Spinal Cord Injury
Also known as: Traumatic spinal cord injury (TSCI, SCI); Metastatic Spinal Cord Compression
Related conditions: Myelopathy
1. Description of the problem
Acute spinal cord injury is defined as any insult to the spinal cord that causes temporary or permanent damage. The injury can result in motor, sensory or autonomic dysfunction. The injuries can be divided into complete or incomplete syndromes based on the extent of the injury, and also can be described based on the level of the injury (cervical, thoracic, or lumbar).
Acute spinal cord injury often results in significant disability that causes huge personal, social, and economic burdens on the patient, family and society.
Incomplete SCI is seen when partial preservation of sensory or motor function is found below the level of the injured spinal cord tissue. Complete SCI is seen when there is no motor or sensory function below the injury, even in the lowest sacral segment.
Several clinical patterns can be seen in SCI depending on the location of the injury:
Cauda equina lesion (actually a lesion below the spinal cord; i.e. not technically a spinal cord injury, but instead a neural injury within the spinal column): causes flaccid, areflexic paralysis, and sensory loss in the area supplied by affected roots, with paralysis of the bladder and rectum.
Brown-Sequard syndrome: an injury resulting in actual or functional hemisection of the spinal cord, usually resulting from blunt or penetrating trauma. Patients have an ipsilateral paresis, ipsilateral corticospinal signs (hypo- then later hyper-reflexia; flaccidity progressing to spasticity), contralateral loss of pain and temperature sensation, and ipsilateral loss of vibration and joint position sensation.
Central cord syndrome: common spinal cord injury usually resulting from hyperextension injury to the cervical spine; causes weakness more marked in the arms than the legs, with urinary retention and sensory loss below the level of the lesion.
Anterior cord syndrome: motor paralysis associated with loss of light touch and pinprick response below the level of injury. This is usually the result of injury to the anterior spinal artery (such as infarction occurring after aortic dissection or aortic surgery).
Posterior cord syndrome: rare syndrome that can result in pain and paresthesias in the neck, upper arms, and trunk. There is loss of vibratory and proprioceptive sensation below the lesion.
Spinal sord “concussion”: transient neurologic symptoms caused by traumatic SCI with recovery in minutes or hours (<72 h)
Spinal shock can occur after acute injury of the spinal cord, whether complete or incomplete. There is paralysis and anesthesia below the lesion, with hypotonia and areflexia, and autonomic disturbances such as hypotension and bradycardia, which can be life-threatening.
2. Emergency Management
In the patient who presents with acute spinal cord injury, spinal immobilization and airway/breathing/circulatory support are the initial concerns. Associated injuries to the head, torso, abdomen, and extremities are common in this population. Patient with high cervical injuries usually require intubation and respiratory support. Hypotension is treated with fluid resuscitation and vasopressor support. Maintenance of cord perfusion, usually MAP >85 mmHg, is recommended. Severe anemia should be treated.
Obviously, while spinal shock may be the cause for hypotension, other causes for hypotension such as ongoing hemorrhage or sepsis must be considered. Bradycardia can be treated with atropine, chronotropes, or even external pacing.
A neurologic and radiographic assessment is performed. Unstable fractures require urgent or emergent surgical stabilization. A neurosurgical or orthopedic spine surgeon should be consulted immediately. Temporary stabilization with placement of a halo external fixator may be necessary.
Bladder catheterization is necessary to avoid overdistention.
Unfortunately, no acute therapies are available to reverse the neural injury beyond mechanical decompression of the spinal cord. Many physicians continue to use acute high-dose methylprednisolone therapy, but the practice is a subject of debate.
The awake non-intoxicated patient without distracting injuries can be evaluated according to NEXUS (National Emergency X-radiography Utilization Study) or Canadian C-Spine criteria.
More commonly seen in the ICU is the intoxicated, obtunded, or multiply injured patient. The EAST Guidelines can be used to guide evaluation of the cervical spine in the obtunded patient. The patient is placed on a spine board with head/neck/spine immobilization by the emergency medical providers or the emergency room staff. A hard cervical collar is placed. Clinical neurologic assessment will allow determination of the patient’s neurologic function and level of injury. This is accomplished by testing strength in the arms and legs, sensation, deep tendon reflexes, and rectal tone.
