Trauma is the leading cause of death in children and young adults; however, the incidence of death and disability from trauma has been slowly decreasing. This decline is partly attributable to increased awareness of safety devices such as seat belts and motorist helmets. Nonetheless, trauma remains a major cause of morbidity and mortality, and it can affect every major organ system in the body. The three main areas of neurosurgical focus are: traumatic brain injury (TBI), spinal cord injury (SCI), and peripheral nerve injury.
The initial assessment of the trauma patient includes the primary survey, resuscitation, secondary survey, and definitive care. Neurosurgical evaluation begins during the primary survey with the determination of the GCS score (usually referred to simply as the GCS) for the patient. The GCS is determined by adding the scores of the best responses of the patient in each of three categories. The motor score ranges from 1 to 6, verbal from 1 to 5, and eyes from 1 to 4. The GCS therefore ranges from 3 to 15, as detailed in Table 42-2. Tracheal intubation or severe facial or eye swelling can impede verbal and eye responses. In these circumstances, the patient is given the score of 1 with a modifier, such as verbal “1T” where T = tube.
Blunt or penetrating trauma to the head can cause injury to the densely vascularized scalp, and significant blood loss can result. Direct pressure initially controls the bleeding, allowing close inspection of the injury. If a simple laceration is found, it should be copiously irrigated and closed primarily. If the laceration is short, a single-layer, percutaneous suture closure will suffice. If the laceration is long or has multiple arms, the patient may need debridement and closure in the operating room, with its superior lighting and wider selection of instruments and suture materials. Careful reapproximation of the galea will provide a more secure closure and better hemostasis. Blunt trauma also can cause crush injury with subsequent tissue necrosis. These wounds require debridement and consideration of advancement flaps to cover the defect.
The usual classification system for bony fractures may be applied to the skull. The fracture may be characterized by skull X-rays or head CT.3 A closed fracture is covered by intact skin. An open, or compound, fracture is associated with disrupted overlying skin. The fracture lines may be single (linear); multiple and radiating from a point (stellate); or multiple, creating fragments of bone (comminuted). Closed skull fractures do not normally require specific treatment. Open fractures require repair of the scalp and operative debridement. Indications for craniotomy include depression greater than the cranial thickness, intracranial hematoma, and frontal sinus involvement.4 Skull fractures generally indicate that a significant amount of force was transmitted to the head and should increase the suspicion for intracranial injury. Fractures that cross meningeal arteries can cause rupture of the underlying vessels and subsequent epidural hematoma (EDH) formation.
Depressed skull fractures may result from a focal injury of significant force. The inner and outer cortices of the skull are disrupted, and a fragment of bone is pressed in toward the brain in relation to adjacent intact skull. The fragment may overlap the edge of intact bone, or may plunge completely below the level of adjacent normal skull. The inner cortex of the bone fragments often has multiple sharp edges that can lacerate dura, brain, and vessels. Craniotomy is required to elevate the fracture, repair dural disruption, and obtain hemostasis in these cases (Fig. 42-7). However, fractures overlying dural venous sinuses require restraint. Surgical exploration can lead to life-threatening hemorrhage from the lacerated sinus.
A. Bone-window axial head computed tomography (CT) of a patient who presented aphasic after being struck with the bottom of a beer bottle. CT demonstrates a depressed skull fracture in the left posterior temporoparietal area. B. Brain-window axial head CT demonstrating intraparenchymal hematoma caused by laceration of cortical vessels by the edge of the fractured bone. Arrowhead indicates traumatic subarachnoid hemorrhage in the sylvanian fissure.
Fractures of the skull base are common in head-injured patients, and they indicate significant impact. They are generally apparent on routine head CT, but should be evaluated with dedicated fine-slice coronal-section CT scan to document and delineate the extent of the fracture and involved structures. If asymptomatic, they require no treatment. Skull base fractures requiring intervention include those with an associated cranial nerve deficit or CSF leak. A fracture of the temporal bone, for instance, can damage the facial or vestibulocochlear nerve, resulting in vertigo, ipsilateral deafness, or facial paralysis. A communication may be formed between the subarachnoid space and the middle ear, allowing CSF drainage into the pharynx via the eustachian tube or from the ear (otorrhea). Extravasation of blood results in ecchymosis behind the ear, known as Battle’s sign. A fracture of the anterior skull base can result in anosmia (loss of smell from damage to the olfactory nerve), CSF drainage from the nose (rhinorrhea), or periorbital ecchymoses, known as raccoon eyes.
Copious clear drainage from the nose or ear makes the diagnosis of CSF leakage obvious. Often, however, the drainage may be discolored with blood or small in volume if some drains into the throat. The halo test can help differentiate. Allow a drop of the fluid to fall on an absorbent surface such as a facial tissue. If blood is mixed with CSF, the drop will form a double ring, with a darker center spot containing blood components surrounded by a light halo of CSF. If this test is indeterminate, the fluid can be sent for beta-2 transferrin testing, a carbohydrate-free isoform of transferrin exclusively found in the CSF.
Many CSF leaks will heal with elevation of the head of the bed for several days. A lumbar drain can augment this method. A lumbar drain is a catheter placed in the lumbar CSF cistern to decompress the cranial vault and allow the defect to heal by eliminating normal hydrostatic pressure. There is no proven efficacy of antibiotic coverage for preventing meningitis in patients with CSF leaks.
Traumatic cranial neuropathies generally can be managed conservatively, with documentation of the extent of impairment and signs of recovery. Patients with traumatic facial nerve palsies may benefit from a course of steroids, although their benefit is unproven. Patients with facial nerve palsy of abrupt onset, who do not respond to steroids within 48 to 72 hours, may be considered for surgical decompression of the petrous portion of the facial nerve. Patients also may present with delayed-onset facial nerve palsy. Again, steroids are used and surgery can be considered, with mixed results.
