eMedicine Specialties > Emergency Medicine > Neurology

Spinal Cord Injuries: Treatment & Medication

Author: Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Contributor Information and Disclosures

Updated: Apr 8, 2009

Treatment

Prehospital Care

  • Most prehospital care providers recognize the need to stabilize and immobilize the spine on the basis of mechanism of injury, pain in the vertebral column, or neurologic symptoms.
  • Patients are usually transported to the ED with a cervical hard collar on a hard backboard.
    • Commercial devices are available to secure the patient to the board.
    • The patient should be secured so that in the event of emesis, the backboard may be rapidly rotated 90 degrees while the patient remains fully immobilized in a neutral position. Spinal immobilization protocols should be standard in all prehospital care systems.

Emergency Department Care

Most patients with spinal cord injuries (SCIs) have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation takes precedence.

Airway management in the setting of spinal cord injury, with or without a cervical spine injury, is complex and difficult. The cervical spine must be maintained in neutral alignment at all times. Clearing of oral secretions and/or debris is essential to maintain airway patency and to prevent aspiration. The modified jaw thrust and insertion of an oral airway may be all that is required to maintain an airway in some cases. However, intubation may be required in others. Failure to intubate emergently when indicated because of concerns regarding the instability of the patient's cervical spine is a potential pitfall.

Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury. Because of the vital sign confusion in acute spinal cord injury and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made.

The most common causes of occult hemorrhage are chest, intra-abdominal, or retroperitoneal injuries and pelvic or long bone fractures. Appropriate investigations, including radiography or CT scanning, are required. In the unstable patient, diagnostic peritoneal lavage or bedside FAST (focused abdominal sonography for trauma) ultrasonographic study may be required to detect intra-abdominal hemorrhage.

Once occult sources of hemorrhage have been excluded, initial treatment of neurogenic shock focuses on fluid resuscitation. Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 liters is the initial treatment of choice. Overzealous crystalloid administration may cause pulmonary edema because these patients are at risk for the acute respiratory distress syndrome.

  • The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters:
    • Systolic blood pressure (BP) should be 90-100 mm Hg. Systolic BPs in this range are typical for patients with complete cord lesions. The most important treatment consideration is to maintain adequate oxygenation and perfusion of the injured spinal cord. Compelling animal and human studies recommend maintenance of systolic blood pressure higher than 90 and prevent any hypotensive episodes.16,7
    • Heart rate should be 60-100 beats per minute in normal sinus rhythm.
    • Hemodynamically significant bradycardia may be treated with atropine.
    • Urine output should be more than 30 mL/h. Placement of a Foley catheter to monitor urine output is essential. Rarely, inotropic support with dopamine is required. It should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation. Usually, low doses of dopamine in the 2- to 5-mcg/kg/min range are sufficient.
    • Prevent hypothermia.
  • Associated head injury occurs in about 25% of patients with spinal cord injury. A careful neurologic assessment for associated head injury is compulsory. The presence of amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, and a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning.
  • Ileus is common. Placement of a nasogastric tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function. Antiemetics should be used aggressively.
  • The patient is best treated initially in the supine position. Occasionally, the patient may have been transported prone by the prehospital care providers. Logrolling the patient to the supine position is safe to facilitate diagnostic evaluation and treatment. Use analgesics appropriately and aggressively to maintain the patient's comfort if he or she has been lying on a hard backboard for an extended period.
  • Prevent pressure sores. Denervated skin is particularly prone to pressure necrosis. Turn the patient every 1-2 hours. Pad all extensor surfaces. Undress the patient to remove belts and back pocket keys or wallets. Remove the spine board as soon as possible.

