Spinal cord injury (SCI) is perhaps the worst of all survivable traumas. The devastating results of SCI in terms of loss of independence, psychologic impact, and socioeconomic costs are staggering. 16,42 Although repair of the injured spinal cord remains a topic confined to the laboratory bench, effective clinical tools are available to assist in the proper understanding of spinal injury syndromes and the application of effective and safe resuscitative measures. It is important to remember that the ultimate outcome of SCI depends on the quantity and quality of axons surviving at the level of injury. 17,33,58
The initial management of the patient with acute SCI is to resuscitate if necessary and to do no further harm. Therefore, all patients with acute SCI first benefit from the health care professional who makes the diagnosis. Few traumatic illnesses are as vulnerable to acute aggravation caused by improper management, or with more tragic results, than SCI. Emergency personnel can often make the diagnosis in the field, but the index of suspicion required to preserve function in incompletely injured patients who are comatose or unresponsive requires a special sensitivity. All patients with head injuries, especially those with frontal or facial trauma, should be suspect for occult SCI. Additionally, patients with multiple long bone and pelvic fractures, or focal neurologic deficit, have an elevated risk of spinal column injury. 4 A penetrating injury in the proximity of the spine may injure the spinal cord by direct force or by percussive effect, which may result in a spinal cord contusion or hematoma. Any fall from a significant height (above 10 ft) or high-speed injury mechanism (faster than 35 mile/h) may be sufficient to cause SCI, especially in the older population in whom degenerative spinal stenosis may be superimposed. 4 Therefore, protection of spinal alignment in patients unable to cooperate with an examination after a trauma is required, followed by a systematic approach to detection.
Primary and Secondary Tissue Damage
To better understand the anatomic and physiologic aftermath of SCI, investigators have developed the concept that various types of tissue damage result. 19,48 So-called “primary” injury refers specifically to the mechanical disruption of axons as a result of stretch or laceration. Treatment to reverse neurologic deficit resulting from this form of injury does not currently exist. However, spinal cords from injured patients rarely demonstrate complete severance, and experimentally injured spinal cords appeared to have little tissue damage immediately after injury despite severe neurologic deficit. This leads to the concept that a progressive form, or “secondary” injury, was present. Multiple mechanisms have been postulated as responsible for secondary injury including “free radical” formation, 28 uncontrolled calcium influx, 39,64 ischemia, and lipid peroxidation. 10,26,27 More recently, investigators have noted more protracted forms of injury that are controlled on the molecular level. For example, programmed cell death (apoptosis) is widespread and expressed for weeks to months after the injury. 40 Whether these later events are destructive or beneficial remains a matter of intense study. It is however likely that multiple pathologic events are responsible for the progressive form of spinal tissue damage after SCI.
Preservation of the Patient’s Life
Management at the Scene
Prehospital management should seek primarily to protect the patient from further injury and to provide early resuscitation and transport to an appropriate acute care facility. Regional trauma centers that provide a multidisciplinary team of health care professionals should be the destination of choice. The ABCs, as outlined by the Advanced Trauma Life Support System, should be implemented as a primary resuscitative effort. 1 Acute respiratory and hemodynamic failure causes the most deaths soon after SCI. 32 Optimal management is based on an understanding of the causes of these physiologic changes and timely intervention. Specific measures are outlined below:
Oxygenation is important in attenuating further ischemic injury to the damaged spinal cord. Upper cervical injuries (occurring rostral to C3) are often the cause of acute fatality because of loss of respiratory drive. With some function above C4, individuals can generate tidal volumes of 100 to 150 mL because of excursion of the scalene and sternocleidomastoid muscles. Intubation at the scene is best performed with a blind nasoendotracheal intubation, or with manual inline traction and oral intubation. 1,36 Fiber optic confirmation, if available, is also helpful. Hyperextension of the neck during intubation is to be avoided because it may create further spinal stenosis because of displacement of injured spinal segments and/or infolding of the ligamentum flavum.