Closed head injury (CHI) is the most common type of TBI and a significant cause of morbidity and mortality in the United States. There are two important factors that affect the outcome of CHI in general. The initial impact causes the primary injury, defined as the immediate injury to neurons from transmission of the force of impact. The long, delicate axons of the neurons can shear as they undergo differential acceleration or deceleration along their projecting pathways. Prevention strategies, such as wearing helmets, remain the best means to decrease disability from primary injury. Subsequent neuronal damage due to the sequelae of trauma is referred to as secondary injury. Hypoxia, hypotension, hydrocephalus, intracranial hypertension, thrombosis, and intracranial hemorrhage may all be mechanisms of secondary injury. One focus of basic research in TBI, critical care medicine, and neurosurgical intervention is to decrease the effects of secondary injury.
The Brain Trauma Foundation’s most recent summary of management recommendations for TBI patients was published in 2007 and is endorsed by the American Association of Neurological Surgeons, Congress of Neurological Surgeons, and the World Health Organization. The guidelines standardize the care of these patients with the hope of improving outcomes. Some of the common patterns of CHI, including concussion, contusion, and diffuse axonal injury, are discussed in Types of Closed Head Injury.5
The initial evaluation of a trauma patient remains the same whether or not the primary surveyor suspects head injury. The first three elements of the ABCDs of resuscitation—airway, breathing, and circulation—must be assessed and stabilized. Hypoxia and hypotension are known to worsen outcome in TBI (due to secondary injury), making cardiopulmonary stabilization critical. Patients who cannot follow commands require intubation for airway protection and ventilatory control. The fourth element, assessment of “D,” for disability, is undertaken next. Motor activity, speech, and eye opening can be assessed in a few seconds and a GCS score assigned.
The following is an example of how a primary surveyor may efficiently assess disability and GCS: Approach the patient and enter his or her field of view. Observe whether the patient is visually attentive. Clearly command: “Tell me your name.” Then ask the patient to lift up two fingers on each side sequentially, and wiggle the toes. A visually or verbally unresponsive patient should be assessed for response to peripheral stimuli such as nail-bed pressure, or deep central painful stimulation, such as a firm, twisting pinch of the sensitive supraclavicular skin. Watch for eye opening and movement of the extremities, whether purposeful or reflexive. Assess the verbal response. The motor, verbal, and eye-opening scores may be correctly assigned using this rapid examination. An initial assessment of the probability of significant head injury can be made, assuming that pharmacologic and toxic elements have not obscured the examination. The surveyor must also take note of any external signs of head injury, including bleeding from the scalp, nose, or ear, or deformation of the skull or face.
Several medical steps may be taken to minimize secondary injury and the systemic consequences of head injury. Patients with a documented CHI and evidence of intracranial hemorrhage or a depressed skull fracture should receive a 17-mg/kg phenytoin loading dose, followed by 1 week of therapeutic maintenance phenytoin, typically 300 to 400 mg/d. Phenytoin prophylaxis has been shown to decrease the incidence of early posttraumatic seizures.6 There is no evidence to support long-term use of prophylactic antiepileptic agents. Blood glucose levels should be closely monitored by free blood sugar checks and controlled with sliding scale insulin. Fevers also should be evaluated and controlled with antipyretics, as well as source-directed therapy when possible. Hyperglycemia and hyperthermia are toxic to injured neurons and contribute to secondary injury. Head-injured patients have an increased prevalence of peptic ulceration and GI bleeding. Peptic ulcers occurring in patients with head injury or high ICP are referred to as Cushing’s ulcers. Ulcer prophylaxis should be used. Compression stockings or athrombic pumps should be used when the patient cannot be mobilized rapidly for prophylaxis of deep venous thrombosis.
TBI can be classified as mild, moderate, or severe. For patients with a history of head trauma, classification is as follows: severe head injury if the GCS score is 3 to 8, moderate head injury if the GCS score is 9 to 12, and mild head injury if the GCS score is 13 to 15. Many patients present to emergency rooms and trauma bays with a history of TBI. A triage system must be used to maximize resource utilization while minimizing the chance of missing occult or progressing injuries.
TBI patients who are asymptomatic, who have only headache, dizziness, or scalp lacerations, and who did not lose consciousness, have a low risk for intracranial injury and may be discharged home without a head CT scan.7,8 Head-injured patients who are discharged should be sent home with reliable family or friends who can observe the patient for the first postinjury day. Printed discharge instructions, which describe monitoring for confusion, persistent nausea, weakness, or speech difficulty, should be provided to the caretaker. The patient should return to the emergency department for evaluation of such symptoms.
Patients with a history of altered consciousness, amnesia, progressive headache, skull or facial fracture, vomiting, or seizure have a moderate risk for intracranial injury and should undergo a prompt head CT. If the CT is normal, and the neurologic examination has returned to baseline (excluding amnesia of the event), then the patient can be discharged to the care of a responsible adult, again with printed criteria for returning to the emergency room. Otherwise the patient must be admitted for a 24-hour observation period.
Patients with depressed consciousness, focal neurologic deficits, penetrating injury, depressed skull fracture, or changing neurologic examination have a high risk for intracranial injury. These patients should undergo immediate head CT and admission for observation or intervention as needed.
