Acute Spinal Cord Injury

Acute Spinal Cord Injury

0899-5885/00 $15.00 + .00 Neurotrauma Acute Spinal Cord Injury Nursing Considerations for the First 72 Hours Virginia Prendergast, RN, NP-C, and Ci...

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Neurotrauma

Acute Spinal Cord Injury Nursing Considerations for the First 72 Hours Virginia Prendergast, RN, NP-C, and Cindy Sullivan, RN, NP-C

The first known reference to spinal cord injury (SCI) is documented in the Edwin Smith Papyrus in 2500 BC. The writer recorded that a person with a crushed vertebra in his neck was "unconscious" of his neck, two arms, and two legs and was speechless. The writer went on to state that this is "an ailment not to be treated." 32 Since then of course, the management for patients with SCI has undergone tremendous change. Controversy has always existed about initial treatment, surgical approaches, and subsequent care. Despite these challenges, nurses are relied on to perform accurate assessments and intervene appropriately to preserve remaining neurologic function for the approximately 10,000 persons in the United States hospitalized each year with an SCI. 15 This article presents an overview of spinal anatomy, mechanisms of injury, and the assessment and management of patients with an acute SCI.

Overview of Spinal Anatomy The spine or vertebral column provides structural support for the human body. This colFrom Masferrer Neurosurgical, Colorado Springs, Colorado (VP); and Neurosurgical Service, Barrow Neurological Institute, Phoenix, Arizona (CS)

umn is made of 33 progressively larger stacked vertebrae descending from the cranium to the coccyx. The vertebrae are classified and numbered in spinal segments, that is, cervical (7), thoracic (12), lumbar (5), sacrum (5), and coccygeal (4). The vertebral body, lying in the anterior portion of the spine, is the largest bony component of the spine. Located in a posteriolateral direction from the vertebral body are the pedicles, which give rise to the superior and inferior facets. These facets provide mutual interlocking surfaces for adjacent superior and inferior vertebrae. Completing the slightly ovoid shape of the spinal column are the lamina, which join together posteriorly, thus forming the spinous processes (Fig. 1). The vertebral bodies and interbody disks, reinforced by ligaments and paraspinal muscles, maintain the stability of the spine. The vertebral bodies are bound together by the anterior and posterior longitudinal ligaments. The ligamentum flavum (yellow ligament) extends through the lamina, thereby reinforcing the posterior aspect of the vertebral column. Inside this protective column lies the spinal cord, insulated by the meninges and surrounded by cerebrospinal fluid (Fig. 2). The spinal cord originates at the caudal end of the medulla oblongata at the level of the foramen magnum. It usually tapers to an end called the conus medullaris at approximately

CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 I Number 4 I December 2000

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Spinous process

Facet

Disc Figure 1 Vertebral anatomy Anterior and axial view of a cervical vertebrae. (Courtesy of Barrow Neurological Institute of St. Joseph's Hospital and Medical Center, Phoenix, AZ.)

Figure 2 Sagittal spinal anatomy. Midsagittal section of upper cervical spine with ligaments. (Courtesy of Barrow Neurological Institute of St. Joseph's Hospital and Medical Center, Phoenix, AZ.)

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the first lumbar vertebra. The remaining lumbar nerve roots are suspended in cerebrospinal fluid until they exit via the foramen. The anterior spinal artery, branching off from the vertebral artery at the level of the fourth cervical vertebrae, supplies circulation to the anterior two thirds of the spinal cord. The remaining blood supply is via radicular arteries from the aorta. The largest of these arteries is the artery of Adamkiewicz, supplying the majority of blood flow from TS to the conus.

