369. TRAUMATIC INJURIES OF THE HEAD AND SPINE - Allan H. Ropper

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Head injuries are frequent in industrialized countries and affect many individuals in the prime of life. Almost 10 million head injuries occur annually in the United States alone, about 20% of which are serious enough to cause brain damage. Among men under 35 years, accidents, usually motor vehicle collisions, are the chief cause of death, and 70% of these involve head injury. Minor head injuries are so common that almost all physicians encounter patients requiring immediate care or suffering from various sequelae. Traumatic spinal cord injuries often occur in conjunction with head injury. The two are best considered together in the context of trauma to the nervous system.

A recent decline in mortality from head and spinal cord injuries can be attributed mainly to the use of seat belts and motorcycle helmets and the development of ambulance systems with trained personnel. In addition, a systematic approach to the evaluation of patients with head and spine trauma, beginning at the scene of the accident, has contributed to the improvement in outcome. Also, the wide availability of computed tomography (CT) and magnetic resonance imaging (MRI) has contributed to advances in diagnosis and intensive care treatment and an understanding of the pathologic lesions that are produced by trauma.

TYPES OF HEAD INJURIES

SKULL FRACTURES

A blow to the skull causes a fracture if the elastic tolerance of the bone is exceeded. Intracranial lesions accompany two-thirds of skull fractures, and the presence of a skull fracture increases manyfold the chances of an underlying subdural or epidural hematoma. Consequently, fractures are important primarily as markers of the site and severity of injury. They are also the cause of cranial nerve injuries and the source of entry pathways to the cerebrospinal fluid (CSF) for bacteria (meningitis), air (pneumocephalus), and leakage of CSF.

Fractures are classified as linear, basilar, compound, or depressed. Linear fractures, which are most often associated with subdural or epidural hematomas, account for 80% of all skull fractures. They are usually oriented from the point of impact toward the base of the skull. Basilar skull fractures are often extensions of adjacent fractures over the convexity of the skull but may occur independently owing to stresses on the floor of the middle cranial fossa or occiput. They are usually located parallel to the petrous bone or along the sphenoid bone toward the sella turcica and ethmoidal groove. Although most are uncomplicated, basilar skull fractures can cause CSF leakage, pneumocephalus, and cavernous-carotid fistulas. Hemotympanum (blood behind the tympanic membrane), delayed ecchymosis over the mastoid process (Battle's sign), or periorbital ecchymosis ("racoon sign") all signify fracture of the basilar skull. Because routine x-ray examination may fail to disclose basilar fractures, they should be suspected if these clinical signs are present. CSF may leak through the cribriform plate or the adjacent sinus and manifest as a watery discharge from the nose (CSF rhinorrhea). Persistent rhinorrhea and recurrent meningitis are indications for surgical repair of torn dura underlying the fracture. The precise site of the leak is often difficult to determine, but useful diagnostic tests include the instillation of water-soluble contrast into the CSF followed by CT with the patient in various positions, and injection of radionuclide compounds or fluorescein into the CSF with an assessment of uptake of these compounds by absorptive nasal pledgets. The site of an intermittent leak is rarely delineated, and most resolve spontaneously. Sellar fractures, even ones associated with serious neuroendocrine dysfunction, are sometimes radiologically occult. Fractures of the dorsum sella may cause sixth or seventh nerve palsies or optic nerve damage. An air-fluid level in the sphenoid sinus suggests a fracture of the sellar floor.

Petrous bone fractures, especially those oriented along the long axis of the bone, may be associated with facial palsy, disruption of ear ossicles, and CSF otorrhea. Transverse petrous fractures are less common; they almost always damage the cochlea or labyrinths and often the facial nerve. External bleeding from the ear is usually from local abrasion of the external canal but can also result from petrous fracture.

Fractures of the frontal bone are often depressed, involving the frontal and paranasal sinuses and the orbits; permanent anosmia results if the olfactory filaments in the cribriform plate are disrupted. Depressed skull fractures are typically compound, but they are often neurologically asymptomatic because the impact energy is dissipated in breaking the bone; however, some are associated with brain contusions and focal neurologic signs

caused by damage to the underlying cortical area. Prompt debridement and exploration of compound fractures are required in order to avoid infection.

CRANIAL NERVE INJURIES

The cranial nerves likely to be injured with head trauma include the olfactory, optic, oculomotor, and trochlear nerves; the first and second branches of the trigeminal nerve; and the facial and auditory nerves. Anosmia and an apparent loss of taste (actually a loss of perception of aromatic flavors, with elementary tastes retained) occur in ~10% of persons with serious head injuries, particularly with falls on the back of the head. This sequela results from displacement of the brain and shearing of the olfactory nerve filaments and may occur in the absence of a fracture. Recovery is the rule, leaving residual hyposmia, but if bilateral anosmia persists for several months, the prognosis is poor. Fractures of the sphenoid bone may rarely bruise or transect the optic nerve, resulting in unilateral partial or complete blindness and an unreactive pupil, usually equal in size to that of the other side and with a preserved consensual light response. Partial optic nerve injuries from closed trauma result in blurring of vision, central or paracentral scotomas, or sector defects. Direct orbital injury may cause short-lived blurred vision for close objects and pupillary paralysis because of reversible iridoplegia. Diplopia limited to downward gaze, which suggests trochlear nerve damage, occurs as an isolated problem after minor injury and can develop after a delay of several days; it may also result from fracture of the lesser wing of the sphenoid bone. The diplopia is corrected if the head is tilted away from the affected eye. Direct facial nerve injury by a basal fracture is present immediately in 3% of severe injuries; it may also be delayed 5 to 7 days. Fractures through the petrous bone, particularly the less common transverse type, are liable to produce this injury. Delayed facial palsy, the mechanism of which is unknown, has a good prognosis. Injury to the eighth cranial nerve from a fracture of the petrous bone causes loss of hearing, vertigo, and nystagmus immediately after injury. Deafness from nerve injury must be distinguished from that due to rupture of the eardrum, blood in the middle ear, or disruption of the ossicles from fracture through the middle ear. A high-tone hearing loss occurs with direct cochlear concussion.