Overall, respiratory complications closely correspond to the severity of SCI and systemic shock. Pulmonary toilet and airway management is important in preventing subacute failure of oxygenation because of the buildup of respiratory secretions and frank infection. Therefore, early and aggressive airway and pulmonary management with proactive treatment of pre-existing pulmonary disease and aggressive pulmonary toilet and early mobilization are commonly used. Despite these measures, however, up to 62% of SCI patients have serious respiratory morbidity. 37
Acute SCI can cause a syndrome analogous to a “functional sympathectomy” in lesions above T6, resulting from the interruption of cardiac accelerator nerves. One should think of the heart after acute SCI as having decreased chronotropic and ionotropic capacity. The normal tachycardia in response to hypotension may be blocked. A “relative” hypovolemia exists because of an increase in venous capacitance. Intravenous replacement therapy should maintain systolic blood pressure between 80 and 100 mm Hg. 60 Treatment of bradycardia (<40 beats/min) should begin with atropine 0.2 to 0.5 mg intravenously. In patients more than 50 years of age, Swan-Ganz catheterization and volume resuscitation to a pulmonary capillary wedge pressure of 18 mm Hg and a target systolic arterial pressure between 80 and 100 mm Hg should be used. 56,60 In younger patients volume expansion is used to increase intravascular supply and stroke volume, but one should be careful not to overcompensate. If hypotension persists, an intravenous β-agonist (dopamine 5–15 μg · kg−1 · min−1 or dobutamine 3–20 μg · kg−1 · min−1) is used. The use of primary α-agonists (such as levoephedrine) should be avoided because it will increase cardiac afterload and impair cardiac output.
Penetrating SCI presents a far greater challenge with regard to neurologic recovery. When all patients with myelopathy after penetrating injuries are considered, only 22% have incomplete injuries, with a nearly 10-fold male:female ratio. In the series by Zipnick et al, 66 only 26% of patients with cervical penetrating injuries had hypotension, prompting concern in the hypotensive patients that blood loss rather than relative hypovolemia may be responsible. 66
In common use spinal shock is a misnomer. Among spinal professionals use of the term may well have two meanings. The first describes an acute neurologic syndrome indicating complete paralysis, loss of sensation, absent reflexes, and muscular hypotonia at the time of initial evaluation. This occurs in approximately 50% of patients. The etiologies behind this phenomenon include primary axonal and cellular dysfunction, ionic conduction block caused by sodium/potassium shifts, maintenance of spinal inhibitory pathways, hyperpolarization of caudal motor neurons, and loss of fusimotor drive in caudal spinal segments. 38 These mechanisms evolve for a period of hours to days and may mask the functioning of less injured spinal tissue. According to Stauffer, there is a 99% likelihood of spinal shock, as defined, resolving in 24 hours. 57
The concept of “spinal shock” has recently been criticized for a number of important reasons. Importantly, there is no universal agreement on the time at which the phase of spinal shock ends. Furthermore, the state of spinal shock has no prognostic significance. Ko et al provided a careful review of reflex recovery after SCI. 34 They reported the emergence of the delayed plantar response as the first recovered reflex, usually within a few days of injury, followed by the bulbocavernosum and cremasteric reflex. 34 Deep tendon reflexes recovered by 1 to 2 weeks. Less than 8% of patients had no reflexes on the day of injury, and reflex recovery did not follow a caudal–rostral pattern. The delayed plantar response has prognostic significance when delayed for ≥48 hours, indicating poor potential for ambulation.
The concept of “spinal shock” as it relates to neurologic dysfunction should therefore be reconsidered. The initial neurologic examination in patients with SCI should not be used as a basis to determine the extent of primary spinal cord damage, nor should it overshadow the potential that residual neurologic function may be spontaneously obtained once these local events return toward normal. Unfortunately, the degree of neurologic impairment early after injury is often a major determinant affecting the aggressiveness of treating physicians. Given that no clear-cut data exist to support aggressive surgical care or traction to reduce spinal malalignment, the decision-making process is only further complicated by the notion of spinal shock. The potential exists that these local microenvironmental events can mask residual postinjury neurologic function. Therefore, even patients who appear complete on presentation may obtain some degree of functional recovery once these pathochemical events have subsided. Furthermore, careful examination of the pattern and detail of reflex recovery may prove much more valuable with regard to prognosis for ambulation.
The second entity reflects the loss of vasomotor tone as a consequence of the injury and refers primarily to systemic hypotension, or “shock.” As mentioned previously, this may not be caused by volume loss but rather the loss of sympathetic vasomotor tone and should be treated with volume resuscitation and β-agonists. 60
Optimizing Return of Neurologic Function
The number and quality of surviving axons traversing the injured site play an essential role in recovery after SCI. Therefore, an important concept in the acute phase of management is the prevention of reinjury to the spinal cord. Nearly all of the pathochemical processes thought to play an important role in secondary injury are made worse by hypoxemia, hypotension, and fever. 28,65 Therefore, those treatments outlined above play no small role in the patient’s eventual neurologic outcome. Stabilization of abnormal motion segments itself plays an important role in preventing reinjury. In addition, it is widely held that early realignment of the spine and therefore indirect decompression of the spinal canal may also optimize functional recovery. These issues are discussed below.