Types of Closed Head Injury
A concussion is defined as temporary neuronal dysfunction following nonpenetrating head trauma. The head CT is normal, and deficits resolve over minutes to hours. Definitions vary; some require transient loss of consciousness, while others include patients with any alteration of mental status. Memory difficulties, especially amnesia of the event, are very common. Concussions may be graded. One method is the Colorado grading system.9 Head trauma patients with confusion only are grade 1, patients with amnesia are grade 2, and patients who lose consciousness are grade 3. Studies have shown that the brain remains in a hypermetabolic state for up to a week after injury. The brain is also much more susceptible to injury from even minor head trauma in the first 1 to 2 weeks after concussion. This is known as second-impact syndrome, and patients should be informed that, even after mild head injury, they might experience memory difficulties or persistent headaches.
A contusion is a bruise of the brain, and occurs when the force from trauma is sufficient to cause breakdown of small vessels and extravasation of blood into the brain. The contused areas appear bright on CT scan, as seen in Fig. 42-8. The frontal, occipital, and temporal poles are most often involved. The brain sustains injury as it collides with rough, bony surfaces. Contusions themselves rarely cause significant mass effect as they represent small amounts of blood in injured parenchyma rather than coherent blood clots. Edema may develop around a contusion, causing mass effect. Contusions may enlarge or progress to frank hematoma, particularly during the first 24 hours. Contusions also may occur in brain tissue opposite the site of impact. This is known as a contre-coup injury. These contusions result from deceleration of the brain against the skull.
Severe bilateral contusions in the basal aspect of the frontal lobes, caused by the brain moving over the rough, irregular skull base during sudden cranial acceleration.
Diffuse axonal injury is caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration. Axons may be completely disrupted and then retract, forming axon balls. Small hemorrhages can be seen in more severe cases, especially on MRI. Hemorrhage is classically seen in the corpus callosum and the dorsolateral midbrain.
These injuries are complex and must be evaluated individually. The two main subtypes are missile (e.g., due to bullets or fragmentation devices) and nonmissile (e.g., due to knives or ice picks). Some general principles apply. If available, skull X-rays and CT scans are useful in assessing the nature of the injury. Cerebral angiography must be considered if the object passes near a major artery or dural venous sinus. Operative exploration is necessary to remove any object extending out of the cranium, as well as for debridement, irrigation, hemostasis, and definitive closure. Small objects contained within brain parenchyma are often left in place to avoid iatrogenic secondary brain injury. Antibiotics are given to decrease the chances of meningitis or abscess formation. High-velocity missile injuries (from high-powered hunting rifles or military weapons) are especially deadly, because the associated shock wave causes cavitary tissue destruction of an area that is much larger than the projectile itself. Projectiles that penetrate both hemispheres or traverse the ventricles are almost universally fatal.
Traumatic Intracranial Hematomas
The various traumatic intracranial hematomas contribute to death and disability secondary to head injury. Hematomas can expand rapidly and cause brain shift and subsequent herniation. Emergent neurosurgical evaluation and intervention often are necessary.
EDH is the accumulation of blood between the skull and the dura. EDH usually results from arterial disruption, especially of the middle meningeal artery. The dura is adherent to bone, and some pressure is required to dissect between the two. EDH has a classic, three-stage clinical presentation that is probably seen in only 20% of cases. The patient is initially unconscious from the concussive aspect of the head trauma. The patient then awakens and has a “lucid interval,” while the hematoma subclinically expands. As the volume of the hematoma grows, the decompensated region of the pressure-volume curve is reached, ICP increases, and the patient rapidly becomes lethargic and herniates. Uncal herniation from an EDH classically causes ipsilateral third nerve palsy and contralateral hemiparesis.
On head CT the blood clot is bright, biconvex in shape (lentiform), and has a well-defined border that usually respects cranial suture lines. An EDH is typically found over the convexities but may rarely occur in the posterior fossa as well.
Open craniectomy for evacuation of the congealed clot and hemostasis generally is indicated for EDH. Patients who meet all of the following criteria may be managed conservatively: clot volume <30 cm3, maximum thickness <1.5 cm, and GCS score >8.10 Prognosis after successful evacuation is better for EDH than subdural hematoma (SDH). EDHs are associated with lower-energy trauma with less resultant primary brain injury. Good outcomes may be seen in 85% to 90% of patients, with rapid CT scan and intervention.11
An acute SDH is the result of an accumulation of blood between the arachnoid membrane and the dura. Acute SDH usually results from venous bleeding, typically from tearing of a bridging vein running from the cerebral cortex to the dural sinuses. The bridging veins are subject to stretching and tearing during acceleration/deceleration of the head, because the brain shifts in relation to the dura, which firmly adheres to the skull. Elderly and alcoholic patients are at higher risk for acute SDH formation after head trauma due to brain atrophy.
On head CT scan, the clot is bright or mixed-density, crescent-shaped (lunate), may have a less distinct border, and does not cross the midline due to the presence of the falx. Most SDHs occur over the cerebral hemispheres, but they may also occur between the hemispheres or layer over the tentorium.
Open craniotomy for evacuation of acute SDH is indicated for any of the following: thickness >1 cm, midline shift >5 mm, or GCS drop by two or more points from the time of injury to hospitalization. Nonoperatively managed hematomas may stabilize and eventually reabsorb, or evolve into chronic SDHs.12 This management requires frequent neurologic examinations until the clot stabilizes based on serial head CT scans.