SEIZURES

Convulsions are surprisingly uncommon immediately after a head injury, but a brief period of tonic extensor posturing or a few clonic movements of the limbs just after the moment of impact may occur. However, the superficial cortical scars that evolve from contusions are highly epileptogenic and may later manifest as seizures, even after many years (Chap. 360). The severity of injury determines the risk of future seizures. It has been estimated that 17% of individuals with brain contusion, subdural hematoma, or prolonged loss of consciousness will develop a seizure disorder and that this risk extends for an indefinite period of time, whereas the risk is only 2% after mild injury; the majority of convulsions in the latter group occur within 5 years of injury.

CONCUSSION

Concussion refers to an immediate but transient loss of consciousness that is associated with a short period of amnesia and described as the experience or appearance of being dazed or "star struck." It typically occurs after a blunt impact that creates a sudden deceleration of the cranium and a movement of the brain within the skull. Severe concussion may precipitate a brief convulsion or autonomic signs such as facial pallor, bradycardia, faintness with mild hypotension, or sluggish pupillary reaction, but most patients are neurologically normal. Higher primates are particularly susceptible to concussion; in contrast, billy goats, rams, and woodpeckers can tolerate impact velocity and deceleration 100-fold greater than that experienced by humans. The mechanism of loss of consciousness in concussion is believed to be a transient electrophysiologic dysfunction of the reticular activating system in the upper midbrain caused by rotation of the cerebral hemispheres on the relatively fixed brainstem (Chap. 24).

Gross and light-microscopic changes in the brain are usually absent following concussion, but biochemical and ultrastructural changes, such as mitochondrial ATP depletion and local disruption of the blood-brain barrier, suggest that complex abnormalities occur. CT and MRI scans are usually normal; however, approximately 3% of patients will be found to have an intracranial hemorrhage of some type.

The amnesia of concussion typically follows at least a few moments of unresponsiveness, but rarely there is no loss of consciousness. The memory loss spans the time of, and moments before, mild impact injuries but may encompass previous weeks (rarely months) in cases of more severe trauma. The extent of retrograde amnesia has been suggested as a rough measure of the severity of injury. Any anterograde amnesia is usually brief and

disappears rapidly in alert patients. Memory is regained in an orderly way from the most distant to recent memories, with islands of amnesia occasionally remaining in severe cases. The mechanism of peritraumatic amnesia is not known. Hysterical posttraumatic amnesia is not uncommon and should be suspected when inexplicable abnormalities of behavior occur, such as recounting events that cannot be recalled on later testing, a bizarre affect that emulates the lay notion of amnesia or psychosis (Ganser syndrome), forgetting one's own name, or a persistent anterograde deficit that is excessive in comparison with the degree of injury.

A single, uncomplicated head injury only infrequently produces permanent neurobehavioral changes in patients who are free of preexisting psychiatric problems and substance abuse. However, there has been increasing attention to minor problems in memory and concentration that may have an anatomic correlate in small shearing or other microscopic lesions (see below).

CONTUSION, BRAIN HEMORRHAGE, AND SHEARING LESIONS

A surface bruise of the brain, or contusion, consists of varying degrees of petechial hemorrhage, edema, and tissue destruction. Contusions and deeper hemorrhages result from mechanical forces that displace the hemispheres forcefully relative to the skull by deceleration of the brain against the inner skull, either under a point of impact (coup lesion) or, as the brain swings back, in the antipolar area (contrecoup lesion). Trauma sufficient to cause prolonged unconsciousness usually produces some degree of contusion. Because the motion of the hemispheres brings them into contact with the prominences of the sphenoid and other frontal basal bones, blunt impact, as from an automobile dashboard or from falling forward while drunk, typically causes contusions on the orbital surfaces of the frontal lobes and the anterior and basal portions of the temporal lobes. With lateral forces, as from the doorframe of a car, the contusions are situated on the lateral convexity of the hemispheres. In both instances there may be obverse contrecoup contusions.

Contusions are visible on CT and MRI scans, appearing early as inhomogeneous hyperdensities on CT and as hyperintensities on MRI; the signal changes reflect small scattered areas of cortical and subcortical blood and localized brain edema (Fig. 369-1); there is also some degree of subarachnoid bleeding, which may be detected by scans or lumbar puncture. Confluent, roughly spherical contusions can be distinguished from cerebral hemorrhages by their involvement of the cortical surface. Contusions may acquire a surrounding ringlike contrast enhancement after a week that may be mistaken for tumor or abscess. Glial and macrophage reactions begin within 2 days and result years later in scarred, hemosiderin-stained depressions on the surface (plaques jaunes) that are one source of posttraumatic epilepsy.

The clinical signs produced by contusions vary with their location and size; a hemiparesis or gaze preference, similar to the signs of a middle cerebral artery stroke, is fairly typical. Large bilateral contusions produce coma with extensor posturing. Contusions limited to the frontal lobes produce an abulic-taciturn state and those in the temporal lobe may cause an aggressive, combative, or delirous syndrome, described below. The secondary effects of progressive edema are the most threatening aspect of contusion injury and lead to coma and signs of secondary brainstem compression (pupillary enlargement).

