are usually used because the ventricles are often so compressed that ventricular catheter placement is difficult (see Fig. 59-11).

It is this group of patients who may remain comatose for extended periods. This clinical picture is classified as a persistent vegetative state (Chapter 16). This entity carries an extremely poor prognosis (Fig. 59-12).

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Figure 59-12 Persistent Vegetative State.

Posterior Fossa Lesions

Cerebellar and posterior fossa traumatic brain lesions account for only 5% of post-TBI sequelae. Epidural hematomas, SDH, and intracerebellar hematomas are the most common traumatic lesions at this level. Because of the limited space within the posterior fossa, strategically placed lesions at this level can rapidly lead to early neurologic decline secondary to both brainstem compression and acute hydrocephalus. Careful assessment of patients for these injuries is critical, especially in high-risk individuals with basal skull fractures. MRI is the study of choice for detecting posterior fossa damage. Normal bony architecture, as imaged with brain CT, frequently prevents identification of posterior fossa lesions artifacts in patients with TBI. Therefore, evacuation of the hematoma with posterior fossa craniectomy is the primary treatment modality when there is a critical mass lesion (Fig. 59-13). In contrast, a ventricular drain is adequate for intraventricular bleeds.

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Figure 59-13 Exploratory Burr Holes and Removal of Posterior Fossa Hematoma.

Traumatic Brain Injury in Military Combat Settings

Significant effort has gone into defining appropriate guidelines of care for traumatic brain injury (TBI) since 1990. In 2005, Guidelines for Field Management of Combat-Related Head Trauma was offered by the Brain Trauma Foundation and also provides levels of evidence found in published literature supporting its conclusions. Nearly all of the supporting scientific literature is Class III evidence. Combat brain trauma tends to occur from high-velocity rifle rounds (as opposed to handguns) and penetrating shrapnel and debris, with or without blast injury. Yet, although there are differences in the circumstances and nature of brain traumas that occur within combat, the same general principles for managing both initial and ongoing care for TBI should be adhered to. This includes the maintenance of PO2 >90 mm Hg and systolic blood pressure >90 mm Hg, the use of mannitol or hypertonic saline if there is evidence of severe neurological dysfunction (Glasgow Coma Scale [GCS] score <8) to help reduce ICP, and the avoidance of hypocapnia (PCO2 <30–35 mm Hg) in all but the acute setting of impending herniation. Differences between combat and civilian care may include limited ability to obtain an adequate exam or history, delay in transportation of patient, or no access to the patient. Inability to secure an area may require assessment of the casualty while under heavy fire. Chemical or radioactive contamination may require medical personnel to don protective clothing that can severely limit assessment, and finally the tactical plans may hamper mobilization of appropriate resources. Supply of bandages, fluids, and medications alone for field medics who are under siege for days or even weeks at a time may be extremely difficult. Not all aspects of the care and assessment of neurologic injuries in a combat setting are negative relative to the civilian world. The dedication of medics for saving casualties and “leaving no one behind” is extraordinarily high and is an important foundation to support the confidence of combat soldiers. Soldiers are among the most physiologically robust and compliant of patients, and medics’ acts of fearlessness to provide care in the battlefield setting are legendary.

One main difference between the civilian and combat setting is the need for multicasualty triage in the field; this is one of the primary responsibilities of combat medics, who have limited ability, if any, to provide mechanical ventilation or ICP management. Measurement of GCS serves to assess severity of TBI and outcome and may be a useful baseline measure for triage decisions. However, its use is only helpful once casualties reach a military hospital level of assessment. Moreover, reliability of combat medics, and even military physicians, in measuring GCS has been shown to be poor compared to civilian personnel, as Emergency Medical Services/paramedics have more medical training.

Recent experience in Afghanistan and Iraq by U.S. neurosurgeons has led to a more aggressive surgical approach in handling brain trauma: aggressive cranial decompression to help manage brain edema, including bilateral hemicraniectomies to allow the brain to swell without pressure from the fixed cranial volume. This minimizes the need for intensive ICP medical management in these initial combat hospital facilities. If patients survived this acute care, better and longer-term management and ultimately cranioplasty repair could be performed at better-equipped facilities in higher-level settings.