Use of steroids in spinal cord injury

  • The National Acute Spinal Cord Injury Studies (NASCIS) II and III, a Cochrane Database of Systematic Reviews article of all randomized clinical trials and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete spinal cord injuries (SCIs) who were treated with high doses of methylprednisolone within 8 hours of injury.17,18
    • The NASCIS II study evaluated methylprednisolone administered within 8 hours of injury. The NASCIS III study evaluated methylprednisolone 5.4 mg/kg/h for 24 or 48 hours versus tirilazad 2.5 mg/kg q6h for 48 hours. (Tirilazad is a potent lipid preoxidation inhibitor.) High doses of steroids or tirilazad are thought to minimize the secondary effects of acute spinal cord injury (SCI). In the NASCIS III trial, all patients (n = 499) received a 30-mg/kg bolus of methylprednisolone intravenously. The study found that, in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 hours was best. In patients treated 3-8 hours after injury, the use of methylprednisolone for 48 hours was best. Tirilazad was equivalent to methylprednisolone for 24 hours.18
    • Both NASCIS studies evaluated the patients' neurologic status at baseline on enrollment into the study, at 6 weeks, and at 6 months. Absolutely no evidence from these studies suggests that giving the medication earlier (eg, in the first hour) provides more benefit than giving it later (eg, between hours 7 and 8). The authors only concluded that there was a benefit if given within 8 hours of injury following the NASCIS trials.18
  • The use of high-dose methylprednisolone in nonpenetrating acute spinal cord injury had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned the validity of the results.19 These authors cited concerns about the statistical analysis, randomization, and clinical endpoints used in the study. Even if the benefits of steroid therapy are valid, the clinical gains are questionable. Other reports have cited flaws in the study designs, trial conduct, and final presentation of the data. The risks of steroid therapy are not inconsequential. An increased incidence of infection and avascular necrosis has been documented.
  • A number of professional organizations have therefore revised their recommendations pertaining to steroid therapy in spinal cord injury (SCI). The Canadian Association of Emergency Physicians is no longer recommending high-dose methylprednisolone as the standard of care. The Congress of Neurological Surgeons has stated that steroid therapy "should only be undertaken with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit."20 The American College of Surgeons has modified their Advanced Trauma Life Support guidelines to state that methylprednisolone is "a recommended treatment" rather than "the recommended treatment."
  • In a recent survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids in spinal cord injury (SCI), but only 24% believed that they were of any clinical benefit.21  Note that the authors discovered that approximately 7% of spine surgeons do not recommend or use steroids at all in acute spinal cord injury. The authors reported that most centers were following the NASCIS II trial protocol.
  • Overall, the benefit from steroids is considered modest at best, but for patients with complete or incomplete quadriplegia, a small improvement in motor strength in one or more muscles can provide important functional gains.
  • The administration of steroids remains an institutional and physician preference in spinal cord injury. Nevertheless, the administration of high-dose steroids within 8 hours of injury for all patients with acute SCI is practiced by most physicians.
  • The current recommendation is to treat all patients with SCI according to the local/regional protocol. If steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus.
  • Local policy will also determine if the NASCIS II or NASCIS III protocol is to be followed.
  • Two North American studies have addressed the administration of GM-1 ganglioside following acute spinal cord injury. The available medical evidence does not support a significant clinical benefit. It was evaluated as a treatment adjunct after the administration of methylprednisolone.22,16

Treatment of pulmonary complications and injury in spinal cord injury

  • Treatment of pulmonary complications and/or injury in patients with spinal cord injury (SCI) includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax.
  • The ideal technique for emergent intubation in the setting of SCI is fiberoptic intubation with cervical spine control. This, however, has not been proven better than orotracheal with in-line immobilization. Furthermore, no definite reports of worsening neurologic injury with properly performed orotracheal intubation and in-line immobilization exist. If the necessary experience or equipment is lacking, blind nasotracheal or oral intubation with in-line immobilization is acceptable. Indications for intubation in SCI are acute respiratory failure, decreased level of consciousness (Glasgow score <9), increased respiratory rate with hypoxia, PCO2 more than 50, and vital capacity less than 10 mL/kg.
  • In the presence of autonomic disruption from cervical or high thoracic spinal cord injury, intubation may cause severe bradyarrhythmias from unopposed vagal stimulation. Simple oral suctioning can also cause significant bradycardia. Preoxygenation with 100% oxygen may be preventive. Atropine may be required as an adjunct. Topical lidocaine spray can minimize or prevent this reaction.

Consultations

  • Consultation with a neurosurgeon and/or an orthopedist is required, depending on local preferences.
  • Because most patients with spinal cord injury have multiple associated injuries, consultation with a general surgeon or a trauma specialist may be required.
  • Depending on the patient's associated injuries, other consultations may be required.

Medication

The goal of therapy is to improve motor function and sensation in patients with spinal cord injuries (SCIs).

Glucocorticoids

High-dose steroids are thought to reduce the secondary effects of acute spinal cord injury (SCI). Studies have shown limited but significant improvement in the neurologic outcome of patients treated within 8 h of injury.


Methylprednisolone (Solu-Medrol)

Used to reduce the secondary effects of acute SCI.

Adult

30 mg/kg IV bolus over 15 min, followed by 5.4 mg/kg/h over 23 h; begin IV infusion 45 min after conclusion of bolus

Pediatric

Administer as in adults

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogen use may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when administered with diuretics

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications

More on Spinal Cord Injuries

Overview: Spinal Cord Injuries
Differential Diagnoses & Workup: Spinal Cord Injuries
Treatment & Medication: Spinal Cord Injuries
Follow-up: Spinal Cord Injuries
Multimedia: Spinal Cord Injuries
References
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References

  1. Kriss VM, Kriss TC. SCIWORA (spinal cord injury without radiographic abnormality) in infants and children. Clin Pediatr (Phila). Mar 1996;35(3):119-24. [Medline].