Deep hemorrhages in the central white matter may result from confluent contusions in the depths of a sulcus. However, ganglionic, diencephalic, and other deep hematomas due to torsion or shearing forces in the brain occur independently of surface damage. Large single hemorrhages after minor trauma may bring to attention a bleeding diathesis or cerebrovascular amyloidosis in the elderly. For unexplained reasons, deep cerebral hemorrhages may not develop until several days after severe injury. Sudden neurologic deterioration in a comatose patient or an unexplained rise in intracranial pressure (ICP) should therefore prompt investigation with a CT scan.

Another type of deep white matter lesion consists of widespread acute disruption, or "shearing," of axons at the time of impact. Characteristically there are small areas of tissue disruption in the corpus callosum and dorsolateral pons, but these areas may not be appreciated in scans. The presence of widespread axonal damage of both hemispheres, a state called diffuse axonal injury, has been proposed as the explanation of persistent coma or vegetative state, but small ischemic-hemorrhagic lesions in the midbrain and low diencephalon are as often the cause. Only severe shearing lesions that contain blood are visualized by CT, usually in the corpus callosum and centrum semiovale (Fig. 369-2); however, within days of the injury, MRI scan demonstrates such lesions throughout the white matter, especially with the use of gradient echo MRI sequences.

On occasion, especially in children, cranial trauma causes diffuse brain swelling within a few hours after injury, even though CT may not reveal focal contusions or hemorrhages. The swelling creates a mass effect with disastrous consequences. Swelling is likely due to microvascular disruption and greatly increased cerebral blood flow. Episodes of moderate hypotension after the injury may play a role in this complication.

Residual symptoms and signs of primary or secondary compressive brainstem hemorrhages or ischemic lesions include cerebellar tremor, pupillary enlargement, eye movement abnormalities, and the "locked-in" syndrome (Chap. 24).

SUBDURAL AND EPIDURAL HEMATOMAS

Hemorrhages beneath the dura (subdural) or between the dura and skull (epidural) may be associated with contusions and other injuries, making it difficult to determine their relative contribution to the clinical state. However, subdural and epidural hematomas more often occur as the sole manifestation of injury, and each has characteristic clinical and radiologic features. Because the mass effect and the rise in ICP caused by these hemorrhages may be life threatening, it is imperative that they be identified immediately by CT or MRI scan and evacuated when appropriate.

Acute Subdural Hematoma These lesions become symptomatic minutes or hours after injury. Up to one-third of patients have a lucid interval before coma supervenes, but most are drowsy or comatose from the moment of injury. Direct cranial trauma is not required for acute subdural hemorrhage to occur; acceleration forces alone, as from whiplash, are adequate, especially in the elderly and those taking anticoagulant medications. A unilateral headache and slightly enlarged pupil on the same side are frequently but not invariably found. Stupor or coma, a hemiparesis, and unilateral pupillary enlargement are the typical signs of larger hematomas; pupillary dilation is contralateral to the hematoma in 5 to 10%. In an acutely deteriorating patient with diminished alertness and with pupillary enlargement, burr (drainage) holes or an emergency craniotomy are appropriate, at times even without prior radiographic confirmation of subdural hematoma. Small subdural hematomas may be asymptomatic and usually do not require therapy. A more subacute syndrome from subdural hematoma occurs days to weeks after injury with drowsiness, headache, confusion, or mild hemiparesis; it is seen in alcoholics and in the elderly. Chronic subdural hematoma is described below.

Most subdural hematomas appear as crescentic collections over the convexity of the hemisphere and are located over the frontotemporal region, less often in the inferior middle fossa or over the occipital poles (Fig. 369-3). The degree of midline shift is disproportionately greater than the apparent size of the clot in any one axial CT scan, but the guidelines relating shift to the level of consciousness outlined in Chap. 24 remain useful. Less common instances of interhemispheric, posterior fossa, or bilateral convexity clots are difficult to diagnose clinically, although drowsiness and the signs expected for each region can be detected (Chap 25). Larger clots are thought to be primarily venous in origin, though additional arterial bleeding sites are often found; some large clots, when explored surgically, appear to be exclusively arterial.

Acute Epidural Hematoma Epidural hematomas evolve more rapidly than subdural hematomas and are therefore more treacherous. They occur in up to 10% of severe trauma cases and are less often associated with underlying cortical damage than are subdural hematomas. Most patients are unconscious when first seen. A "lucid interval" of several minutes to hours before coma supervenes is said to be most characteristic of epidural hemorrhage, although it is not common, and epidural hemorrhage by no means is the only cause of this temporal profile.

An epidural hematoma located over the convexity of either lateral temporal lobe is explained by its origin from a torn dural vessel, most commonly the middle meningeal artery, which is transected by a fracture of the squamous portion of the temporal bone. Frontal, inferior temporal, or occipitoparietal epidural hematomas are less frequent, occurring when fractures disrupt branches of the middle meningeal artery. The hematoma strips the tightly attached dura from the inner table of the skull, producing a characteristic lenticular shaped clot on CT (Fig. 369-4). Epidural hematomas may be less frequent in the elderly because of the tighter attachment of dura to skull that occurs with aging. Posterior fossa epidural hematomas are rare and difficult to detect clinically; most result from surgery in that region, such as resection of an acoustic schwannoma.

