Head Trauma

Scalp and cranium

The scalp consists of five tissue layers ( Fig. 33.1 ). The skull is comprised of the frontal, ethmoid, sphenoid, and occipital bones and two parietal and two temporal bones. Each bone consists of solid inner and outer layers separated by a layer of cancellous bone tissue (the diploe). In adults, the bones of the skull average 2 to 6 mm in thickness; the bones in the temporal region are usually the thinnest of the skull. The cranial bones form a smooth outer surface of the skull, but within the cranial vault are many bony protrusions and ridges. “ Contrecoup” brain injuries , such as contusions, may occur on the opposite side of the head impact (coup) as the brain shifts to the uninjured side and strikes against uneven bone surfaces. After the first few months of life, the cranial bones begin to fuse, ultimately forming the rigid, nonexpandable cranial vault. The inner aspect of the skull is lined with the periosteal dura, which is a thick connective tissue layer that adheres closely to the bone surface. The inner meningeal layer of the dura is the outermost covering of the brain. This dural membrane reflects back on itself to make folds within the cranial space. These folds serve to protect and compartmentalize different components of the brain. The midline falx cerebri separates the two cerebral hemispheres from each other. The tentorium cerebelli partitions the cerebellum and brainstem from the cerebral hemispheres. The U-shaped free margin of this dural fold is important in the pathology of the transtentorial herniation syndromes. Within the margins of the dural reflections, the two dural layers separate to form large dural venous sinuses. Injury to the dural sinuses is associated with significant morbidity and mortality because of the potential for uncontrolled hemorrhage.

Brain and cerebrospinal fluid

The brain is a semisolid structure that weighs approximately 1400 g (3 lb.) and occupies approximately 80% of the cranial vault, with the remaining space occupied primarily by vasculature and cerebrospinal fluid (CSF). The brain is covered by three distinct membranes—the meningeal dura, arachnoid layer, and pia ( Fig. 33.2 ). The location of traumatic hematomas relative to these membranes defines the pathologic condition and determines the consequences of the injury.

The brain is suspended in the CSF, which provides some physical buffering for the brain during trauma. CSF is produced by the choroid plexus, located primarily in the lateral ventricles of the brain. CSF passes from the ventricular system into the subarachnoid space that surrounds the brain and spinal cord. The normal pressure exerted by the CSF is 65 to 195 mm H ₂ O or 5 to 15 mm Hg.

The blood-brain barrier (BBB) maintains the microenvironment of the brain tissue and CSF. Extracellular ion and neurotransmitter concentrations are regulated by movement across this barrier. When the BBB is intact, the ability of neuroactive drugs to penetrate the brain tissue usually depends on their lipid solubility. However, the biomechanics of a brain injury or posttraumatic cerebral edema can cause a disruption of the BBB for up to several hours after the insult. In severe TBI, prolonged disruption of the BBB further contributes to the development of posttraumatic vasogenic cerebral edema and higher maximum intracranial pressure (ICP). Mild TBI patients exposed to repetitive biomechanical forces and those with post-concussive symptoms also appear to have higher BBB permeability on neuroimaging. ^,

Cerebral hemodynamics and increased intracranial pressure

The brain has an extremely high metabolic rate, accounting for approximately 20% of the entire oxygen consumption of the body and requiring approximately 15% of total cardiac output. In the normal brain, cerebral blood flow (CBF) is maintained at constant levels. Optimal regional CBF is maintained by the ability of the cerebral vessels to alter their diameter in response to changing physiologic conditions. This response protects the brain by increasing the delivery of oxygen to tissue, enhancing the removal of metabolic end products, and allowing nearly instantaneous adjustments to meet changing metabolic demands. Hypertension, alkalosis, and hypocarbia promote cerebral vasoconstriction, whereas hypotension, acidosis, and hypercarbia cause cerebral vasodilation.