  2. Pang D. Spinal cord injury without radiographic abnormality in children, 2 decades later. Neurosurgery. Dec 2004;55(6):1325-42; discussion 1342-3. [Medline].

  3. Yucesoy K, Yuksel KZ. SCIWORA in MRI era. Clin Neurol Neurosurg. May 2008;110(5):429-33. [Medline].

  4. National Spinal Cord Injury Statistical Center, Birmingham, Alabama. Spinal Cord Injury: Facts and Figures at a Glance. January 2008;Accessed February 24, 2009. Available at www.spinalcord.uab.edu.

  5. Harris MB, Sethi RK. The initial assessment and management of the multiple-trauma patient with an associated spine injury. Spine. May 15 2006;31(11 Suppl):S9-15; discussion S36. [Medline].

  6. Ho CH, Wuermser LA, Priebe MM, Chiodo AE, Scelza WM, Kirshblum SC. Spinal cord injury medicine. 1. Epidemiology and classification. Arch Phys Med Rehabil. Mar 2007;88(3 Suppl 1):S49-54. [Medline].

  7. Wuermser LA, Ho CH, Chiodo AE, Priebe MM, Kirshblum SC, Scelza WM. Spinal cord injury medicine. 2. Acute care management of traumatic and nontraumatic injury. Arch Phys Med Rehabil. Mar 2007;88(3 Suppl 1):S55-61. [Medline].

  8. Brown CV, Antevil JL, Sise MJ, Sack DI. Spiral computed tomography for the diagnosis of cervical, thoracic, and lumbar spine fractures: its time has come. J Trauma. May 2005;58(5):890-5; discussion 895-6. [Medline].

  9. Grogan EL, Morris JA Jr, Dittus RS, et al. Cervical spine evaluation in urban trauma centers: lowering institutional costs and complications through helical CT scan. J Am Coll Surg. Feb 2005;200(2):160-5. [Medline].

  10. Acheson MB, Livingston RR, Richardson ML, Stimac GK. High-resolution CT scanning in the evaluation of cervical spine fractures: comparison with plain film examinations. AJR Am J Roentgenol. Jun 1987;148(6):1179-85. [Medline].

  11. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. Jul 13 2000;343(2):94-9. [Medline].

  12. Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. Dec 25 2003;349(26):2510-8. [Medline].

  13. Stiell IG, Wells GA, Vandemheen KL. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. Oct 17 2001;286(15):1841-8. [Medline].

  14. Keenen TL, Antony J, Benson DR. Non-contiguous spinal fractures. J Trauma. Apr 1990;30(4):489-91. [Medline].

  15. Powell JN, Waddell JP, Tucker WS, Transfeldt EE. Multiple-level noncontiguous spinal fractures. J Trauma. Aug 1989;29(8):1146-50; discussion 1150-1. [Medline].

  16. Congress of Neurologic Surgeons. Blood pressure management after acute spinal cord injury. Neurosurgery. Mar 2002;50(3 Suppl):S58-62. [Medline].

  17. Bracken MB, Shepard MJ, Hellenbrand KG, et al. Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. J Neurosurg. Nov 1985;63(5):704-13. [Medline].

  18. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. May 28 1997;277(20):1597-604. [Medline].

  19. Nesathurai S. Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma. Dec 1998;45(6):1088-93. [Medline].

  20. Hadley MN, Walters BC, Grabb PA, et al. Pharmacological therapy after acute spinal cord injury. Neurosurgery. 2002;50 Suppl:63-72.

  21. Eck JC, Nachtigall D, Humphreys SC, Hodges SD. Questionnaire survey of spine surgeons on the use of methylprednisolone for acute spinal cord injury. Spine. Apr 20 2006;31(9):E250-3. [Medline].

  22. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor function after spinal-cord injury--a randomized, placebo-controlled trial with GM-1 ganglioside. N Engl J Med. Jun 27 1991;324(26):1829-38. [Medline].

  23. Gaebler C, Maier R, Kutscha-Lissberg F, Mrkonjic L, Vecsei V. Results of spinal cord decompression and thoracolumbar pedicle stabilisation in relation to the time of operation. Spinal Cord. Jan 1999;37(1):33-9. [Medline].

  24. Mirza SK, Krengel WF 3rd, Chapman JR, Anderson PA, Bailey JC, Grady MS. Early versus delayed surgery for acute cervical spinal cord injury. Clin Orthop Relat Res. Feb 1999;(359):104-14. [Medline].

  25. Vaccaro AR, Daugherty RJ, Sheehan TP, et al. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine. Nov 15 1997;22(22):2609-13. [Medline].

  26. Bagnall AM, Jones L, Duffy S, Riemsma RP. Spinal fixation surgery for acute traumatic spinal cord injury. Cochrane Database Syst Rev. Jan 23 2008;CD004725. [Medline].