For SCI to have occurred, either deformation of the spinal elements must have compressed the cord or ongoing compression by displaced spinal elements must be present. Because neither scenario can be confirmed before imaging studies, the patient must be treated as if any significant movement of the spine will cause further damage. Physiologic load is avoided by transporting the patient in recumbency with every attempt to immobilize the spine. These measures include the application of a rigid collar and backboard. In patients with pre-existing spinal deformities such as ankylosing spondylitis, in situ positioning with sandbags placed around the neck and shoulders and taping of the patient to a backboard are used to prevent movement. Any movement of the patient is performed with strict adherence to spinal alignment. At no time should the association of the head and torso be altered from the straight position. Special considerations are indicated for children less than 7 years of age, when the greater relative volume of the cranium to the torso may cause excessive flexion of the cervical spine unless the above measures are used in conjunction with a behind the shoulder pad. 31
A comprehensive neurologic examination is key to the next phase of treatment. First, patients are examined for signs of obvious head, torso, and abdominal injuries. The back is inspected with the patient turned in a lateral decubitus position, at all times maintaining strict spinal precautions. Facial, scalp, and torso injuries are helpful in determining force vectors applied to the spine during injury.
Voluntary movements of the arms and legs are grossly tested and measured (Table 1). Careful inspection of muscle groups is then carried out to determine graded strength from proximal to distal. During the sensory examination any areas of reported numbness are noted and tested first, and the borders of returning sensation are noted both proximal and distal to the insensate area. A fractured wooden swab stick can identify areas of pin sensation without injuring the skin.
The American Spinal Injury Association scale (Table 2) is useful in recording myotomal and dermatomal function. 1 It is important to record the time of these findings, along with any retained zones of sensation, such as sacral sparing. The presence of any neurologic function below the level of injury has important prognostic significance and should be noted. The initial examination is compared with subsequent examinations at determined, frequent intervals so that further deterioration can be easily determined. Progressive loss of neurologic function requires explanation because untreated deterioration carries a very poor prognosis. Sacral sparing is commonly the first indication of incompleteness of injury in a patient with a dense deficit; therefore, special attention is paid to the presence or absence of a bulbocavernosus reflex, the quality of sphincter tone, and voluntary anal contractions.
Secondary tissue damage after SCI is time dependent and therefore potentially treatable. This has led to the testing of a number of pharmacologic agents in the past 15 years. Glucocorticoids were used with some success in treating experimental SCI, leading to clinical trials of methylprednisolone in 1990 (National Acute Spinal Cord Injury Studies [NASCIS] II) 6 and 1997 NASCIS III). 7,8 These studies have concluded that treatment with methylprednisolone (loading dose 30 mg/kg intravenously) is beneficial when given within 8 hours of injury. When the loading dose is given within 3 hours of injury, 24 hours duration of 5.4 mg/kg intravenous drip is required. Patients treated with the loading dose between 3 and 8 hours are given the identical drip, but for 48 hours duration. Patients do not benefit from methylprednisolone if given >8 hours after the injury. Patients with penetrating SCI do not benefit from treatment with methylprednisolone. 30 Other agents, such as the potent lipid peroxidation inhibitor Lazaroid (Upjohn, Kalamazoo) 8 and ganglioside 22 have also undergone clinical evaluation, but their benefit if any is less clear.
Much debate surrounds the risk/benefit ratio of methylprednisolone use in SCI, prompting some North American centers to re-evaluate its use in acute SCI. 9,47 However, it remains the standard treatment in the United States while the debate continues. Given the modest improvement in functional recovery reported by the NASCIS trials, the optimal pharmacologic treatment of acute SCI clearly remains elusive. In general, however, the decision to treat with methylprednisolone should be made coincident with the diagnosis of SCI, and the treatment should be initiated as soon as possible.