It is essential to obtain accurate and complete imaging of the spinal column soon after the injury. Plain films are usually obtained at the bedside. A three-view evaluation of the cervical spine including anteroposterior, lateral, and open mouth odontoid views are typically obtained. CT imaging is obtained in addition to the plain films. CT provides excellent bone imaging and provides information about the degree of neural compression and/or spinal canal compromise.
MRI of the spine is superior in visualizing soft tissues (including the spinal cord), ligaments, intervertebral disks, and epidural masses. MRI may be obtained in the acute setting as well depending on the type of injury and assessment of the consulting spine surgeon. MRI is a very good test to evaluate the level and extent of the injury and can be used to clear the cervical spine in the unconscious or uncooperative patient if obtained early (within 72 hours of injury).
4. Specific Treatment
After the patient is stabilized and the diagnosis of acute spinal cord injury has been made with clinical examination and appropriate imaging, most patients require an intensive care or trauma unit for management of autonomic dysfunction such as hypotension and bradycardia, ventilatory support, and high-level nursing care to avoid secondary complications. The literature suggests that outcomes are better at Level 1 Trauma Centers with the capabilities to treat this patient population. Timing of decompressive surgery remains uncertain, although some literature suggests that early surgery confers benefit in neurologic outcome. Surgical treatment, with closed reduction or open decompression and fixation, is important in stabilizing the spinal column, removing cord compression, and preventing any further injury to the cord from mobile bony segments of the spine. Immediate involvement of a spine surgeon is essential in managing these patients.
Maintenance of spinal cord perfusion pressure (MAP >85 mmHg with intra-arterial monitoring) is standard of care based on expert opinion to maintain tissue blood flow. Care must be taken to avoid hypovolemia. Treatment with high-dose steroids based on the NASCIS trials remains controversial as the clinical benefit, if any, appears to be small. If MPS is given, it should be started within 3 hours of the spinal cord injury, but no later than 8 hours. The initial loading dose of 30 mg/kg over 15 minutes is given, followed by 5.4 mg/kg/h for either 23 hours or 47 hours. It is not recommended to use this treatment in diabetic patients or those with active infection.
Neurogenic shock refers to bradycardia, hypotension, hypothermia and vasodilation secondary to autonomic dysfunction secondary to sympathetic fibers damage. It is very rare if the level of injury is below T6. Intravenous fluid resuscitation is required, along with pressor and inotropic support with agents such as norepinephrine to provide both alpha- and beta-adrenergic stimulation.
Acute therapeutic hypothermia is experimental at this time as an acute therapy for SCI. Similarly, stem cell therapy for cord regeneration is being explored as a subacute treatment option.
Respiratory complications from loss of airway patency, atelectasis, mucous plugging, and chest wall/diaphragmatic weakness are extremely common and often necessitate tracheostomy after a period of endotracheal intubation. Venous thromboembolic disease is also a major driver of morbidity and mortality. DVT prophylaxis with subcutaneous heparin, LMWH, or systemic anticoagulation should be considered. Inferior vena cava filters can be used in those patients who cannot be safely given anticoagulant drugs.
Finally, it should be noted that spinal cord compression secondary to metastatic tumor is treated with high-dose dexamethasone, radiation therapy, and/or decompressive therapy. However, the evidence base is limited.
5. Disease monitoring, follow-up and disposition
After the acute stabilization and hospitalization, aggressive neurologic rehabilitation at a focused neuorehabilitation institute is essential to maximize the patient’s recovery.
Traumatic spinal cord injury results from a direct mechanical distortion of the tissue causing cord dysfunction. Macroscopic examination shows a swollen, reddish, soft and friable cord, along with contusion. Extradural hemorrhage, subdural hemorrhage and subarachnoid hemorrhage may be seen. Vascular changes are caused by the presence of vasoactive agents, triggered by prostaglandins and catecholamines that can lead to vasospasm and thrombosis. Cellular dysfunction, tissue edema, and inflammatory changes cause further secondary injury.
The estimated annual incidence of SCI worldwide is 15-50 cases per 1,000,000 persons, with about 12,000 new cases per year in the U.S. It is most common in young men, with 65% of those patients younger than 35 years.
The most common level of injury is cervical at C5, followed by C4 and C6; the most common caudal injury is T12.