Mechanisms of Spinal Cord Injury SCI occurs as a result of primary mechanisms, which include flexion, hyperextension, combinations of flexion and extension with rotation, vertical compression, and penetrating wounds. 1• 13 Traumatic injury to the vertebral column most commonly occurs at the lower cervical and thoracolumbar junction because these two areas are the most mobile. The injuries are often classified according to the mechanism of injury, such as flexion, hyperextension, and vertical compression. Furthermore, the terms stable and unstable refer to the integrity of the vertebral column and sup-

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porting ligaments. With disruption of these components, great care must be exercised in maintaining the spine in a neutral plane to avoid any further neural injury. 16 Flexion injuries commonly occur as a result of a blow to the back of the head or during instances of deceleration such as occur in motor vehicle accidents. The most severe injuries are teardrop-shaped fractures of the vertebral body. Aside from bony disruption, injury occurs to the disk and anterior and posterior longitudinal ligaments. Therefore, these types of fractures are unstable and require fixation with a halo brace and, in certain instances, fusion of the spine. Wedge-shaped fractures may also occur with flexion injuries but are not always associated with disruption of both main ligaments. In contrast to a teardrop fracture, these fractures are considered stable and are usually treated with a halo brace. The third type of flexion injury, usually occurring with a rotational force, results in subluxation, with the cervical facets becoming disjointed and locked in abnormal alignment. Incremental cervical traction may be used to distract and ultimately realign the spine. However, the patient may occasionally require posterior decompression and fusion to restore alignment if cervical traction fails (Fig. 3).

Figure 3 Cervical subluxation with bilateral locked facets. Lateral view of the cervical spine with subluxation between CS and C6. Inset shows superior view of subluxation. (Courtesy of Barrow Neurological Institute of St. Joseph's Hospital and Medical Center, Phoenix, AZ.)

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Hyperextension injuries may result from a forward fall, with the patient striking his or her face; this is characterized by bruising or lacerations to the forehead or chin. In this instance, SCI may result because of anterior compression of the spinal cord. Great care must be taken to avoid any further extension and subsequent damage to the spinal cord. If there is bony compression of the cord, anterior surgical decompression may be required. Compression injuries may follow a sudden, severe compression of the spinal column, such as can occur in diving or other sports injuries. 19 In the lower cervical spine, a compression fracture may result in the vertebral body bursting under the axial load. Portions of the disrupted body may displace the spinal canal with subsequent neurologic deficits. Because the primary injury occurs to the body, leaving the posterior ligament intact, these injuries are often stable. Although once considered to be primarily a wartime injury, penetrating injuries now rank third as a cause for SCI. Most often, these injuries are caused by knife or gunshot wounds and are rarely unstable. 20 The resultant SCI penetration often occurs because of the blast effect, transection of the cord, or disruption of the vascular supply. Therefore, surgery is rarely indicated except with development of cerebrospinal fluid fistulae 2 or associated visceral or vascular injury.

Anterior cord syndrome can occur with damage to the anterior spinal artery following vertebral fractures and compression. There is characteristic loss of strength and loss of sensations of pain and temperature below the level of the injury. The sensations of vibration and proprioception remain intact. Brown-Sequard syndrome may occur following injuries that transect the cord and is typically seen with stab or gunshot wounds. There is loss of motor function and vibration and position sense ipsilateral to the injury with contralateral loss of sensation of pain and temperature. Changes in the spine occur as a normal part of aging and must be considered in the patient with an SCI. Spinal stenosis can occur with age-related changes such as disk degeneration, osteophyte formation, and hypertrophy of the ligamentum flavum. Because of the narrowed spinal canal, the elderly patient is at greater risk for sustaining an SCI when flexion or extension injuries occur. 24 Numerous secondary pathophysiologic mechanisms of SCI have been identified. These include the systemic effects of neurogenic shock, local vascular damage of neural microcirculation, biochemical changes, edema, electrolyte shifts, free radical formation, lipid hydrolysis, and demyelination. 26 · 27 It is beyond the scope of this article to address the current research and possible interventions for secondary mechanisms of injury. 23, 26, 32

Mechanisms of Injury and Resultant Syndromes

Acute Management

In discussing injury to the spinal cord, the extent of damage is commonly called a complete or an incomplete lesion. In a complete lesion, there is no preservation of neurologic function more than three segments below the level of the injury. When this type of injury lasts more than 24 hours, no distal function is expected. 16 An incomplete lesion infers residual motor or sensory function more than three levels below the level of the injury. 33 Various syndromes may result from incomplete lesions. The central cord syndrome is the most common and usually occurs following a hyperextension injury. Hemorrhage and edema occurring in the central part of the cord results in bilateral upper extremity weakness with sensations of severe burning. In the lower extremities, strength and sensation are preserved.