Chronic Subdural Hematoma A history of trauma may or may not be elicited; 20 to 30% of patients recall no head injury, particularly the elderly and those with a bleeding diathesis. The causative injury may be trivial (striking the head against the branch of a tree, a sudden stop in a car, or minor head contact during a fall or

faint) and is often forgotten because it was remote. Headaches (common but not invariable), slowed thinking, change in personality, a seizure, or a mild hemiparesis emerges weeks or months afterwards. The headache may fluctuate in severity, sometimes with positional changes. Many chronic subdural hematomas are bilateral and produce perplexing clinical syndromes. The initial clinical impression is of a stroke, brain tumor, drug intoxication, depression, or a dementing illness because drowsiness, inattentiveness, and incoherence of thought are more prominent than focal signs such as hemiparesis. Patients with undetected small bilateral subdural hematomas seem to have a low tolerance for surgery, anesthesia, and drugs that depress the nervous system, remaining drowsy or confused for long periods postoperatively. Occasionally a chronic hematoma causes brief episodes of hemiparesis or aphasia that are indistinguishable from transient ischemic attacks.

Skull x-rays are usually normal except for a shift of the calcified pineal body to one side or an occasional unexpected fracture. In very long-standing cases the irregular calcification of membranes that surround the collection may be appreciated. CT performed without contrast infusion shows a low-density mass over the convexity of the hemisphere (Fig. 369-5), but between 2 to 6 weeks after the initial bleeding the clot appears isodense compared to adjacent brain. Bilateral chronic hematomas may fail to be detected because of the absence of lateral tissue shifts; this circumstance is suggested by a "hypernormal" CT scan with fullness of the cortical sulci and small ventricles in an older patient. CT with contrast demonstrates the vascular fibrous capsule surrounding the clot; MRI can reliably identify either a subacute or chronic clot. Lumbar puncture is not recommended for diagnosis because of the risk of worsening tissue shifts but, if performed, shows xanthochromia of the spinal fluid and a variable number of red blood cells. Chronic subdural hematomas can expand gradually and clinically resemble tumors of the brain.

Clinical observation and serial imaging are reasonable in patients with few symptoms and small subdural collections. Treatment with glucocorticoids alone is sufficient in some cases, but surgical evacuation is more often successful. The fibrous membranes that grow from the dura and encapsulate the region require surgical resection to prevent recurrent fluid accumulation. Small hematomas are largely resorbed, leaving only the organizing membranes, which become calcified after many years.

PENETRATING INJURIES, COMPRESSIONS, AND LACERATIONS

Tangential scalp wounds from bullets are capable of producing neurologic signs or delayed seizures because small hemorrhages or contusions arise even in the absence of missile penetration. Bullets entering the brain cause considerable damage because of their tremendous kinetic energy. A cylindrical area of necrosis surrounds the bullet track, but the nature of injury differs for different projectiles. Soft civilian bullets typically shatter on impact and leave a track of metallic fragments with moderate parenchymal damage, whereas military bullets, because of their high velocity and energy, disrupt tissue at great distances from the track and produce massive brain destruction. All of these penetrating injuries cause a rapid increase in ICP for several minutes, followed by a drop depending on the volume of secondary hemorrhage and the degree of developing edema. Infection is a risk mainly from shell fragments, shrapnel, grenades, and mines, because such small projectiles carry surface bacteria and dirt into the brain. Most neurosurgeons administer systemic antibiotics prophylactically and perform local debridement for all types of penetrating injuries. Aneurysms may form as a result of disruption of vessel walls from the shock wave of the passing projectile; facial-orbital entrance wounds have the highest incidence of this complication. The aneurysms have an unpredictable course, but most that rupture do so in the first month. The prognosis for survival after missile injuries is good if consciousness is preserved and poor if coma is present from the outset.

In civilian practice, intracranial foreign bodies such as knives, picks, studgun staples, or high-speed tool bits may be missed unless skull x-rays are taken after what are seemingly minor penetrating injuries. Surgical removal of the object, debridement, and extensive exploration for hemorrhage and necrotic tissue are required.

TRAUMATIC VASCULAR DISSECTION AND OCCLUSION

The kinetic energy of minor or more severe head or neck trauma can produce dissection of the internal carotid or vertebral arteries by stripping the intima or the media. Chiropractic neck manipulation accounts for some cases. Severe blunt impacts to the neck can initiate a dissection several centimeters above the origins of the internal carotid or vertebral arteries. There is usually local neck pain over the affected carotid artery, a Horner's syndrome, and headache over the ipsilateral anterior cranium. Some patients with carotid dissection subsequently have large middle cerebral artery strokes with hemiplegia after a period of fluctuating hemiparesis. In drowsy or comatose patients, evidence of dissection or subsequent stroke is difficult to determine, but its

presence is suggested by unexplained hemiplegia, unilateral miosis, or appearance of cerebral infarction on CT scan.

Traumatic vertebral artery dissection causes vertigo, vomiting, suboccipital or supraorbital headache, and other signs of lateral medullary or cerebellar ischemia. These symptoms may be attributed erroneously to vestibular concussion. In comatose patients, the only indication may be inferior cerebellar infarction on imaging studies. Vasospasm from traumatic subarachnoid blood may also be involved in the development of infarction after head injury.

Cavernous sinus arteriovenous fistulas are rare but serious complications in patients who survive severe head injury. The problem is first evident as a self-audible bruit (many are also audible to the examiner), proptosis, conjunctival injection, or visual impairment. Angiography shows early filling of the cavernous sinus and its draining tributaries. The fistula enlarges, causing increasingly severe local changes around the eye and orbit and decreased chances of visual recovery. About 10%, mostly small fistulas, resolve spontaneously. Many surgical approaches have been tried, including ligation of the carotid artery and direct obliteration of the fistula or cavernous sinus, but a detachable balloon that is delivered by an intravascular catheter has proved most successful.