The prognosis for functional recovery is significantly worse for acute SDH than EDH because it is associated with greater primary injury to brain parenchyma from high-energy impacts. Prompt recognition and intervention minimizes secondary injury. The elderly patients with low admission GCS, or high postoperative ICP do poorly, with as few as 5% attaining functional recovery.13
Chronic Subdural Hematoma
Chronic SDH is a collection of blood breakdown products that is at least 2 to 3 weeks old. Acute hematomas are bright white (hyperdense) on CT scan for approximately 3 days, after which they fade to isodensity with brain, and then to hypodensity after 2 to 3 weeks. A true chronic SDH will be nearly as dark as CSF on CT. Traces of white are often seen due to small, recurrent hemorrhages into the collection. These small bleeds may expand the collection enough to make it symptomatic. This phenomenon is referred to as an acute-on-chronic SDH. Figure 42-9 demonstrates the CT appearance of an acute-on-chronic SDH. Vascularized membranes form within the hematoma as it matures. These membranes may be the source of acute hemorrhage.
Head computed tomography scan of an elderly patient with progressing left hemiplegia and lethargy, demonstrating an acute-on-chronic subdural hematoma. History revealed that the patient sustained a fall 4 weeks before presentation. Arrowheads outline the hematoma. The acute component is slightly denser and is seen as the hyperdense area in the dependent portion.
Chronic SDHs often occur in patients without a clear history of head trauma, as they may arise from minor head injury. Alcoholics, the elderly, and patients on anticoagulation are at higher risk for developing chronic SDH. Patients may present with headache, seizure, confusion, contralateral hemiparesis, or coma.
A chronic SDH >1 cm or any symptomatic SDH should be surgically drained. Unlike acute SDH, which consists of a thick, congealed clot, chronic SDH typically consists of a viscous fluid with the texture and dark brown color reminiscent of motor oil. A simple burr hole can effectively drain most chronic SDHs. However, the optimal treatment of chronic SDH remains controversial.14 Most authorities agree that burr hole drainage should be attempted first to obviate the risks of formal craniotomy. A single burr hole placed over the dependent edge of the collection can be made, and the space copiously irrigated until the fluid is clear. A second, more anterior burr hole can then be placed if the collection does not drain satisfactorily due to containment by membranes. The procedure is converted to open craniotomy if the SDH is too congealed for irrigation drainage, the complex of membranes prevents effective drainage, or persistent hemorrhage occurs that cannot be reached with bipolar cautery through the burr hole. The required surgical prepping and draping are always performed to allow simple conversion to craniotomy, and the scalp incision and burr holes are placed to allow easy incorporation into larger skin flaps.
There are various strategies to prevent reaccumulation of blood. Subdural or subgaleal drains may be left in place for 1 to 2 days. Mild hydration and bedrest with the head of the bed flat may encourage brain expansion. High levels of inspired oxygen may help draw nitrogen out of the cavity. Regardless of the strategy used, follow-up head CT scans are required postoperatively and approximately 1 month later to document resolution.
Isolated hematomas within the brain parenchyma are most often associated with hypertensive hemorrhage or arteriovenous malformations (AVMs). Bleeding may occur in a contused area of brain. Mass effect from developing hematomas may present as a delayed neurologic deficit. Delayed traumatic intracerebral hemorrhage is most likely to occur within the first 24 hours. Patients with contusion on the initial head CT scan should be reimaged 24 hours after the trauma to document stable pathology. Indications for craniotomy include: any clot volume >50 cm3 or a clot volume >20 cm3 with referable neurologic deterioration (GCS 6–8) and associated midline shift >5 mm or basal cistern compression.15
Trauma to the head or neck may cause damage to the carotid or vertebrobasilar systems. Generally, dissection refers to violation of the vessel wall intima. Blood at arterial pressures can then open a plane between the intima and media, within the media, or between the media and adventitia. The newly created space within the vessel wall is referred to as the false lumen. Tissue or organs supplied by dissected vessels may subsequently be injured in several ways. Expansion of the hematoma within the vessel wall can lead to narrowing of the true vessel lumen and reduction or cessation of distal blood flow. Slow-flowing or stagnant blood within the false lumen exposed to thrombogenic vessel wall elements may thrombose. Pieces of thrombus may then detach and cause distal embolic arterial occlusion. Also, the remaining partial-thickness vessel wall may rupture, damaging adjacent structures.
Traumatic dissection may occur in the carotid artery (anterior circulation) or the vertebral or basilar arteries (posterior circulation). Dissections may be extradural or intradural. Intradural dissection can present with subarachnoid hemorrhage (SAH). Traditional angiography remains the basis of diagnosis and characterization of arterial dissection. Angiographic abnormalities include stenosis of the true lumen, or “string-sign,” visible intimal flaps, and the appearance of contrast in the false lumen. Four-vessel cerebral angiography should be performed when suspicion of dissection exists.
Historically, patients with documented arterial dissection have been anticoagulated with heparin and then warfarin to prevent thromboembolic stroke. Trauma patients often have concomitant absolute or relative contraindications to anticoagulation, complicating management. Antiplatelet therapy is often implemented in lieu of full anticoagulation, however, there is no randomized clinical trial comparing the two therapies.16 Consider surgical or interventional techniques for persisting embolic disease and for vertebral dissections presenting with SAH. Surgical options include vessel ligation and bypass grafting. Interventional radiology techniques include stenting and vessel occlusion. Occlusion techniques require sufficient collateral circulation to perfuse the vascular territory previously supplied by the occluded vessel.
Carotid dissection may result from neck extension combined with lateral bending to the opposite side, or trauma from an incorrectly placed shoulder belt tightening across the neck in a motor vehicle accident. Extension or bending stretches the carotid over the bony transverse processes of the cervical vertebrae, while seat belt injuries cause direct trauma. Symptoms of cervical carotid dissection include contralateral neurologic deficit from brain ischemia, headache, and ipsilateral Horner’s syndrome from disruption of the sympathetic tracts ascending from the stellate ganglion on the surface of the carotid artery. The patient may complain of a bruit.