Prehospital care is an important part in the management of acute SCI. The assumption is made that every patient with multiple trauma or head injury has an SCI. The mechanism of injury is factored into care as persons who are victims of motor vehicle accidents, falls, sporting accidents, and work-related injuries are all managed by prehospital personnel as if an acute SCI has occurred. The objective in caring for patients with an acute spinal injury is to prevent further neurologic insult and maintain remaining neurologic function. On arrival at the emergency department, the advanced trauma life support3 protocol is initiated, directing early interventions. The principles of acute management for the patient with a known or suspected SCI include attention to the following parameters in sequence.

ACUTE SPINAL CORD INJURY

Establishment and Protection of Airway The may be obstructed with blood or vomitus or by massive craniofacial trauma. The jaw-thrust technique may be used initially to open the airway with minimal spinal hyperextension. In instances of apnea, respiratory distress, or depressed level of consciousness, endotracheal intubation should be performed as quickly as possible while maintaining the spine in a neutral plane.

Support of Breathing and Oxygenation Cervical and thoracic segments innervate the muscles of respiration, and injury to these spinal segments predisposes the patient to respiratory compromise or failure. Pulmonary complications in this population are major causes of morbidity and mortality (Table 1). [,4,

2'S

The critical care nurse must assess pulmonary function aggressively by observing diaphragmatic movement, chest expansion, and cough. Paradoxical breathing, the collapse of the thorax on inspiration and expansion on expiration, may develop as the new patient with SCI fatigues. 18 Frequent auscultation of lung sounds for equal air exchange and adventitious sounds is imperative because ineffective cough, inability to clear secretions, development of atelectasis, and increased risk of infections are common complications. 25 Serial measurements of respiratory parameters, including tidal volume (VT), vital capacity (VC), and negative inspiratory force (NIF), are valid indicators for assessing respiratory status and assisting with decision making regarding the types of respiratory treatments warranted and the need for intubation and mechanical ventilation. Respiratory failure is

Level

Muscles Innervated

C2-C8

Accessory muscles for rib cage excursion Diaphragm lntercostal muscles for deep breathing and coughing Abdominal muscles for expiration and coughing

C3-C5 T1-T7 T6-T12

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indicated by decreases in VT below 5 mL/kg, VC below 1 S ml/kg, and NIF below - 20 cm H 20. 18 Serial arterial blood gases (ABGs) are also performed for all patients because hypoxemia contributes to the secondary mechanisms of SCI injury and must be avoided. The patient should be repositioned every 2 hours to prevent secretion accumulation. The use of an incentive spirometer promotes deep breathing, strengthens the respiratory muscles, and promotes secretion mobilization. Chest physiotherapy and intermittent positive pressure breathing also promote loosening of secretions. 8 Persons with SCI above the level of T7 will need to be coughed manually to assist in clearance of secretions as the innervation of the muscles for cough are impairedrn Finally, nasotracheal suctioning can be used for patients who do not mobilize retained secretions. Failure to maintain adequate ventilation leads to intubation and, most often, mechanical ventilation of the patient.

Maintenance of Systemic and Spinal Cord Perfusion Cardiovascular compromise is most profound in persons with SCI above the level of T6 because of the interruption of the sympathetic chain located adjacent to Tl-TS. The syndrome of neurogenic shock occurs as a result of decreased sympathetic tone, unopposed cardiac vagotonia, and decreased systemic arteriolar resistance. Hence, neurogenic shock is best remembered by the triad of hypotension, bradycarclia, and warm, hyperemic skin. Hypotension secondary to neurogenic shock will not improve solely with the administration of fluid boluses. The abnormally increased venous capacitance results in decreased afterload and preload, thereby decreasing cardiac output. The use of vasopressors, such as dopamine or dobutamine, is typically needed to promote vasoconstriction and increase cardiac output. There is some discussion in the literature regarding the optimum parameters for mean arterial pressure (MAP). Drawing a corollary from management of cerebral ischemia, there has been the suggestion of defining a MAP greater than 85 mm Hg as the optimal perfusion for the spinal cord 51 However, no such parameter has been scientifically established nor are there methods currently available to measure spinal cord perfusion. Furthermore,