INTRACRANIAL PRESSURE AND CEREBRAL BLOOD FLOW

Raised ICP arising from contusion, hematoma, and subsequent progressive edema accounts for at least 50% of deaths after head injury; outcome is inversely related to the level of ICP. Aggressive treatment of raised ICP in modern intensive care units is believed to contribute to improved survival after severe head injury, but many other factors pertain, and the role of direct monitoring of ICP to guide therapy, while favored in many centers, is still uncertain.

For several minutes to an hour after acute head injury, cerebral blood flow increases in most patients, although metabolic demands and oxygen consumption of the cerebrum are diminished. Autoregulationthe ability of the cerebral vasculature to maintain a constant blood flow in response to decreased or increased perfusion pressureis impaired globally and even more so in damaged regions. The rise in cerebral blood volume caused by the failure of autoregulation is thought to account for approximately two-thirds of the rise in ICP after severe head injury. The blood-brain barrier also becomes more permeable in contused regions, promoting edema formation. Resting ICP is spontaneously interrupted by rises in ICP, termed plateau waves, which arise as a result of a loss of cerebrovascular tone and a resultant increase in cerebral blood volume. Plateau waves may be precipitated by iatrogenic maneuvers such as suctioning, physical therapy, excess fluid administration, or pain but also by mild, often unnoticed hypotension that causes cerebrovascular dilation. Signs of clinical deterioration, such as pupillary enlargement, may occur after plateau waves; occasionally, brain death ensues. Other secondary systemic phenomena after severe head injury, particularly hypotension and hypoxia, cause brain damage and greatly alter outcome. The regulation of ICP and its relationship to cerebral blood flow (CBF) are discussed in Chap. 376.

CLINICAL SYNDROMES AND TREATMENT OF HEAD INJURY

MINOR INJURY

The patient who is fully alert and attentive after head injury but who has one or more symptoms of headache, faintness, nausea, a single episode of emesis, difficulty with concentration, or slight blurring of vision has a good prognosis with little risk of subsequent deterioration. Such patients have usually sustained a concussion and are expected to have a brief amnestic epoch. Children and young adults are particularly prone to drowsiness, vomiting, and irritability, which is sometimes delayed for several hours after apparently minor injuries. Occasionally, vasovagal syncope occurs several minutes to an hour after the injury and may cause undue concern. Constant generalized or frontal headache is common in the days following trauma; it may be migrainous (throbbing and hemicranial) in nature. After several hours of observation, patients with this category of injury may be accompanied home and observed by a family member or friend. Most patients with a minor syndrome do not have a skull fracture on skull x-ray or hemorrhage on CT. The decision to perform these tests depends largely on clinical signs suggesting that the impact was severe (e.g., prolonged concussion, periorbital or mastoid hematoma, repeated vomiting), on the seriousness of other bodily injuries, and on the degree of surveillance that can be expected at home. Persistent severe headache and repeated vomiting in the context of

normal alertness and no focal neurologic signs are usually benign, but radiologic studies should be obtained and observation in the hospital is justified.

INJURY OF INTERMEDIATE SEVERITY

Patients who are not comatose but who have persistent confusion, behavioral changes, subnormal alertness, extreme dizziness, or focal neurologic signs such as hemiparesis should be admitted to the hospital and soon thereafter have a CT scan. Usually a contusion or hematoma is found. The clinical syndromes most common in this group, in addition to postconcussive headache, dizziness, and vomiting, include (1) delirium with a disinclination to be examined or moved, expletive speech, and resistance if disturbed (anterior temporal lobe contusions); (2) a quiet, disinterested, slowed mental state (abulia) with dull facial appearance and irascibility (inferior frontal and frontopolar contusions); (3) a focal deficit such as aphasia or mild hemiparesis (due to subdural hematoma or convexity contusion, or, less often, carotid artery dissection); (4) confusion with inattention, poor performance on simple mental tasks, and fluctuating or slightly erroneous orientation (associated with several types of injuries, including the first two described above as well as medial frontal contusions and interhemispheric subdural hematoma); (5) repetitive vomiting, nystagmus, drowsiness, and unsteadiness (usually labyrinthine concussion, but occasionally due to a posterior fossa subdural hematoma or vertebral artery dissection); and (6) diabetes insipidus (damage to the median eminence or pituitary stalk). It needs to be emphasized that intermediate-grade injuries are often complicated by drug or alcohol intoxication.

Clinical observation is necessary to detect increasing drowsiness, change in respiratory pattern, or pupillary enlargement and to ensure restriction of free water (unless there is diabetes insipidus). Asymmetry in limb posture, limb movement, or gaze preference suggests a subdural or epidural hematoma or large contusion. Most patients in this category improve over several days. During the first week, the state of alertness, memory, and other cognitive performance often fluctuate, and irascibility or agitation is common. Behavioral changes are worst at night, as with most other encephalopathies, and may be treated with small doses of antipsychotic medications. Subtle abnormalities of attention, intellect, spontaneity, and memory tend to return to normal weeks or months after the injury, sometimes surprisingly abruptly; persistent losses in cognition are discussed below.