Traumatic vessel wall injury to the portion of the carotid artery running through the cavernous sinus may result in a carotid-cavernous fistula (CCF). This creates a high-pressure, high-flow pathophysiologic blood flow pattern. CCFs classically present with pulsatile proptosis (the globe pulses outward with arterial pulsation), retro-orbital pain, and decreased visual acuity or loss of normal eye movement (due to damage to cranial nerves III, IV, and VI as they pass through the cavernous sinus). Symptomatic CCFs should be treated to preserve eye function. Fistulae may be closed by balloon occlusion using interventional neuroradiology techniques. Fistulae with wide necks are difficult to treat and may require total occlusion of the parent carotid artery.
Vertebrobasilar dissection may result from sudden rotation or flexion/extension of the neck, chiropractic manipulation, or a direct blow to the neck. Common symptoms are neck pain, headache, and brain stem stroke or SAH. The risks and benefits of aspirin therapy are unclear when a vertebral dissection extends intracranially. The theoretically increased friability of the vessel wall may increase the risk of SAH when coupled with an antiplatelet agent. Consultation of a stroke neurologist is recommended in this situation.
Brain death occurs when there is an absence of signs of brain stem function or motor response to deep central pain in the absence of pharmacologic or systemic medical conditions that could impair brain function.
A neurologist, neurosurgeon, or intensivist generally performs the clinical brain death examination. Two examinations consistent with brain death 12 hours apart, or one examination consistent with brain death followed by a consistent confirmatory study generally is sufficient to declare brain death (see below). Hospital regulations and local laws regarding documentation should be followed closely.
Establish the absence of complicating conditions before beginning the examination. The patient must be normotensive, euthermic, and oxygenating well. The patient may not be under the effects of any sedating or paralytic drugs.
Documentation of no brain stem function requires the following: nonreactive pupils; lack of corneal blink, oculocephalic (doll’s eyes), oculovestibular (cold calorics) reflexes; and loss of drive to breathe (apnea test). The apnea test demonstrates no spontaneous breathing even when Paco2 is allowed to rise above 60 mmHg.
Deep central painful stimuli are provided by bilateral forceful twisting pinch of the supraclavicular skin and pressure to the medial canthal notch. Pathologic responses such as flexor or extensor posturing are not compatible with brain death. Spinal reflexes to peripheral pain, such as triple flexion of the lower extremities, are compatible with brain death.
Confirmatory studies are performed after a documented clinical examination consistent with brain death. A study consistent with brain death may obviate the need to wait 12 hours for a second examination. This is especially important when the patient is a potential organ donor, as brain-dead patients often have progressive hemodynamic instability. Lack of cerebral blood flow consistent with brain death may be documented by cerebral angiography or technetium radionuclide study. A “to-and-fro” pattern on transcranial Doppler ultrasonography indicates no net forward flow through the cerebral vasculature, consistent with brain death. An electroencephalogram (EEG) documenting electrical silence has been used, but generally is not favored because there is often significant artifact which impairs interpretation.
The spine is a complex biomechanical structure. The spine provides structural support for the body as the principal component of the axial skeleton, while protecting the spinal cord and nerve roots. Trauma may fracture bones or cause ligamentous disruption. Often, bone and ligament damage occur together. Damage to these elements reduces the strength of the spine and may cause instability, which compromises both supportive and protective functions. Spine trauma may occur with or without neurologic injury.
Neurologic injury from spine trauma is classified as either incomplete or complete. If there is some residual motor or sensory neurologic function below the level of the lesion, as assessed by clinical examination, the injury is defined as incomplete.17 A patient with complete neurologic dysfunction persisting 24 hours after injury has a very low probability of return of function in the involved area.
Neurologic injury from spine trauma may occur immediately or in delayed fashion. Immediate neurologic injury may be due to direct damage to the spinal cord or nerve roots from penetrating injuries, especially from stab wounds or gunshots. Blunt trauma may transfer sufficient force to the spine to cause acute disruption of bone and ligament, leading to subluxation, which is a shift of one vertebral element in relation to the adjacent level. Subluxation decreases the size of the spinal canal and neural foramina and causes compression of the cord or roots. Such neural impingement can also result from retropulsion of bone fragments into the canal during a fracture. Transection, crush injury, and cord compression impairing perfusion are mechanisms leading to SCI. Delayed neurologic injury may occur during transportation, examination of an improperly immobilized patient, or during a hypotensive episode.
The Mechanics of Spine Trauma
Trauma causes a wide variety of injury patterns in the spine due to its biomechanical complexity. A mechanistic approach facilitates an understanding of the patterns of injury, as there are only a few types of forces that can be applied to the spine. Although these forces are discussed individually, they often occur in combination. Several of the most common injury patterns are then presented to illustrate the clinical results of these forces applied at pathologically high levels.
Bending the head and body forward into a fetal position flexes the spine. Flexion loads the spine anteriorly (the vertebral bodies) and distracts the spine posteriorly (the spinous process and interspinous ligaments). High flexion forces occur during front-end motor vehicle collisions, and backward falls when the head strikes first. Arching the neck and back extends the spine. Extension loads the spine posteriorly and distracts the spine anteriorly. High extension forces occur during rear-end motor vehicle collisions (especially if there is no headrest), frontward falls when the head strikes first, or diving into shallow water.
Force applied along the spinal axis (axial loading) compresses the spine. Compression loads the spine anteriorly and posteriorly. High compression forces occur when a falling object strikes the head or shoulders, or when landing on the feet, buttocks, or head after a fall from height. A pulling force in line with the spinal axis distracts the spine. Distraction unloads the spine anteriorly and posteriorly. Distraction forces occur during a hanging, when the chin or occiput strikes an object first during a fall, or when a passenger submarines under a loose seat belt during a front-end motor vehicle collision.