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there has been concern that hypertension must be avoided because of the theoretic implications of contributing to intramedullary hemorrhage or edema. Whereas this aspect of initial management remains unresolved, the insertion of arterial lines and pulmonary artery catheters contributes to accurate, ongoing assessment and management of the patient's circulatory status and preservation of normotension. Immobilization of Spine

The cervical region is the most common site of SCI because it is the most mobile part of the spine. 10 During transportation to the hospital, sandbags should be placed on either side of the patient's head to further minimize cervical spine movement10• 14 and patients should be secured to a backboard with the spine in alignment. In addition, it is recommended that patients have their heads taped to the backboard for transportation. 14 On arrival in the emergency department, the patient should be removed from the backboard within 2 hours to avoid development of decubitus ulcers. In-line immobilization without traction is the current standard of care for patients with a suspected SCI. 14 This is accomplished by placing the head and neck in a neutral position, then immobilizing the neck in a rigid collar. Stabilization of fractures of the cervical spine is generally accomplished with skeletal tongs or a halo ring and traction. Weights are applied in small increments, with alignment determined by serial roentgenograms. Once cervical alignment is achieved, a halo vest may be applied to maintain stabilization. Thoracic spine fractures (Tl-TlO) are relatively uncommon because this region is stabilized by the rib cage, 10 and they are therefore frequently considered stable fractures. Thoracolumbar injuries (Tll-Tl2) are the second most common site of fractures and dislocations5 because of increased mobility at this level. Initially, patients should be kept supine and log rolled to avoid further flexion, extension, or rotation of the spine. With compression fractures of the spine, external bracing is used to provide stability and support for 12 weeks while the fracture heals. 23 When fractures are associated with disruption of the pedicles and lamina, posterior surgical fusion is often performed and is followed by external bracing. Because of the high incidence of associated ligamentous dis-

ruption, these injuries are often considered unstable (Fig. 4). Neurologic Examination It is essential for an accurate baseline exami-

nation to be performed that documents the patient's neurologic status, providing an anatomic level of injury as well as an indication of the extent of neural damage. Changes in management will be based on this initial survey; therefore, consistent methods of assessment should be used. For those patients with a complete SCI, a period of spinal shock occurs. This interval period, highly variable in duration, may last a minimum of 3 or 4 days or as long as 6 weeks. Conditions such as urinary tract infections or decubitus ulcers may prolong the duration of spinal shock. During this time, there is flaccid paralysis and minimal reflex activity. 4 Following the period of spinal shock, injuries to the spinal cord result in loss of voluntary motor function below the level of injury, increased muscle tone, and hyperreflexia. The motor and sensory aspects of spinal shock are described as resolving within an hour. Therefore, motor function and sensory levels

Figure 4 Fracture dislocation of thoracolumbar spine. Lateral view of flexion-rotation type of fracture dislocation with disruption through the level of the disc, posterior longitudinal ligament, and spinal fracture. (Courtesy of Barrow Neurological Institute of St. Joseph's Hospital and Medical Center, Phoenix, AZ.)

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at admission should be attributed to neural injury and not spinal shock. 2 Predictions regarding prognosis related to motor function may be the most accurate if based on a complete neurologic examination 72 hours after the initial injury instead of the examination performed in the emergency department. The initial examination may have been influenced by factors such as level of alertness, the presence of drugs, and evolving neurologic deficits. 7 The two key areas for serial nursing assessments include documentation of motor and sensory function. The sequential survey of main muscle groups corresponds to the level of neural innervation (Table 2). Each muscle should be assessed individually and compared with that on the contralateral side. Improvements or deteriorations in function will influence subsequent diagnostic testing and intervention. Although there are a variety of scales available to record muscle strength, the key point is to assess and document the motor function in a reliable and consistent manner. For the sensory examination, the patient response to pinprick is also compared in a sequential, side-to-side manner. A dermatome chart can be placed at the patient's bedside or on the graphic chart to monitor changes (Fig. 5). There may be a band of increased sensation at or just below the level of the lesion. With cervical injuries, visceral sensation is lost as well. The patient will therefore not complain of abdominal pain that may be associated with constipation or the development of stress ulcers. For more detailed examinations, patient response to light touch can be recorded as a manner of testing the preservation of anterior cord function. Proprioception, or joint sense, can likewise be used to assess the posterior columns of the spinal cord.