Cerebral vasoactivity is also very sensitive to changes in the partial pressures of carbon dioxide and oxygen (P co ₂ and P o ₂ , respectively). The response to changes in P co ₂ is nearly linear between P co ₂ values of 20 and 60 mm Hg. In this range, lowering P co ₂ by as little as 1 mm Hg decreases the diameter of cerebral vessels by 2% to 3%, corresponding to an overall change in CBF of 1.1 mL/100 g of tissue/min. This is the physiologic rationale for intentional hyperventilation in the setting of rapid and marked increases in ICP. Hyperventilation causes P co ₂ to fall, resulting in cerebral vasoconstriction. However, this is no longer recommended as a mechanism for reducing ICP. The cerebral vessels also respond to changes in P o ₂ . As P o ₂ declines, cerebral vessels dilate to ensure adequate oxygen delivery to brain tissue. When brain injury occurs, increased CBF, vascular dilation, and a disrupted BBB promote vasogenic edema and can further increase ICP. Therefore, avoiding or reversing hypoxia is essential in managing the brain-injured patient.

CBF also depends on the cerebral perfusion pressure (CPP), which is the pressure gradient across the brain. CBF remains fairly constant when CPP is 50 to 160 mm Hg. This is referred to as autoregulation and occurs with a mean arterial pressure (MAP) of 60 to 150 mm Hg. The determinants of CPP are MAP and the resistance to CBF produced by the mean systemic venous pressure and ICP. Because ICP is higher than mean systemic venous pressure, ICP effects predominate, and CPP can be approximated as follows:

If CPP falls below 40 mm Hg, autoregulation is lost and CBF declines, resulting in tissue ischemia and altered cerebral metabolism. Avoidance of hypotension or elevation in ICP in the head-injured patient helps ensure that CPP can be maintained.

The recommended target CPP value is between 60 and 70 mm Hg. However, the risks of aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors, including the risk of developing adult respiratory failure, should be considered.

Increased intracranial pressure

Increased ICP is defined as a CSF pressure greater than 15 mm Hg (or 195 mm H ₂ O) and is a frequent consequence of a severe TBI. Initially, as ICP increases as a result of a traumatic mass lesion or edema, CSF is displaced from the cranial vault to the spinal canal, offsetting the increased blood or brain volume. When this compensatory mechanism is overwhelmed, the elastic properties of the brain substance allow tissue compression to provide buffering for the increasing pressure. Depending on the location and rate of mass expansion and edema formation, the intracranial compensatory mechanisms can accommodate an increased volume of 50 to 100 mL. Beyond that, even small changes in intracranial relationships, such as from vasodilation, CSF obstruction, or areas of focal edema, may increase ICP. If ICP increases to the point at which CPP is compromised, vasoparalysis occurs and autoregulation is impaired. The CBF then depends directly on the systemic MAP. With the loss of autoregulation, massive cerebral vasodilation occurs. Systemic pressure is transmitted to the capillaries, contributes to vasogenic edema, and further increases ICP.

ICP above 22 mm Hg is associated with increased mortality requiring intervention and treatment. If ICP is not controlled, herniation will occur, resulting in brainstem compression and cardiorespiratory arrest. Simple techniques to reduce ICP include head of bed elevation to 30 degrees and keeping the neck in a neutral position. Common therapies include use of osmotic and diuretic agents such as mannitol or hypertonic saline (HTS), and CSF drainage. Therapeutic hyperventilation, once almost universally used, is potentially harmful and is now recommended only as a temporizing measure for a select group of patients for whom other measures are not available or have failed.

Cushing reflex

Progressive hypertension associated with bradycardia and diminished respiratory effort is a specific response to acute, potentially lethal increases in ICP. This response is called Cushing reflex or Cushing phenomenon, and its occurrence indicates that the ICP has reached life-threatening levels. However, only one-third of cases of life-threatening increased ICP manifest the full triad of hypertension, bradycardia, and respiratory irregularity.