SEVERE INJURY

Patients who are comatose from the onset require immediate neurologic attention and often resuscitation. After intubation, with care taken to avoid deforming the cervical spine, the depth of coma, pupillary size and reactivity, limb movements, and Babinski responses are assessed. As soon as vital functions permit and cervical spine x-rays and a CT scan have been obtained, the patient should be transported to a critical care unit. The finding of an epidural or subdural hematoma or large intracerebral hemorrhage is an indication for prompt surgery and intracranial decompression in otherwise salvageable patients. Subsequent treatment is probably best guided by direct measurement of ICP but may proceed on a presumptive basis using clinical status and CT scan as guides. All potential exacerbating factors must be eliminated. Hypoxia, hyperthermia, hypercarbia, awkward head positions, and high mean airway pressures from mechanical ventilation all increase cerebral blood volume and ICP. Many, but not all, patients will have lower ICP when the head and trunk are elevated. Active management of raised ICP includes hyperosmolar dehydration with 20% mannitol (0.25 to 1 g/kg every 3 to 6 h), preferably using directly measured ICP as a guide. Otherwise, a serum osmolality of ~300 mosmol/L is desirable. It is customary to restrict free water administration in order to maintain high serum osmolarity, but there is no rationale for a reduction in the total volume of fluids administered if they are iso- or hyperosmolar, e.g., normal saline. Induced hypocarbia to an initial level of 28 to 33 mmHg PCO2 is rapidly effective in reducing

ICP, but its duration of effect is limited and its use has fallen out of favor, perhaps excessively so.

Persistently raised ICP after inception of this conservative therapy generally indicates a poor outcome. Although the addition of high-dose barbiturates may further lower ICP, there is no beneficial effect on overall outcome. In many instances, barbiturates cause a parallel reduction in ICP and BP without a net improvement in cerebral perfusion. Systolic BP should be maintained 100 mmHg by vasopressor agents, if necessary. Mean BP levels 110 to 120 mmHg may exaggerate brain edema, but some neurosurgeons allow the BP to rise above normal on the basis that this may abort plateau waves. A conventional approach to extreme hypertension utilizes diuretics and -adrenergic blocking agents, angiotensin-converting enzyme inhibitors, or intermittent doses of barbiturates. A number of other antihypertensive drugs, including some calcium channel blockers and nitrates, are said to be relatively contraindicated because they may raise ICP. Antacids administered by nasogastric tube or direct-acting drugs are utilized to keep gastric pH 3.5 and prevent gastrointestinal bleeding as described

below. The use of large doses of glucocorticoids in severe head injury does not improve outcome. Several studies suggest that early nutritional support results in faster neurologic recovery from head injury. If the patient remains comatose, it is worthwhile to repeat the CT or MRI scan to exclude a delayed surface or intracerebral hemorrhage. Intensive care salvages some critically ill head-injured patients by concentrating efforts on simple treatments that avoid medical complications, particularly pneumonia and sepsis and preventable increases in ICP.

SYSTEMIC DERANGEMENTS RESULTING FROM SEVERE HEAD TRAUMA

Injuries outside the cranium should be searched for at the outset, because they are likely to be forgotten if not initially noted. In particular, associated spinal, long bone, and abdominal injuries may cause delayed difficulties in management. Over half of patients who persist in coma for 24 h after head injury develop abnormalities of electrolytes or fluid balance. Diabetes insipidus should be suspected if urine output increases and urine specific gravity is low (Chap. 329). Replacement of water losses suffices for mild cases, but vasopressin may be required. Secretion of aldosterone and antidiuretic hormone (vasopressin, AVP) in response to stress favor the retention of sodium and free water, respectively. The latter usually predominates, leading to mild hypervolemic hyponatremia, but this is obscured if osmotic dehydrating agents have been used.

Some patients with head injuries suffer hypoxia acutely after injury without obvious pulmonary infiltrates. Aspiration pneumonia presents a great risk; lung injury from aspirated gastric contents, infection, and atelectasis may combine to produce the adult respiratory distress syndrome (ARDS) and severe arteriovenous shunting (Chap. 265). ARDS also occurs owing to disseminated intravascular coagulopathy, fat embolism, or, rarely, "neurogenic" pulmonary edema (see below). The effect of positive end-expiratory pressure (PEEP) on ICP is complex, but PEEP should not be withheld if necessary for oxygenation. Atelectasis is common in all poorly responsive patients and is treated with chest physical therapy and adequate ventilator tidal volumes. Pulmonary embolism is also a major threat to bedridden patients, and intermittent pneumatic calf compression or modest doses of subcutaneous heparin may be useful prophylaxis. The latter has not predisposed to intracerebral or gastrointestinal bleeding. Early recognition of deep leg vein thrombosis and aggressive treatment by occlusion of the inferior vena cava may prevent later emboli.

Patients with severe long bone injuries are subject to widespread cerebral fat embolism. For uncertain reasons, this complication is seen less often than previously, perhaps because of better fluid replacement. In the typical case, head injury is a minor part of the overall trauma; nonetheless, severe cranial injury masks the syndrome. Several days after the bone fractures occur, restlessness, delirium or drowsiness progressing to coma in severe cases, seizures, generalized brain edema, and hypoxia develop. About half the patients have retinal and punctate conjunctival hemorrhages or fat that is visible in retinal vessels. A petechial rash (prominent in the anterior axillary folds and supraclavicular fossae), diffuse interstitial infiltrates on the chest x-ray, fat in the urine, and/or renal failure occur in some patients. Severe reduction in arterial oxygen content is common from widespread lung injury (ARDS). Cerebral fat embolism causes a cerebral purpura, mainly in the white matter, due to capillary occlusion by fat globules. There is evidence that patients in whom this complication is recognized and treated early have a better prognosis. Massive doses of glucocorticoids and administration of positive-pressure ventilation with high end-expiratory pressures have been claimed to be useful.