Force applied tangential to the spinal axis rotates the spine. Rotation depends on the range of motion of intervertebral facet joints. High rotational forces occur during off-center impacts to the body or head or during glancing automobile accidents.
Certain patterns of injury resulting from combinations of the previously mentioned forces occur commonly and should be recognized during plain film imaging of the spine. Always completely evaluate the spine. A patient with a spine injury at one level has a significant risk for additional injuries at other levels.
The cervical spine is more mobile than the thoracolumbar spine. Stability comes primarily from the multiple ligamentous connections of adjacent vertebral levels. Disruption of the cervical ligaments can lead to instability in the absence of fracture. The mass of the head transmits significant forces to the cervical spine during abrupt acceleration or deceleration, increasing risk for injury.
A Jefferson fracture is a bursting fracture of the ring of C1 (the atlas) due to compression forces. There are usually two or more fractures through the ring of C1. The open-mouth odontoid view may show lateral dislocation of the lateral masses of C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse ligament. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures dislocated <7 mm usually are treated with a rigid collar, while those dislocated 7 mm or greater usually are treated with a halo vest. Surgical intervention is not indicated.
The odontoid process, or dens, is the large ellipse of bone arising anteriorly from C2 (the axis) and projecting up through the ring of C1 (the atlas). Several strong ligaments connect the dens to C1 and to the base of the skull. Odontoid fractures usually result from flexion forces. Odontoid fractures are classified as type I, II, or III. A type I fracture involves the tip only. A type II fracture passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. Surgery often is undertaken for widely displaced fractures (poor chance of fusing) and for those that fail external immobilization. Type I fractures usually fuse with external immobilization only.
Traditionally considered a hyperextension/distraction injury from placement of the noose under the angle of the jaw, hangman’s fractures also may occur with hyperextension/compression, as with diving accidents, or hyperflexion. The injury is defined by bilateral C2 pars interarticularis fractures. The pars interarticularis is the bone between superior and inferior facet joints. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of external immobilization.
Jumped Facets—Hyperflexion Injury
The facet joints of the cervical spine slope forward. In a hyperflexion injury, the superior facet can “jump” over the inferior facet of the level above if the joint capsule is torn. Hyperflexion/rotation can cause a unilateral jumped facet, whereas hyperflexion/distraction leads to bilateral jumped facets. Patients with unilateral injury usually are neurologically intact. Those with bilateral injury, however, typically suffer from spinal cord damage, since the anteroposterior diameter of the spinal canal is compromised by bilateral injury, leading to spinal cord compression (Fig. 42-10).
A. Lateral cervical spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displacement of the C5 body with respect to the C6 body. B. Sagittal T2-weighted magnetic resonance imaging of the same patient, revealing compromise of the spinal canal and compression of the cord. Note the bright signal within the cord at the level of compression, indicating spinal cord injury. C. Lateral cervical spine X-ray of same patient after application of cervical traction and manual reduction. Note restoration of normal alignment. D. Lateral cervical spine X-ray after posterior cervical fusion to restabilize the C5–C6 segment of the spine.
The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the thoracolumbar spine has a higher threshold for injury than the cervical spine. A three-column model is useful for categorizing thoracolumbar injuries.18 The anterior longitudinal ligament and the anterior half of the vertebral body constitute the anterior column. The posterior half of the vertebral body and the posterior longitudinal ligament constitute the middle column. The pedicles, facet joints, laminae, spinous processes, and interspinous ligaments constitute the posterior column.
Compression fracture is a compression/flexion injury causing failure of the anterior column only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-11).
A. Lateral lumbar spine X-ray showing a compression fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. B. Axial computed tomography scan through the same fracture. Arrowhead demonstrates a transverse discontinuity in the superior endplate of the L2 body.
Burst fracture is a pure axial compression injury causing failure of the anterior and middle columns. It is unstable, and perhaps half of patients have neurologic deficit due to compression of the cord or cauda equina from bone fragments retropulsed into the spinal canal.
Chance fracture is a flexion-distraction injury causing failure of the middle and posterior columns, sometimes with anterior wedging. Typical injury is from a lap seat-belt hyperflexion with associated abdominal injury. It often is unstable and associated with neurologic deficit.
Fracture-dislocation is failure of the anterior, middle, and posterior columns caused by flexion/distraction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation causing decreased canal diameter (Fig. 42-12).
Sagittal reconstruction of an axial fine-slice computed tomography scan through the lumbar spine demonstrating a severe fracture-dislocation through the body of L2.
Initial Assessment and Management
The possibility of a spine injury must be considered in all trauma patients. A patient with no symptoms referable to neurologic injury, a normal neurologic examination, no neck or back pain, and a known mechanism of injury unlikely to cause spine injury is at minimal risk for significant injury to the spine. Victims of moderate or severe trauma, especially those with injuries to other organ systems, usually fail to meet these criteria or cannot be assessed adequately. The latter often is due to impaired sensorium or significant pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient care until completion of clinical and radiographic evaluation.
The trauma patient should be kept on a hard flat board with straps and pads used for immobilization. A hard cervical collar is kept in place. These steps minimize forces transferred through the spine, and therefore decrease the chance of causing dislocation, subluxation, or neural compression during transport to the trauma bay. The patient is then moved from the board to a flat stretcher. The primary survey and resuscitation are completed. Physical examination and initial X-rays follow.
For the examination, approach the patient as described in the section on Neurologic Examination earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature of the trauma, and if there was loss of consciousness, numbness, or inability to move any or all limbs. Assess motor function by response to commands or pain, as appropriate. Assess pinprick, light touch, and joint position, if possible. Determining the anatomically lowest level of intact sensation can pinpoint the level of the lesion along the spine. Testing sensation in an ascending fashion will allow the patient to better discern the true stimulus as opposed to determine when it is extinguished. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.