Table 2

Figure 5 Dermatome. (Courtesy of Barrow Neurological Institute of St. Joseph's Hospital and Medical Center, Phoenix, AZ.)

Administration of Methylprednisolone The current practice of steroid administration following acute SCI has been studied in three trials by the National Acute Spinal Cord Injmy

SPINAL LEVELS AND KEY MUSCLE.GROUPS

Spinal Level

Muscle

Test

C5 C6

Deltoid/biceps Wrist extensors Triceps Flexor digitorum profundus Hand intrinsics lliopsoas Quadriceps Tibialis anterior Extensor hallucis longus Gastrocnemius

Shoulder abduction or elbow flexion Cock up wrist Extend elbow Finger flexion to middle finger Little finger abductor Hip flexors Knee extensors Ankle dorsiflexor Dorsiflex great toe Ankle plantar flex

Cl

cs

T1 L2 L3 L4 L5

81

505

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Study (NASCIS). The results suggest that patients who received steroids had significant improvement in motor function compared with patients treated with placebo at 6 weeks, 6 months, and 1 year postinjury. 6 As a result of these studies, the current standardized treatment for patients with SCI who are seen within 3 hours of injury is to receive an initial intravenous (IV) bolus of 30 mg/ kg of methylprednisolone over 15 minutes, followed 45 minutes later by a 5.4 mg/kg per hour continuous intravenous infusion of methylprednisolone for 23 hours. Patients who are treated within the 3- to 8-hour window should receive the same initial bolus and should have the 5.4 mg/kg per hour drip of methylprednisolone for 48 hours. The efficacy of steroids for patients with SCI secondary to gunshot wounds has not been proven in retrospective studies. 17• 22 Gastrointestinal Considerations

A nasogastric tube inserted and placed to low, intermittent suction decreases vomiting and possible aspiration. Decompression of the abdomen may also improve pulmonary function. Frequently, patients with SCis develop a paralytic ileusthatmay last for several days. Administration of agents such as metoclopramide to decrease gastric paresis may be beneficial. The concomitant administration of H2 blockers is advocated for stress ulcer prophylaxis. The nutritional needs of the patient should also be addressed via oral, enteral, or intravenous supplementation within 72 hours. Genitourinary Considerations An indwelling urinary catheter should be

placed in the emergency department to allow for careful monitoring of intake and output records. Additionally, the catheter prevents bladder distention from urinary retention. Following resolution of neurogenic shock, intermittent catherization may begin. A bowel regimen consisting of stool softener and evacuants should be initiated within the first 72 hours.

available. Use of subcutaneous, low-dose heparin, or low-molecular-weight heparin should be administered once the risk of intramedullary or epidural hemorrhage has been resolved.

Diagnostic Evaluation The radiographic study of the patient with a known or suspected SCI includes basic spine films at the minimum, or more complex diagnostic studies. In most centers, emergency department protocols usually include openmouth odontoid, anterioposterior, and lateral films for cervical clearance. It is essential that the views include C7 to Tl to exclude a lower cervical injury. In the cervical spine, flexion and extension films may be obtained to exclude ligamentous injury when the patient presents with neurologic deficits or complaints of neck pain. Anterioposterior and lateral films of the thoracic and lumbar spine are obtained in trauma patients to exclude vertebral pathology. Whereas plain films may provide a gross indication of spinal alignment, CT scans are superior in detecting bony abnormalities that may not be well visualized on conventional films. This is especially true with fractures of the odontoid.11 With the advent of spiral CT imaging, high-resolution images can be obtained rapidly. 2 In contrast to plain films or CT images, MR studies yield excellent information on the softtissue structures such as the spinal cord, disks, and ligaments. This study is especially recommended for patients who may have ligamentous injury, for those whose deficits are not explained by plain or CT images, or for those who develop delayed deficits. Such examples include patients with epidural hematomas or nonhemorrhagic cord contusion.11 Disruption of ligaments may not be appreciated on the plain films or on the CT, yet they may be highlighted on the MR study, thus influencing management. Artifact caused by patient motion results in poor quality MR images, so the nurse may need to provide reassurance or medications for pain and anxiety during the testing.