Direct injury

Direct head trauma occurs when the head is struck, or its motion is suddenly arrested, by an object. The resulting damage to the skull and brain depends on the consistency, mass, surface area, and velocity of the object striking the head. Direct injury can also be caused by compression of the head. External signs of trauma are frequently noted at the site of impact or compression force where the skull initially bends inward at the point of contact. If the force is sufficient, a skull fracture can occur. The cranium absorbs some of this applied energy, whereas some energy is transmitted to the brain by shock waves that travel distant to the site of impact or compression. With sufficient and prolonged application of a compression force, the ability of the skull to absorb the force is overcome, and multiple linear skull fractures occur. These resulting fractures can be depressed if a high-energy rapid compression force is applied to a small area of the skull. The extent of direct injury depends on the vasoelastic properties of the underlying region of brain tissue, duration of the force applied, magnitude of the force reaching the brain tissue, and surface area of the brain that is affected.

Indirect injury

In indirect brain injury, the cranial contents are set into motion by forces other than the direct contact of the skull with an object. A common example is an acceleration-deceleration injury in which no direct mechanical impact is sustained, but the cranial contents are set into vigorous motion. As the bridging subdural vessels are strained, subdural hematomas (SDHs) may result.

In an indirect injury, differential acceleration of the cranial contents occurs, depending on the physical characteristics of the brain region. As one brain region slides past another, shear and strain occur. These movements result in diffuse injuries, such as a concussion or TAI. Additional injury occurs as the movement of the intracranial contents is abruptly arrested, and the brain strikes the skull or a dural structure. Contrecoup contusions are an example of such an injury. In a penetrating injury, the object produces pressure waves that can strike structures distal to the path of the missile.

Epidural hematoma

An EDH is bleeding that occurs between the inner table of the skull and dura. Most EDHs result from a direct-impact injury that causes a forceful deformity of the skull. Often, a fracture occurs across the middle meningeal artery, or vein, or a dural sinus. The temporoparietal region is the most likely site for an EDH. The high arterial pressure of the bleeding vessel dissects the dura away from the skull, permitting hematoma formation. EDHs are rare in older adults and children younger than 2 years because of the close attachment of the dura to the skull in both patient populations.

Subdural hematoma

An SDH is a hemorrhage that occurs between the dura and brain and is usually caused by acceleration-deceleration injuries. SDH occurs most commonly in patients with brain atrophy, such as alcoholic or older patients, because bridging vessels traverse greater distances than in patients with no atrophy. As a result, the vessels are more likely to rupture with rapid movement of the head. Once they are ruptured, blood can fill the potential space between the dura and arachnoid. SDH is much more common than EDH, occurring in up to 30% of patients with severe head trauma. The slow bleeding of venous structures delays the development of clinical signs and symptoms. As a result, the hematoma compresses the underlying brain tissue for prolonged periods and can cause significant tissue ischemia and damage. Approximately 20% of patients will present with a bilateral SDH. The prognosis of SDH does not entirely depend on the size of the hematoma but rather on the degree of brain injury caused by the pressure of the expanding hematoma on underlying tissue or by other intracranial injuries. Mortality is highest in older adults, patients who have a GCS score of 8 or less, and those with signs of acute herniation syndrome on initial ED presentation. Posterior fossa SDHs make up less than 1% of all reported SDHs. They are caused by occipital trauma that tears bridging vessels or venous sinuses and have a very poor prognosis.

Traumatic subarachnoid hemorrhage

A traumatic SAH is blood within the CSF and meningeal intima and probably results from tears of small subarachnoid vessels. Traumatic SAH is detected on the first CT scan in up to one-third of patients with severe TBI and ultimately is identified in almost 50% of patients with severe head trauma. It is therefore the most common CT scan abnormality seen after head trauma. Traumatic intracranial hemorrhage is typically associated with significant morbidity and mortality. Most patients with traumatic SAH and a normal GCS do not require neurosurgical intervention.