  27. American Spinal Injury Association. Guidelines for Facility Categorization and Standards of Care: Spinal Cord Injury. 1981.

  28. Annual Report for the Model Spinal Cord Injury Care Systems [database online]. Birmingham, Alabama, USA: National Spinal Cord Injury Statistical Center; December 2007.

  29. Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev. 2002;CD001046. [Medline].

  30. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. May 17 1990;322(20):1405-11. [Medline].

  31. Burney RE, Maio RF, Maynard F, Karunas R. Incidence, characteristics, and outcome of spinal cord injury at trauma centers in North America. Arch Surg. May 1993;128(5):596-9. [Medline].

  32. CJEM. Steroids in acute spinal cord injury. CJEM. Jan 2003;5(1):7-9. [Medline].

  33. Ducker TB, Zeidman SM. Spinal cord injury. Role of steroid therapy. Spine. Oct 15 1994;19(20):2281-7. [Medline].

  34. Fehlings MG, Perrin RG. The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence. Injury. Jul 2005;36 Suppl 2:B13-26. [Medline].

  35. Fisher CG, Noonan VK, Dvorak MF. Changing face of spine trauma care in North America. Spine. May 15 2006;31(11 Suppl):S2-8; discussion S36. [Medline].

  36. Green BA, Eismont FJ, O'Heir JT. Spinal cord injury--a systems approach: prevention, emergency medical services, and emergency room management. Crit Care Clin. Jul 1987;3(3):471-93. [Medline].

  37. Hadley MN, Walters BC, Grabb PA, et al. Guidelines for the management of acute cervical spine and spinal cord injuries. Clin Neurosurg. 2002;49:407-98. [Medline].

  38. Hurlbert RJ. Strategies of medical intervention in the management of acute spinal cord injury. Spine. May 15 2006;31(11 Suppl):S16-21; discussion S36. [Medline].

  39. Hurlbert RJ, Hamilton MG. Methylprednisolone for acute spinal cord injury: 5-year practice reversal. Can J Neurol Sci. Mar 2008;35(1):41-5. [Medline].

  40. Janssen L, Hansebout RR. Pathogenesis of spinal cord injury and newer treatments. A review. Spine. Jan 1989;14(1):23-32. [Medline].

  41. Krompinger WJ, Fredrickson BE, Mino DE, Yuan HA. Conservative treatment of fractures of the thoracic and lumbar spine. Orthop Clin North Am. Jan 1986;17(1):161-70. [Medline].

  42. Marshall LF, Knowlton S, Garfin SR, et al. Deterioration following spinal cord injury. A multicenter study. J Neurosurg. Mar 1987;66(3):400-4. [Medline].

  43. Meyer PR. Surgery of Spine Trauma. New York, NY: Churchill Livingstone; 1989.

  44. Meyer PR Jr, Cybulski GR, Rusin JJ, Haak MH. Spinal cord injury. Neurol Clin. Aug 1991;9(3):625-61. [Medline].

  45. Reid DC, Henderson R, Saboe L, Miller JD. Etiology and clinical course of missed spine fractures. J Trauma. Sep 1987;27(9):980-6. [Medline].

  46. Saboe LA, Reid DC, Davis LA, Warren SA, Grace MG. Spine trauma and associated injuries. J Trauma. Jan 1991;31(1):43-8. [Medline].

  47. Sansam KA. Controversies in the management of traumatic spinal cord injury. Clin Med. Mar-Apr 2006;6(2):202-4. [Medline].

  48. Savitsky E, Votey S. Emergency department approach to acute thoracolumbar spine injury. J Emerg Med. Jan-Feb 1997;15(1):49-60. [Medline].

  49. Tator CH. Acute management of spinal cord injury. Br J Surg. May 1990;77(5):485-6. [Medline].

  50. Woodring JH, Lee C. The role and limitations of computed tomographic scanning in the evaluation of cervical trauma. J Trauma. Nov 1992;33(5):698-708. [Medline].

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Further Reading

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Keywords

spinal cord injury, SCI, anterior cord syndrome, Brown-Séquard syndrome, central cord syndrome, conus medullaris syndrome, cauda equina syndrome, incomplete SCI syndromes, spinal cord concussion, spinal cord injury syndromes, SCIWORA, spinal cord injury without radiologic abnormality

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Contributor Information and Disclosures

Author

Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Abbott Point of Care Inc Research Grant and Speaker''''''''''''''''s Bureau Speaking and teaching; Bristol-Myers Squibb Inc Honoraria Speaking and teaching; Sanofi-Aventis, Inc Honoraria Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Tom Scaletta, MD, President, Emergency Excellence (EmEx) (www.emergencyexcellence.com); Assistant Professor of Emergency Medicine, Rush Medical College, Cook County Hospital; Chairperson, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine
Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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