Most patients with severe head injuries develop gastric erosions, but only a few have clinically significant hemorrhages. Gastrointestinal bleeding usually occurs in the first days to 1 week after injury. Unlike the majority of patients in shock or with stress ulceration, head-trauma patients often have elevated gastric acidity. Prophylactic treatment with gastric coating agents as discussed above, with H2 receptor blockers, or with

frequent antacid administration probably reduces gastric hemorrhage in other stress states and is commonly used in head trauma.

Acute head trauma may cause transient apnea and cardiac arrest. In the absence of overwhelming brain damage, recovery from the arrest is the rule. Subsequently, a sympathoadrenal discharge or raised ICP causes systemic hypertension, either with the classically associated bradycardia of the Cushing response or, almost as frequently, with tachycardia. Cardiac arrhythmias are common, most notably sinus bradycardia, supraventricular tachycardias, nodal rhythm, and heart block. T-wave inversion and alterations in the ST segment may simulate subendocardial ischemia. In some instances these changes are due to cardiac muscle contusion.

Neurogenic pulmonary edema is a form of respiratory failure in which the alveoli fill with fluid, as in congestive heart failure, but left ventricular end-diastolic pressure is normal after the infiltrates are established. The nature of this pulmonary vascular leak is not settled, but it may be the result of a sudden shift of intravascular volume from the systemic to the pulmonary circulation or there may be a direct cerebral neurogenic influence on the pulmonary microvasculature. The alveolar capillary leak may continue despite a return of pulmonary vascular pressure to normal.

Many patients demonstrate a mild coagulopathy, and 5 to 10% have various degrees of disseminated intravascular coagulation, a harbinger of poor outcome. There is a correlation between the severity of injury and the level of increased fibrin degradation products in blood, and one cause of the coagulopathy may be the release of highly thromboplastic material from damaged brain tissue.

PROGNOSIS

Extensive work by Jennet's group in Glasgow and by the Traumatic Coma Data Bank has provided data on the outcome in severe head injury. Verbal output, eye opening, and the best motor response of the limbs have been found to be predictive of outcome and are summarized using the "Glasgow Coma Scale" (Table 369-1). Over 85% of patients with aggregate scores of 3 or 4 die within 24 h. However, a number of patients with slightly higher scores but a poor initial prognosis, including absent pupillary light responses, survive, suggesting that an initially aggressive approach is justified in most patients. Patients 20 years, particularly children, may make remarkable recoveries after having grave early neurologic signs. In one large study of severe head injury, 55% of children had a good outcome at 1 year, compared with 21% of adults. Older age, increased ICP, hypoxia and hypotension, and CT scan evidence of compression of the cisterns surrounding the brainstem and shift of midline structures are all poor prognostic signs. Delayed evacuation of large intracerebral clots is also associated with a poor prognosis.

Evoked potentials have prognostic value in head injury, similar to their use in ischemic-hypoxic brain injury, and their accuracy in predicting a poor outcome probably exceeds that of purely clinical methods. The results obtained from somatosensory evoked potentials are clearest, with the bilateral absence of cortical potentials (more caudal potentials present) predicting death or a vegetative state in over 90% of patients. A normal or mildly abnormal test, however, does not reliably predict a good functional outcome.

NEUROPSYCHOLOGICAL OUTCOME AFTER HEAD INJURY

A structural basis has been sought for the posttraumatic nervous instability termed the postconcussion syndrome, which consists of fatigue, dizziness, headache, and difficulty in concentration after mild or moderate injury. Most instances are difficult to distinguish from asthenia and depression. However, with intermediate-grade injury there is probably a substantial incidence of difficulty with attention and memory as well as other subtle cognitive deficits. Based on experimental models, some investigators believe that subtle axonal shearing lesions or biochemical alterations account for these symptoms despite normal findings on brain imaging, evoked potentials, and electroencephalogram. In moderate and severe trauma, neuropsychological changes are found routinely, but some of these deficits identified in formal testing are not important in daily functioning. Test scores tend to improve rapidly during the first 6 months after injury, then more slowly for years.

SPINAL CORD TRAUMA

Approximately 10,000 patients a year in the United States, mostly young and otherwise healthy, become paraplegic or quadriplegic because of spinal cord injuries; there are an estimated 200,000 quadriplegics in the nation. Most spinal cord injuries in civilian life result from fracture or dislocation of the surrounding vertebral column. Vertical compression with flexion is the main mechanism of injury in the thoracic cord, and hyperextension or flexion is the main cause of injury in the cervical cord. Preexisting spondylosis, a congenitally narrowed spinal canal, hypertrophied ligamentum flavum (Chap. 16), and instability of the apophyseal joints from diseases such as rheumatoid arthritis predispose to severe spinal cord damage even after minor degrees of injury.

PATHOPHYSIOLOGY AND PATHOLOGY OF SPINAL CORD INJURY

Considerable spinal cord damage results from secondary phenomena that arise in the minutes and hours following injury. Even when a complete transverse myelopathy is evident immediately after impact, some

secondary changes and the resultant damage may be reversible. The immediate compression of the cord causes pericapillary hemorrhages that coalesce and enlarge, particularly in the gray matter. Infarction of gray matter and early white matter edema are evident within 4 hours of experimental blunt injury. Eight hours after injury, there is global infarction at the traumatized level, and only at this point does necrosis of white matter and paralysis below the level of the lesion become irreversible. The necrosis and central hemorrhages enlarge to occupy one or two levels above and below the point of primary impact. Gliosis progresses over several months, and the affected regions may cavitate, causing a syringomyelic syndrome.

A large number of interventions for acute spinal compression injury have been of uncertain benefit, but high doses of methylprednisolone (typically 30 mg/kg followed by 5.4 mg/kg hourly for 23 h) administered within 8 hours of injury is associated with a slightly improved outcome. The critical factor for recoverable function is the time from injury to the institution of any therapy.