Emergency radiologic evaluation of the patient’s spine requires coordination with other aspects of the patient’s condition. 13 Although proper identification of a patient’s spinal fractures is a priority, the efficient gathering of this information in the presence of ongoing resuscitative measures should be the goal. The lateral cervical radiograph obtained in the emergency room is still widely used as the minimum requirement in assessing the patient’s spine. 21,41,53,54 Complete spine films are performed at the earliest convenient time point, remembering that 10% to 15% of patients with a spinal fracture have a noncontiguous spinal fracture. Visualization of C1 through the top of T1 is necessary to avoid missed injuries. Plain films of the cervical spine demonstrating widening of the interspinous process distance, rotation of the facet joints, or more than 11° of segmental angulation, as compared with other contiguous segments, or 3.5 mm of translation are considered unstable. 55,62,63 Dynamic images, i.e., flexion–extension studies, are reserved for patients who are neurologically intact but have significant axial pain. Spiral computed tomography may enhance views of transitional areas, such as the occipitocervical and cervicothoracic junction. 2,3
Emergent magnetic resonance imaging (MRI) scanning is indicated in unexplained neurologic deficit, discordant skeletal and neurologic levels of injury, and worsening neurologic status. Spinal cord injury lesions enhanced with gadolinium A T2-weighted sagittal image may demonstrate posterior ligamentous injury. After an extensive review, Fehlings et al determined that in patients with cervical SCI, the midsagittal T1- and T2-weighted images provided the most quantifiable and reliable assessment of spinal cord compression. 20
Computed tomography myelography is used when MRI is not feasible. Axial computed tomography studies provide a great deal of useful information with regard to the location and degree of bony injury and the percentage of canal compromise. Canal compromise is best determined by two-dimensional reconstructions of the spinal computed tomography and MRI if available. Injury to the vertebral arteries may result from fractures within the foramen transversarium or from sufficient spinal distraction to cause endothelial stretch injury. Patients with altered mental status and cervical spine injury are suspect for vertebral arterial injury and may require vertebral angiography. Recently, MRI has been useful as a noninvasive means of determining vertebral artery patency. 23 Thoracolumbar fractures are typically classified as unstable based on significant vertebral displacement, highly comminuted burst fracture, or significant posterior ligamentous injury. Spinal cord injury without radiographic abnormality is a syndrome caused by ligamentous failure and spinal deformation, which reduces to normal alignment after injury. This phenomenon occurs in children and in some adults at the atlantoaxial junction. 49
Stabilization of the injured spinal segment and decompression of the spinal canal, either through axial traction or realignment, are typical goals of nonoperative treatments. Stability requires that the spine tolerate physiologic loads without progressive pain, deformity, or neurologic deficit. Thoracolumbar injuries limited to compression of the anterior column alone or burst fractures with less than 50% canal compromise and stable posterior ligamentous structures can often be treated in a rigid brace. Thoracic and thoracolumbar fracture dislocations are treated with open reduction and instrumentation. Cervical dislocations and severe compression fractures are frequently considered for reduction by means of axial traction. Patients with pre-existing spinal deformity, such as ankylosing spondylitis, are not candidates for axial traction. The timing and technique of traction are discussed below.
Traction may be initiated as soon as a malalignment is noted on emergency lateral cervical radiography. Reports of patients improving in neurologic function after the application of cervical traction have been noted. 11,24,31 However, clinical studies do not conclusively indicate that “early” traction and reduction of malalignment improve recovery, partly because of a lack of agreement on what constitutes “early.” Preclinical studies of experimental SCI indicate a window of 6 to 8 hours during which decompression can reverse neurologic deficits. 14,15 Whereas few would argue against patients with cervical dislocations undergoing reduction of the deformity, the real controversy exists regarding the significance of traction with regard to neurologic recovery. 24,46 Most experimental and clinical studies of SCI suggest that the primary force of impact is the major determinant of neurologic outcome.
Some controversy exists about whether patients are better served by MRI determination of disc herniation before active reduction of deformity through traction. 50,51 Disc herniation as a result of cervical traction in facet dislocations is either extremely rare or without significant risk of neurologic injury. 18,24,59 Realignment of the spine with carefully applied axial traction remains a core belief of many spinal surgeons. In the absence of strong evidence that pretraction MRI significantly alters treatment, traction and realignment are typically applied at the earliest opportunity.
Technique of Traction.
Stabilization of the injured spine requires elimination of pathologic movement at the injury site and may prevent progressive spinal cord damage caused by repeated contusion or compression. In cervical fractures and severe ligamentous injuries, traction is routinely used as an interim measure while the injury is investigated, although rigid collar support might be effective in patients undergoing radiographic evaluation who do not have significant post-traumatic deformities. The application of modern halo rings may be preferable to tongs because they allow conversion to a halo jacket, and most are able to be secured to an operating room table if surgery becomes necessary. However, halo ring application is more complicated than tongs. In children conventional Gardner–Wells tongs are not appropriate and pediatric halos should be used. Muscle relaxation and sedation assist in reduction of deformities, but the patient should be awake sufficiently to report neurologic changes and cooperate with the examination.