Subdural hygroma

A SDHG is a collection of clear, xanthochromic blood-tinged fluid in the dural space. The pathogenesis of an SDHG is not certain. It may result from a tear in the arachnoid that permits CSF to escape into the dural space or effusions from injured vessels through areas of abnormal permeability in the meninges or in the underlying parenchyma. They may accumulate immediately after trauma or in a delayed manner.

Diffuse axonal injury and traumatic axonal injury

Prolonged traumatic coma not caused by mass lesions or ischemic insult is thought to result from diffuse axonal injury (DAI). Although the term diffuse axonal injury has been widely adopted, the distribution of axonal injury is usually not diffuse but multifocal. Axonal injury occurs on a spectrum, with milder cases primarily localized. Furthermore, DAI has been used to describe axonal injury from nontraumatic causes in other neurologic conditions. Accordingly, the term traumatic axonal injury is preferred, particularly in milder cases. In more severe cases, when the axonal injury is more widespread, the term diffuse traumatic axonal injury more appropriately describes the condition.

In TAI, axons sustain a primary insult in which they are torn (axotomy) or stretched, resulting in the formation of axon retraction balls that interrupt synaptic connection and normal axonal function. Secondary insult including disruption of the extracellular brain matrix and influx of inflammatory mediators leads to axonal swelling and disconnection and can lead to axon death (see Fig. 33.2 ). Moreover, acute uncoupling of CBF, metabolism, and apoptosis are thought to be the important factors linked to axonal cell death after TAI. ^{, ,}

Most patients with TAI present with persistent traumatic coma that begins immediately at the time of trauma; however, some patients may recover consciousness briefly before lapsing into prolonged coma. Because diagnostic studies cannot predict the extent of the axonal damage, the severity of the injury is determined by the clinical course. Clinical grades of diffuse TAI have been based on length of coma: (1) grade I (mild)—coma for 6 to 24 hours; (2) grade II (moderate)—coma for longer than 24 hours but not decerebrate; (3) grade III (severe)—coma for longer than 24 hours and decerebrate or flaccid. Currently, no early clinical or biomarker predictor exists that differentiates patients with mild, moderate, or severe diffuse TAI.

Cerebral contusions

Contusions are bruises on the surface of the brain, usually caused by impact injury. Contusions are produced when parenchymal blood vessels are damaged, resulting in scattered areas of petechial hemorrhage and subsequent edema. Contusions develop in the gray matter on the surface of the brain and taper into the white matter. Subarachnoid blood is frequently found overlying the involved gyrus.

Most often, contusions occur at the poles and inferior surfaces of the frontal and temporal lobes, where the brain comes into contact with bone protuberances in the base of the skull. If the contusion occurs on the same side as the impact injury, it is a coup injury; if it occurs on the opposite side, the contusion is a contrecoup injury. Contusions can also develop in the brain tissue that underlies a skull fracture. Multiple areas of contused tissue may be produced with a single impact, often in association with other intracranial injuries. With time, the associated hemorrhages and edema of a contusion can become widespread and serve as a nidus for hemorrhage or swelling, thus producing a local mass effect. Compression of the underlying tissue can cause local areas of ischemia, and tissue infarction is possible if the compression is significant and unrelieved. Eventually, these ischemic areas become necrotic, and cystic cavities form within them.

Intracerebral hematoma

Intracerebral hematomas (ICHs) are formed deep within the brain tissue and are usually caused by shearing or tensile forces that mechanically stretch and tear deep small-caliber arterioles as the brain is propelled against irregular surfaces in the cranial vault. Resulting small petechial hemorrhages coalesce to form ICHs, with 85% in the frontal and temporal lobes. An ICH is often found in the presence of extra-axial hematomas and in many patients multiple ICHs are present. Isolated ICHs may be detected in as many as 12% of all patients with severe head trauma.