Overall Treatment Protocols

TBI is one of the primary medical challenges of the current Iraq and Afghanistan wars. Significant effort has gone into further definition of guidelines for their care. In 2005, Guidelines for Field Management of Combat-Related Head Trauma were published. Nearly all supporting scientific literature is Class III evidence. None is Class I. Combat brain trauma tends to occur from high-velocity rifle rounds (as opposed to handguns) and penetrating shrapnel and debris, with or without blast injury. It is debatable whether civilian outcome studies, where injury etiology is typically different, can be used to draw conclusions for combat-related brain trauma.

However, although there are clearly differences in the setting, circumstances, and nature of the typical combat TBI, it was found that the same general principles for managing both initial and ongoing care are applicable. These include the maintenance of PO2 >90, systolic blood pressure >90, the use of mannitol or hypertonic saline with evidence of severe neurologic dysfunction (generally GCS score <8) to help reduce ICP, and the avoidance of hypocapnia (Pco2 <30–35) are vital. Surgery is indicated where there is a focal decompressible lesion in the acute setting of impending herniation.

Recent military experience has led to a more aggressive surgical approach in handling brain trauma. Because two surgeons were often working together in a highly efficient and staffed operating theater environment, in many cases receiving severe head trauma within minutes of the injury, even the soldier with a low GCS score underwent aggressive cranial decompression to help manage brain edema (Fig. 59-14). This minimizes the need for intensive ICP medical management in these initial combat hospital facilities. It will take time and long-term follow-up to eventually evaluate the prognosis for useful brain recovery with such aggressive and bolder therapeutic approaches.

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Figure 59-14 Brain Injury in Military Combat.

A recent civilian study with TBI demonstrated that decompressive craniectomy is associated with a better-than-expected functional outcome in patients having medically uncontrollable ICP and/or brain herniation. This therapeutic approach was compared with outcomes in other previously reported control cohorts. Thus, there is a very pressing need to standardize treatment of TBI. It is estimated that the annual fiscal savings in the United States would include $262 million in medical costs and $3.84 billion in lifetime societal costs. This is absolutely staggering as it puts into perspective what the annual economic loss must be for management of acute traumatic brain injury.

Long-Term Prognosis of Traumatic Brain Injury

Typically it is often difficult to accurately determine a patient’s eventual functional outcome despite the physician’s desire to answer this very critical issue for the patient’s family. Although it is relatively easy to identify individuals at both ends of the trauma severity spectrum, it is more difficult in the gray middle-zone area. Useful factors include injury severity, the initial Glasgow Coma Scale score, response to therapy, global that is shear versus focal injuries, associated injuries, age, medical comorbidities, and the ability to rapidly commence medical and surgical interventions. The final degree of neurologic recovery often stabilizes 6 months to 1 year after TBI.

Additional Resources

Aarabi B. Surgical Outcome in 435 Patients who sustained missile head wounds during the Iran-Iraq War. Neurosurgery. 1990;27:692-695.

Aarabi B, Taghipour M, Alibaii E, et al. Central Nervous System Infections after Military Missile Head Wounds. Neurosurgery. 1998;42:500-509.

Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care.

Chesnut RM. Management of brain and spine injuries. Crit Care Clin. 2004;20:25-55.

Fakhry SM, Trask AL, Waller MA, et al. Management of brain-injured patients by an evidence-based medicine protocol improves outcomes and decreases hospital charges. J Trauma. 2004;56:492-500.

Faul M, Wald MM, Rutland-Brown W, et al. Using a cost-benefit analysis to estimate outcomes of a clinical treatment guideline: testing the Brain Trauma Foundation guidelines for the treatment of severe traumatic brain injury. J Trauma. 2007 Dec;63(6):1271-1278.

Guidelines for Field Management of combat-related head trauma, Brain Trauma Foundation, New York, NY, 2005.

2007 Guidelines for the management of severe traumatic brain injury. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons. J Neurotrauma. 2007;24(Suppl. 1)):S1-106. A detailed overview

Personal communication, Brett Schlifka, MD, Maj, USA, 2006.

Riechers GR, Ramage A, Brown W, et al. Physician knowledge of the Glasgow Coma Scale. J Neurotrauma. 2005;22(11):1327-1334.

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