Deep Vein Thrombosis Prophylaxis

Measures to reduce the development of deep vein thrombosis (DVT) should begin on admission for the patient with SCI. Various types of foot or full-leg compression devices are

Operative Management Controversy about the optimal timing for surgical decompression and fusion for patients with

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SCI is well cited in the literature. 2• 9• 24 Amar and Levy2 posit that the changes that occur at the time of injury are the main determinants of outcome, and early surgical intervention does not significantly alter outcome. In their view, the patient should stabilize and recover from any other injuries sustained at the time of injury. Equally important, a number of studies have not demonstrated any significant neurologic improvement in patients with complete injuries following surgical decompression. 9• 24 When indicated, early surgery is performed to decompress the spinal canal from bone or disk fragments, provide stabilization in cases of ligmentous injury, or repair damage caused by penetrating injuries. The anterior approach is generally indicated for injuries caused by extension, whereas a posterior approach is considered for most flexion injuries. External immobilization is often used postoperatively until osseous union is complete. Although the spine may fuse spontaneously within 8 to 12 weeks, surgical decompression and fusion may be performed as early as 4 or 5 days after injury. The benefits of surgical stabilization include allowing the patient to get out of bed, which in turn provides for improved pulmonary function and for the introduction of physical and occupational therapy.

Future Directions in SCI There is the expression "spinal cord injuries are forever." For the individual with an SCI, the total number of years of impairment is significant given that the average age at the time of injury is 31 years and that life expec-

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tancy of the patient with SCI reaches 70% of normal. 29 • 30 Recent statistics reveal that approximately 56% of patients with SCI are between the ages of 16 and 30 years, which translates to over $7 billion in direct costs for lifetime care of patients with SCI. 13, 21 In 1997, estimates of preventable SCI ranged from 66% to 74%. 28 Because of such compelling figures, many health care providers in the neurosciences have focused attention on programs stressing prevention of injury. The Think First Foundation (Park Ridge, IL), developed in 1986 by the American Association of Neurological Surgeons and Congress of Neurological Surgeons, is a program geared to reduce incidence of head and spinal injury. Classes at elementary through high school level are taught through the combined efforts of a young person who is brain- or spinal-cord injured and a health care professional. There is evidence that prevention programs have been successful for other preventable injuries such as alcohol-related driving fatalities. Following a widespread advertising campaign against drunk driving, a 30% decrease was noted in such fatalities in 1994 as compared to 1984. 28 Aside from the potential success of preventive programs, research efforts continue to explore ways to alter the course of secondary injuries. Aspects related to the biomechanical forces of injury, nerve growth factors, spinal cord ischemia, and optimal spinal cord perfusion warrant further investigation. 12• 26 • 31 Nursing research related to quality of life issues for those patients with SCI could help identify additional areas of intervention for all members of the health care team.

SUMMARY The effects of spinal cord injury can be devastating. An understanding of spinal anatomy and the mechanisms of injury provide the basis for correlating presenting signs and symptoms with the extent of neural damage. Understanding the principles of acute care management will help guide the nurse in executing interventions aimed at preservation of neurologic functions. Research must continue to focus on· quality-of-life issues and methods of preventing both primary and secondary injuries.