The two key components of cervical traction are the amount of weight and the direction of applied force, creating a classic force vector. Facet dislocations often require a slight degree of flexion to help mobilize “locked” facets. After reduction the direction of traction force is opposed to the vector of injury. For example, flexion injuries are placed in slight extension. An improvement of 12% has been observed in cadaveric cervical spinal canals after traction. 12 Overdistraction may occur through the use of inappropriately large weights to reduce unstable spinal elements, especially in distraction-type injuries. This may worsen spinal cord damage and risks injury to the vertebral arteries. An injury that is not reducible by this method usually requires open reduction, although some surgeons use traction up to one half the patient’s body weight (approximately 100 lb). Thoracolumbar fractures and dislocations are treated with open reduction and stabilization.
The role of spinal traction and early reduction of displaced spinal elements remains a mainstay of treatment, although scientific support is lacking. In some centers early recognition of the injury and definitive operative stabilization are the preferred course of treatment in patients who are hemodynamically stable. Early reduction of spinal malalignment and mobilization of the patient are the usual goals of early hospital-based management and, in combination with more chronic measures outlined below, usually represent the best treatment for patients who do not require surgery.
After stabilization of the patient’s hemodynamic and respiratory status, along with proper immobilization of the injured spine, the focus shifts to improving the patient’s overall condition and avoiding long-term complications, such as metabolic imbalance, deep vein thrombosis (DVT)/pulmonary embolism, and cutaneous ulcers.
Nutritional and Metabolic Response to Injury.
Most patients lose weight (mean 10%) in the first 4 weeks after SCI. Nitrogen excretion parallels changes in body weight. Calcium excretion is increased for 3 weeks after injury and usually plateaus at 150% above baseline. 29,52 It is important to remember that metabolic losses and nutritional needs are far in excess of immobilized patients, and appropriate caloric and metabolic support should be calculated and met as intravenous feedings or enteral support is feasible. 5,52
Prevention of Secondary Complications
Deep Vein Thrombosis/Pulmonary Embolism.
Deep venous thrombosis and pulmonary emboli are commonly associated with the patient with SCI, in as much as 80% and 10% of patients, respectively. 25 The severity of the motor deficit and a thoracic level of injury increase the risk of thromboembolic complications. 25,35,45 Early application of prophylactic measures, such as sequential compression devices of the lower extremities, increases endothelial production of protocycline-like substances and seems to lower the incidence of DVT from 49% to 72% to 5%. 45 Other measures to prevent DVT are more controversial, although it is the general opinion that early mobilization and heparin therapy (5000 subcutaneously twice a day) may be beneficial. Because the incidence of DVT peaks at 7–8 days, heparin therapy may be delayed a few days after injury. Anticoagulation therapy is continued until the patient is ambulatory or for 3 months postinjury in nonambulatory patients. 25,45 The incidence of pulmonary embolism is difficult to determine because minor emboli may be difficult to detect, as hemoptysis from suctioning and chest wall anesthesia masking pleuritic pain. A sudden deterioration of blood gases (hypoxia and hypocapnia) in a patient with SCI is the most common sign of pulmonary embolism. Fatal pulmonary emboli caused by saddle emboli are far more difficult to prevent than DVT or nonfatal pulmonary embolism.
Skin breakdown has its roots in the early management of patients and occurs in 28% to 85% of patients. 43,44 For example, patients retained on a rigid backboard for more than 8 hours may suffer cutaneous ill effects. Decubiti are best prevented through a combination of frequent patient turning (every 2 hours initially), padding of pressure points, nutritional support, and identification and treatment of cutaneous erosions in the early stages.
Other systemic effects of SCI include ileus, treated with nasogastric suction and Reglan as needed. Bladder atonia is managed with an indwelling catheter for 1 to 2 weeks, followed by intermittent straight catheterization every 4 to 6 hours. Aggressive management of fevers not only assists in the rapid treatment of common infections, such as pneumonia and urinary tract infections, but may also play a role in preventing further damage to the spinal tissue in the acute stage. Because of the loss of autonomic regulation, it is important to maintain the patient in a temperature-regulated environment. Joint immobility from disuse may be caused by heterotopic bone formation and may respond to early mobilization and range of movement exercises.
Skilled nonoperative acute management is an important facet of care surrounding any patient with SCI. With proper resuscitative techniques, the special combination of life-saving measures and protection of the spinal cord from further injury can be achieved. Efficient diagnosis, neurologic vigilance, and spinal traction and immobilization, when indicated, are important measures. Prevention of more chronic complications, such as infection, thromboembolism, and decubiti, are initiated in the acute management stage. The combination of these efforts will help patients with SCI reach their highest levels of recovery.
- Proper evaluation and injury detection are key to capturing patients with SCI.
- Preservation of the patient’s life requires an understanding of the unique hemodynamic and respiratory features of acute SCI.
- Treatments that promote neurologic recovery continue to evolve but seem to involve rapid ster-oid treatment and spinal decompression and stabilization.
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