American Spinal Injury Association Classification
The American Spinal Injury Association provides a method of classifying patients with spine injuries. The classification indicates completeness and level of the injury and the associated deficit. A form similar to that shown in Fig. 42-13 should be available in the trauma bay and completed for any spine injury patient. The association also has worked to develop recommendations and guidelines to standardize the care of SCI patients in an effort to improve the quality of care.
The American Spinal Injury Association system for categorizing spinal cord injury patients according to level and degree of neurologic deficit.
Penetrating, compressive, or ischemic cord injury can lead to several characteristic presentations based on the anatomy of injury. The neurologic deficits may be deduced from the anatomy of the long sensory and motor tracts and understanding of their decussations (Fig. 42-14). Four patterns are discussed. First, injury to the entire cord at a given level results in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal canal diameter and crushing the cord. Second, injury to half the cord at a given level results in Brown-Séquard syndrome, with loss of motor control and proprioception ipsilaterally and loss of nociception and thermoception contralaterally. The typical mechanism is a stab or gunshot wound. Third, injury to the interior gray matter of the cord in the cervical spine results in a central cord syndrome, with upper extremity worse than lower extremity weakness and various degrees of numbness. The typical mechanism is transient compression of the cervical cord by the ligamentum flavum buckling during traumatic neck hyperextension. This syndrome occurs in patients with preexisting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with paralysis and loss of nociception and thermoception bilaterally. The typical mechanism is an acute disc herniation or ischemia from anterior spinal artery occlusion.
Spinal cord injury patterns. a. = artery. (Adapted with permission from Hoff J, Boland M: Neurosurgery, in Schwartz SI, et al (eds): Principles of Surgery, 7th ed., New York: McGraw-Hill, 1999, p 1837. Copyright © The McGraw-Hill Companies, Inc.)
Anteroposterior and lateral plain films provide a rapid survey of the bony spine. Plain films detect fractures and dislocations well. Adequate visualization of the lower cervical and upper thoracic spine often is impossible because of the shoulder girdle. Complete plain film imaging of the cervical spine includes an open-mouth view to assess the odontoid process and the lateral masses of C1. Fine-slice CT scan with sagittal and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI provides the best soft tissue imaging. Canal compromise from subluxation, acute disc herniations, or ligamentous disruption is clearly seen. MRI also may detect EDHs or damage to the spinal cord itself, including contusions or areas of ischemia.
The National Acute Spinal Cord Injury studies (NASCIS I and II) provide the basis for the common practice of administering high-dose steroids to patients with acute SCI. A 30-mg/kg IV bolus of methylprednisolone is given over 15 minutes, followed by a 5.4-mg/kg per hour infusion begun 45 minutes later. The infusion is continued for 23 hours if the bolus is given within 3 hours of injury, or for 47 hours if the bolus is given within 8 hours of injury. The papers indicate greater motor and sensory recovery at 6 weeks, 6 months, and 1 year after acute SCI in patients who received methylprednisolone.19,20 However, the NASCIS trial data have been extensively criticized, as many argue that the selection criteria and study design were flawed, making the results ambiguous. Patients who receive such a large corticosteroid dose have increased rates of medical and ICU complications, such as pneumonias, which have a deleterious effect on outcome. Thus, clear consensus on the use of spinal-dose steroids does not exist.21 A decision to use or not use spinal-dose steroids may be dictated by local or regional practice patterns, especially given the legal liability issues surrounding SCI. Patients with gunshot or nerve root (cauda equina) injuries, or those who are pregnant, <14 years old, or on chronic steroids were excluded from the NASCIS studies and should not receive spinal-dose steroids. In addition to steroids, hypothermia for SCI has also received attention. There is even less evidence supporting the use of this treatment, and thus, it is not currently recommended.22
Rigid external orthotic devices can stabilize the spine by decreasing range of motion and minimizing stress transmitted through the spine. Commonly used rigid cervical orthoses include Philadelphia and Miami-J collars. Cervical collars are inadequate for C1, C2, or cervicothoracic instability. Cervicothoracic orthoses brace the upper thorax and the neck, improving stabilization over the cervicothoracic region. Minerva braces improve high cervical stabilization by bracing from the upper thorax to the chin and occiput. Halo-vest assemblies provide the most external cervical stabilization. Four pins are driven into the skull to lock the halo ring in position. Four posts arising from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of companies manufacture lines of spinal orthotics. A physician familiar with the technique should fit a halo-vest. Assistance from a trained orthotics technician improves fitting and adjustment of the other devices.
Neurosurgical intervention has two goals. First is the decompression of the spinal cord or nerve roots in patients with incomplete neurologic deficits. These patients should be decompressed expeditiously, especially if there is evidence of neurologic deterioration over time. Second is the stabilization of injuries judged too unstable to heal with external immobilization only. Spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neurologic deficits who have bony or ligamentous injury requiring open fixation, may be medically stabilized before undergoing surgery. Surgical stabilization may be indicated for some injuries that would eventually heal with conservative treatment. It also can allow early mobilization, aggressive nursing care, and physical therapy. Solid surgical stabilization may also allow a patient to be managed with a rigid cervical collar who would otherwise require halo-vest immobilization.