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REFERENCES 1. Allen AR: Surgery of experimental lesions of the spinal cord equivalent to crush injury of fracture dislocation of the spinal column: A preliminary report. JAMA 57:878-880, 1991 2. Amar AP, Levy ML: Surgical controversies in the management of spinal cord injury. ] Am Coll Surg 188:550-566, 1999 3. American College of Surgeons: Advanced trauma life support program for physicians. Chicago, American College of Physicians, 1997 4. Atkinson PP, Atkinson JL: Spinal shock. Mayo Clin Proc 71:384-389, 1996 5. Bauer RD, Errico TJ: Thoracolumbar spine injuries. In Errico TJ, Bauer RD, Waugh T (eds): Spinal Trauma. Philadelphia, JB Lippincott, 1991, pp 195-269 6. Bracken MB, Shepard MJ, Holford TR, et al: Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1 year follow up. ] Neurosurg 89:699-706, 1998 7. Brown PJ, Marino RJ, Herbison GJ, et al: The 72 hour examination as a predictor of recovery in motor complete quadriplegia. Arch Phys Med Rehab 72:546-552, 1991 8. Browner CM, Duistermars PJ: Preventing pulmonary compromise in the acute spinal cord-injured patient. BNI Quarterly 5:35-39, 1989 9. Chen TU, Dickman CA, Eleraky M, et al: The role of decompression for acute incomplete cervical spinal cord injury in cervical spondylosis. Spine 23:23982403, 1998 10. Chiles BW, Cooper PR: Acute spinal injury. New Eng J Med 334:514-520, 1996 11. Cornelius RS, LeachJL: Imaging evaluation of cervical spine trauma. Neuroimaging Clin North Am 5:451463, 1995 12. Cusick JF, Yoganandan N, Pintar F, et al: Cervical spine injuries from high-velocity forces: A pathoanatomic and radiologic study.] Spinal Disord 9:1-7, 1996 13. DeVivo MJ: Causes and costs of spinal cord injury in the United States. Spinal Cord 35:809-813, 1997 14. Fehlings MG, Lauw D: Initial stabilization and medical management of acute spinal cord injury. Am Fam Phys 54:155-162, 1996 15. Go BK, DeVivo MJ, Richards JS: The epidemiology of spinal cord injury. In Stover SL, DeLisa ]A, Whiteneck GG (eds): Spinal Cord Injury: Clinical Outcomes from the Model Systems, 1995, pp 21-55

16. Greenberg MS: Spine and spinal cord. In Handbook of Neurosurgery, ed 4. Lakeland, FL, Greenberg Graphics, 1997, pp 1669-1697 17. Heary RF, Vaccaro AR, Mesa]], et al: Steroids and gunshot wounds to the spine. Neurosurgery 41:576584, 1997 18. Hughes MC: Critical care nursing for the patient with a spinal cord injury. Crit Care Nurs Clin North Am 2:33-40, 1990 19. Huston CJ: Cervical spine injury. AJN 98:33, 1998 20. Jallo GI: Neurosurgical management of penetrating spinal injury. Surg Neural 47:328-330, 1997 21. Kirshblum SC, O'Connor KC: Predicting neurologic recovery in traumatic cervical spinal cord injury. Arch Phys Med Rehabil 79:1456-1466, 1998 22. Levy ML, Gans W, Wijesinghe HS, et al: Use of methylprednisolone as an adjunct in the management of patients with penetrating spinal cord injury: Outcome analysis. Neurosurgery 39:1141-1149, 1996 23. Marion DW: Head and spinal cord injury. Neural Clin 16:485-502, 1998 24. Murphy KP, Optiz JL, Cabanela ME, et al: Cervical fractures and spinal cord injury: Outcome of surgical and nonsurgical management. Mayo Clin Proc 65:949-959, 1990 25. Roth EJ, Lu A, Primack S, et al: Ventilatory function in cervical and high thoracic spinal cord injury: Relationship to level of injury and tone. Am] Phys Med Rehabil 76:262-267, 1997 26. Segatore M, Way C: Neuroprotection after spinal cord injury: State of the science. SCI Nursing 14:8-17, 1997 27. Tator CH: Spinal trauma: Pathophysiology and pathology of spinal cord injury. In Wilkins RH, Rengachary SS (eds): Neurosurgery. New York, McGrawHill, 1996, pp 2847-2859 28. Tyrock AH, Davis JW, Kaups KL, et al: Spinal cord injury. Arch Surg 132:778-781, 1997 29. Yeo]D, Walsh], Rutkowski S, eta!: Mortality following spinal cord injury. Spinal Cord 36:329-336, 1998 30. Yu D: A crash course in spinal cord injury. Postgrad Med 104:109-122, 1998 31. Vale FL, BurnsJ,JacksonAB, eta!: Combined medical and surgical treatment after acute spinal cord injury: Results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management.] Neurosurg 87:239-246, 1997 32. Sonntag VK: History of degenerative and traumatic diseases of the spine. In Greenblatt SH: A History of Neurosurgery. Park Ridge, IL, American Association of Neurological Surgeons, 1997, pp 355-372 33. Waters RL, Adkins RH, Yakura J, et al: Profiles of spinal cord injury and recovery after gunshot injury. Clin Orthop 267:14-21, 1991

Address reprint requests to Virginia Prendergast, RN, NP-C Masferrer Neurosurgical 75 Printers Parkway, Suite 145 Colorado Springs, CO 80910