Intracerebellar hematoma

Primary traumatic intracerebellar hematomas are rare but can occur after a direct blow to the occipital area. Often, these patients have an associated skull fracture, posterior fossa EDH or SDH, or supratentorial contrecoup hematomas and contusions.

Hypotension

Hypotension, defined as SBP less than 90 mm Hg, has been found to have a negative impact on severe brain injury outcome. Systemic hypotension reduces cerebral perfusion, thereby potentiating ischemia and infarction. Hypotension is associated with a near-doubling of the mortality from TBI and worse outcomes for patients who survive. ^,

Hypoxia

Hypoxia, defined as a P o ₂ less than 60 mm Hg, is relatively common in the brain-injured patient. Causes include: (1) transient or prolonged apnea caused by brainstem compression or injury after the traumatic event; (2) partial airway obstruction caused by blood, vomitus, or other debris in the airway of the traumatized patient; (3) injury to the chest wall that interferes with normal respiratory excursion; (4) pulmonary injury that reduces effective oxygenation; and (5) ineffective airway management, such as the inability to bag-valve-mask or intubate the patient in an effective or timely manner. When hypoxia is documented, the overall mortality from severe TBI may double. ^{, ,} Significant hyperoxia with resultant oxygen toxicity is also associated with worse outcome after TBI, although this relationship is less clearly defined. In TBI, normoxia should be maintained.

Hypocarbia and hypercarbia

Pa co ₂ is one of the most potent drivers of CBF. Hypocarbia (Pa co ₂ ≤35 mm Hg) results in vasodilation, while hypercarbia (Pa co ₂ ≥46 mm Hg) leads to cerebral vasoconstriction. In TBI, both hypocarbia and hypercarbia are associated with increased morbidity. Hypercarbia causes cerebral vasodilatation with a resultant increase in cerebral edema and ICP, and thus is associated with a worsened neurologic outcome. Hypocarbia, generally secondary to hyperventilation, results in reduced CBF and a transient decrease in ICP. For patients with impending brain herniation brief therapeutic hyperventilation may be considered. However, in most patients, hyperventilation should be avoided in favor of maintenance of normal to slightly reduced Pa co ₂ levels.

Anemia

Anemia caused by blood loss can be detrimental to the head-injured patient by reducing the oxygen-carrying capacity of the blood, thus reducing the amount of necessary substrate delivered to the injured brain tissue. When anemia (hematocrit, 30%) occurs in patients with severe brain injury, the mortality rate increases. However, transfusion of red blood cells also has adverse effects in TBI patients. At this time, evidence is insufficient to recommend a restrictive or liberal approach to transfusion in the brain-injured patient and transfusion threshold should be tailored to the individual patient.

Hyperpyrexia

Hyperpyrexia (core body temperature >38.5°C [101.3°F]) is also correlated with worse outcomes after TBI, and its magnitude and duration are contributory factors. Pathophysiology likely involves increased metabolism in injured brain areas, thus recruiting blood flow, with a resultant increase in ICP.

General

The goals of the acute neurologic assessment of head trauma patients include detection of life-threatening injuries and identification of neurologic changes in the immediate post-trauma period. An accurate neurologic assessment in this period serves as a basis for comparison in subsequent examinations. An efficient neurologic examination in the emergency setting includes evaluation of mental status, GCS score, pupillary size and responsiveness, and motor strength and symmetry. If a formal GCS measure is not possible or is difficult because of comorbid confounders, the patient’s mental status should be described in as much detail as possible. Declining mental status after head trauma suggests increasing ICP from an expanding mass lesion or worsening cerebral edema, which may rapidly become life-threatening. The strongest predictors of outcome following moderate and severe TBI are advanced age, pupillary reactivity, and GCS motor score. Additional predictors include the presence of extracranial injuries, CT characteristics including midline shift and subarachnoid bleeding, hypotension, hypoxia, and specific laboratory parameters (including glucose, hemoglobin, and coagulation profiles). ^,