Regional SCI centers with nurses, respiratory therapists, pulmonologists, physical therapists, physiatrists, and neurosurgeons specifically trained in caring for these patients may improve outcomes. Frequently encountered ICU issues include hypotension and aspiration pneumonia. Chronically, prevention and treatment of deep venous thrombosis, autonomic hyperreflexia, and decubitus ulcer formation are important. Many patients with cervical or high thoracic cord injuries require prolonged ventilatory support until the chest wall becomes stiff enough to provide resistance for diaphragmatic breathing. Patients with high cervical cord injuries (C4 or above) will often require permanent ventilatory support. Patients should be transferred to SCI rehabilitation centers after stabilization of medical and surgical issues.
The peripheral nervous system extends throughout the body and is subject to injury from a wide variety of trauma. Peripheral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and sensory functions. The key information-carrying structure of the nerve is the axon. The axon transmits information from the neuronal cell body and may measure from <1 mm to >1 m in length. Axons that travel a significant distance are often covered with myelin, which is a lipid-rich, electrically insulating sheath formed by Schwann cells. Myelinated axons transmit signals much more rapidly than unmyelinated axons because the voltage shifts and currents that define action potentials effectively jump from gap to gap over the insulated lengths of the axon.
Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium form bundles known as fascicles. Fascicles run through a tubular collagenous tissue known as perineurium. Groups of fascicles are suspended in mesoneurium. Fascicles and their mesoneurium run through another tubular collagenous tissue known as epineurium. The epineurium and its contents form the nerve.
There are four major mechanisms of injury to peripheral nerves. Nerves may be lacerated, stretched, compressed, or contused. Knives, passing bullets, or jagged bone fractures may lacerate nerves. Adjacent expanding hematomas or dislocated fractures may stretch nerves. Expanding hematomas, external orthoses such as casts or braces, or blunt trauma over a superficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause damage to the various anatomic components of the nerve. The patterns of damage are categorized in Types of Injury section.
Certain nerve segments are particularly vulnerable to injury. The following four characteristics make a nerve segment more vulnerable: proximity to a joint, superficial course, passage through a confined space, and being fixed in position.
The traditional classification system for peripheral nerve injury is the Seddon classification. Seddon described three injury patterns as defined in the Neurapraxia, Axonotmesis, and Neurotmesis sections. The Seddon classification provides a simple, anatomically based approach to peripheral nerve injury.23
Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. Axon degeneration does not occur. Return of normal axonal function occurs over hours to months, often in the 2- to 4-week range.
Axonotmesis is the disruption of axons and myelin. The surrounding connective tissues, including endoneurium, are intact. The axons degenerate proximally and distally from the area of injury. Distal degeneration is known as Wallerian degeneration. Axon regeneration within the connective tissue pathways can occur, leading to restoration of function. Axons regenerate at a rate of 1 mm per day. Significant functional recovery may occur for up to 18 months. Scarring at the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.
Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous components, such as the epineurium, may or may not be intact. Proximal and distal axonal degeneration occurs. The likelihood of effective axonal regeneration across the site of injury depends on the extent of neuroma formation and on the degree of persisting anatomic alignment of the connective tissue structures. For instance, an injury may damage axons, myelin, and endoneurium, but leave perineurium intact. In this case, the fascicle sheath is intact, and appropriate axonal regeneration is more likely to occur than if the sheath is interrupted.
Management of Peripheral Nerve Injury
The sensory and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early surgical exploration. Clean, sharp injuries may also benefit from early exploration and reanastomosis. Most other peripheral nerve injuries should be observed. EMG/NCS studies should be done 3- to weeks postinjury if deficits persist. Axon segments distal to the site of injury will conduct action potentials normally until Wallerian degeneration occurs, rendering EMG/NCS before 3 weeks uninformative. Continued observation is indicated if function improves. Surgical exploration of the nerve may be undertaken if no functional improvement occurs over 3 months. If intraoperative electrical testing reveals conduction across the injury, continue observation. In the absence of conduction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not heal. A nerve graft may be needed to bridge the gap between the proximal and distal nerve ends. The sural nerve often is harvested, as it carries only sensory fibers and leaves a minor deficit when resected. The connective tissue structures of the nerve graft may provide a pathway for effective axonal regrowth across the injury.
The brachial plexus may be injured in a variety of ways. Parturition or a motorcycle accident can lead to plexus injury due to dislocation of the glenohumeral joint. Attempting to arrest a fall with one’s hands can lead to a stretch injury of the plexus due to abrupt movement of the shoulder girdle. An apical lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with injury to the various components of the brachial plexus, and understanding them all would require extensive neuroanatomic discussion. Two well-known eponymous syndromes are Erb’s palsy and Klumpke’s palsy. Injury high in the plexus to the C5 and C6 roots resulting from glenohumeral dislocation causes Erb’s palsy with the characteristic “bellhop’s tip” position. The arm hangs at the side, internally rotated. Hand movements are not affected. Injury low in the plexus, to the C8 and T1 roots, resulting from stretch or compression injury, causes Klumpke’s palsy with the characteristic “claw hand” deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.
The radial nerve courses through the axilla, then laterally and posteriorly in the spiral groove of the humerus. Improper crutch use can cause damage to the axillary portion. The section of the nerve traversing the spiral groove can be damaged by humerus fractures or pressure from improper positioning during sleep. This classically occurs when the patient is intoxicated and is called “Saturday night palsy.” The key finding is wrist drop (i.e., weakness of hand and finger extensors). Axillary (proximal) injury causes triceps weakness in addition to wrist drop.
Common Peroneal Neuropathy
The common peroneal nerve forms the lateral half of the sciatic nerve (the medial half being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to form the deep and superficial peroneal nerves. The superficial, fixed location at the fibular neck makes the common peroneal nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg at the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior), eversion weakness, and numbness over the anterolateral surface of the lower leg and dorsum of the foot. In contrast, a foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to compressive fibers or adhesions that may be lysed, with the possibility of return of function.