MANAGEMENT OF SPINAL CORD INJURY SYNDROMES

Any patient with an injury that involves the spine or head potentially has an associated instability of the spinal column. The care of such patients begins at the scene of the accident: the neck should be immobilized, and care should be taken during transport and during the physical and radiologic examinations to prevent extension or rotation of the neck and torsion-rotation of the thoracic spine. Intubation, if necessary, can be accomplished by a blind nasotracheal technique or over an endoscope in order to avoid neck extension. High thoracic or cervical cord transection causes hypotension and bradycardia because of a functional sympathectomy (sometimes corroborated by bilateral ptosis and miosisHorner's syndrome), which responds to infusion of crystalloid or colloid.

The neurologic assessment in the awake patient with possible spinal injury focuses on neck or back pain, diminished limb power, a sensory level on the trunk, and on deep tendon reflexes, which are usually absent below the level of acute cord injury. The level of injury can be approximated from the upper dermatome of sensory loss. Injuries above C5 cause quadriplegia and respiratory failure. At C5 and C6 the biceps are weak, whereas the deltoid and the supra- and infraspinatus are spared. C7 injuries cause weakness of the triceps, wrist extensors, and forearm pronators. Injuries at T1 and below cause paraplegia. Compression in the lower thoracic and lumbar spine causes a conus medullaris or cauda equina syndrome. Cauda equina injuries are usually incomplete, involving peripheral nerves rather than spinal cord, and therefore are surgically remediable for longer periods after injury than spinal cord compression. In a comatose patient, absent reflexes, especially with small pupils or paradoxical breathing and hypotension, signify a high cervical cord injury. The principles of spinal cord localization are considered in detail in Chap. 368.

Reversible and preventable causes of spinal cord compression must be detected and surgically remedied. These include dislocation of a vertebral body, or an unstable vertebral fracture that can lead to misalignment and cord compression in the future. Treatment of fractures through the pedicles, facets, or vertebral bodies varies; some fractures heal with immobilization and time, usually 2 to 3 months, while others require surgical fusion to ensure stability. Many traumatic myelopathies have no clearly associated fracture or dislocation, but there is generally rupture of the supporting ligaments that has produced transient cord compression during the impact. If x-rays suggest any aberration in the position of vertebrae, then realignment should generally be undertaken quickly. CT or MRI exam is the most useful for demonstrating spinal misalignment and fractures. The role of myelography is not as compelling as it was in the past, but many neurosurgeons choose to instill a few drops of water-soluble contrast medium into the spinal subarachnoid space to demonstrate a block to the flow of CSF by CT or conventional myelography. Decompression within 2 hours of severe injury may lead to some recovery of spinal cord function. With incomplete myelopathies, especially if the limbs are becoming progressively weaker, early realignment is performed even many hours after injury. The surgical approaches to decompressing the spinal column depend on the specific nature of the injury. In complete transverse myelopathies beyond 6 to 12 hours after injury, decompressive laminectomies are usually unsuccessful in restoring function.

Atlantoaxial dislocation can cause immediate death from respiratory failure, an event that may occur unexpectedly even without other neurologic signs. Rheumatoid arthritis predisposes to this injury. Atlantooccipital dislocations occur predominantly in children and are almost always fatal. "Jefferson's fractures" are burst fractures of the ring of the atlas resulting from a force descending on the vertex of the skull, as in diving accidents; they are usually asymptomatic. "Hangman's fractures" are produced by hyperextension and longitudinal distraction of the upper cervical spine, as occurs with penal hanging or striking the chin on a

steering wheel in a head-on collision. These are usually fractures through the pedicles of C2 with subluxation anteriorly of C2 on C3. Traction reduction and prolonged immobilization usually allow proper healing.

Hyperflexion dislocation of the cervical vertebrae commonly causes quadriplegia. Occasionally, a markedly displaced injury is unassociated with neurologic dysfunction, presenting only with neck pain. Any degree of subluxation must be considered as potentially unstable.

Compression fracture of the cervical spine can cause neurologic damage if a bone fragment is driven backward (burst fracture) into the spinal cord. "Teardrop fractures" with crushing of a vertebral body, leaving a fragment of bone anteriorly, are usually associated with ligamentous disruption and spinal instability. Single compression fractures of the thoracic spine are usually stable because the thoracic cage provides support, but they may be associated with anterior spinal cord compression and require decompression and stabilization with the insertion of metal rods.

Mild cervical hyperextension injuries may cause only disruption of supporting ligamentous structures and can be well tolerated. More severe injuries cause vertebral displacement and cord compression. The "central cord syndrome" is produced by brief compression of the cervical cord and disruption of the central gray matter. It usually occurs in patients with an already narrow spinal canal, either congenitally or from cervical spondylosis. There is weakness of the arms with pinprick loss over the arms and shoulders, and relative sparing of leg power and sensation on the trunk and legs. Abnormality of bladder function is variable. The prognosis for recovery is good.

Thoracolumbar fracture is produced by impact in the high or middle back, usually while the patient is bent over. Impingement on the spinal canal results in a complex combination of cauda equina and conus medullaris dysfunction. Purely lumbar fractures with displacement of a vertebral body produce cauda equina compression. Surgical decompression is usually recommended, even with severe neurologic deficits, because there is considerable potential for recovery of the nerve roots of the cauda.

The subsequent care of patients with spinal cord injury is best undertaken in specialized centers. General principles of medical and urologic management are discussed in Chap. 368.

BIBLIOGRAPHY

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