Glasgow Coma Scale

The GCS is a 15-point scale used to quantify the patient’s LOC and as an objective method of following the patient’s neurologic status ( Table 33.2 ). It was originally developed during a time when CT scanning was not available to communicate changes in neurologic status in comatose patients with TBI ( Fig. 33.4 ). The score assigns points based on the patient’s best eye opening (spontaneous opening = 4 to no response = 1), motor response (obeys commands = 6 to no response = 1), and verbal response (oriented = 5 to no response = 1). Recent literature has supported the integration of a pupillary component to the GCS score. Due to its ease of use, it has been adopted in the routine assessment of all trauma patients, including those with MTBI who are not comatose. However, the GCS score can reflect impairment from conditions other than brain injury, such as distracting injuries, intoxication from drugs and alcohol, hypoxemia, and sedative medications. Furthermore, patients can deteriorate from an expanding intracranial hematoma after what appears clinically to be a mild brain injury. Although TBI is often categorized into mild, moderate, and severe based on the GCS score, it actually represents a spectrum of injury and the trend in GCS score is more indicative of outcome than any one score in isolation.

Pupillary examination

An evaluation of the patient’s pupil size and responsiveness is performed early in the initial assessment of the head-injured patient. Pupillary asymmetry, the loss of the light reflex, or a dilated pupil suggests herniation syndrome as increasing pressure on the CN III resulting in compromise of the parasympathetic fibers and pupillary dilation on the affected side. Of note, use of the pupillary examination for localization of an intracranial lesion is neither sensitive nor specific. Further, traumatic mydriasis, resulting from direct injury to the eye and periorbital structures, may confuse the assessment of the pupillary responsiveness. A pupillometer, though not commonly available, may be of some use in objectively determining pupillary reactivity. As with the GCS score, a change in pupillary response is more indicative of intracranial pathology than the initial findings.

Motor examination

The patient’s acute motor examination assesses for strength and symmetry. If the patient is not cooperative or is comatose, motor movement should be elicited by the application of humane external or noxious stimuli (such as a sternal rub). Any movement should be recorded, and voluntary purposeful movement must be distinguished from abnormal motor posturing. If RSI is to be performed, attempts should be made to perform the motor examination before paralytic agents are given as paralysis obscures involuntary reflexes.

Decorticate posturing implies injury above the midbrain and presents as abnormal flexion of the upper extremity and extension of the lower extremity. The arm, wrist, and elbow slowly flex, and the arm is adducted. The leg extends and rotates internally, with plantar flexion of the foot. Decerebrate posturing is the result of a more caudal injury, and therefore is associated with a worse prognosis. The arms extend abnormally and assume an adducted position. The wrist and fingers are flexed, and the entire arm is internally rotated at the shoulder. The neck undergoes abnormal extension, and the teeth may become clenched. The leg is internally rotated and extended, and the feet and toes are plantar-flexed.

Brainstem function

In the acute setting, brainstem activity is assessed by the patient’s respiratory pattern, pupillary size, and eye movements. The oculocephalic response (“doll’s eyes” maneuver) tests the integrity of the pontine gaze centers. The oculovestibular response (using cold water calorics) also permits assessment of the brainstem. Comatose patients no longer demonstrate nystagmus when cold water is placed in the ear canal; the only response is tonic deviation of the eyes toward the instilled cold water. This response is dampened by cerumen or blood in the patient’s ear canal, and the tympanic membrane needs to be intact for this test to be performed. Neither maneuver should be attempted until cervical spine fractures have been ruled out. In patients who are awake and cooperative, a formal CN examination should be performed. In the severely head-injured patient, the CN examination is often limited to the pupillary responses (CN III), gag reflex (CNs IX and X), and corneal reflex (CNs V and VII). Facial symmetry (CN VII) can sometimes be assessed if the patient grimaces with noxious stimuli.