The most common cause of SCI is motor vehicle accidents, then domestic falls and industrial accidents, followed by sports injury.
Mortality at the scene is common. Of those who survive to hospitalization, mortality at one year is 13%. Male to female ratio of 4:1. The most important two clinical prognostic factors are age and completeness of injury. Better prognosis is seen in younger patients with incomplete injury. MRI findings with maximum spinal cord compression, spinal cord hemorrhage or edema are signs of poor prognosis. The most common cause of death in these patients is pneumonia, followed by pulmonary emboli, and then sepsis.
Special considerations for nursing and allied health professionals.
It is very important for the team taking care of a patient with SCI to pay attention to prevention and early recognition of common complications. At least daily efforts at ventilator weaning in intubated patients and good chest physical therapy are very important to reduce ventilator days and to prevent pneumonia and atelectasis, which are common complications following SCI. Lower extremity sequential compression devices should be used on all patients with SCI along with early use of heparin or low-molecular-weight heparin for DVT prophylaxis if there is no contraindication. DVT prophylaxis should be continued for 12 weeks in any patient with complete SCI. On the other hand, inferior vena cava filter placement is not recommended routinely for DVT prophylaxis in this patient population. However, filter placement and even full anticoagulation are used in some patients.
Special attention should be paid to the patient’s nutritional status, bladder and bowel dysfunction, pressure ulcer prevention, and prevention of gastric stress ulcers, which are very common, especially if the patient is being treated with steroids. Adequate pain control and attention to mood/depression are essential components of the acute and chronic care of this patient population. Early physical therapy and rehabilitation are essential once the patient is stable. Referral to a dedicated neurorehabilitation center should be considered.
What's the evidence?
McDonald, JW, Sadowsky, C. “Spinal-cord injury”. Lancet. vol. 359. 2002. pp. 417-25.
Bracken, MB. “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. vol. 277. 1997 May 28. pp. 1597-604.
Waters, RL. “Motor and sensory recovery following incomplete tetraplegia”. Arch Phys Med Rehabil. vol. 75. 1994 Mar. pp. 306-11.
Waring, WP. “2009 review and revisions of the international standards for the neurological classification of spinal cord injury”. J Spinal Cord Med. vol. 33. 2010. pp. 346-52.
DeVivo, MJ. “Recent trends in mortality and causes of death among persons with spinal cord injury”. Arch Phys Med Rehabi. vol. 80. 1999. pp. 1411-9.
Furlan, JC, Fehlings, MG. “Cardiovascular complications after acute spinal cord injury: pathophysiology, diagnosis, and management”. Neurosurg Focus. vol. 25. 2008.
Zwimpfer, TJ, Bernstein, M. “Spinal cord concussion”. J Neurosurg. vol. 72. 1990. pp. 894-900.
Hoffman, J. “Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma”. N Engl J Med. vol. 343. 2000. pp. 94-99.
Marion, DW. “EAST practice management guidelines for identifying cervical spine injuries following trauma, 2000 update”.
Muchow, RD. “Magnetic resonance imaging in the clearance of the cervical spine in blunt trauma: a meta-analysis”. J Trauma. vol. 64. 2008. pp. 179-89.
Hurlbert, RJ, Hamilton, MG. “Methylprednisolone for acute spinal cord injury: 5-year practice reversal”. Can J Neurol Sci. vol. 35. 2008. pp. 41-5.
Cortez, R, Levi, AD. “Acute spinal cord injury”. Current Treatment Options in Neurology. vol. 9. 2007. pp. 115-25.
Jia, X. “Critical care of traumatic spinal cord injury”. J Intensive Care Med. 2011 Apr 11.
Short, DJ, El Masry, WS, Jones, PW. “High-dose methylprednisolone in the management of acute spinal cord injury: a systematic review from a clinical perspective”. Spinal Cord. vol. 38. 2000. pp. 273-86.
Sayer, FT. “Methylprednisolone treatment in acute spinal cord injury: the myth challenged through a structured analysis of published literature”. Spine J. vol. 6. 2006 May-Jun. pp. 335-43.
George, R. “Interventions for the treatment of metastatic extradural spinal cord compression in adults”. Cochrane Database Syst Rev. 2008 Oct 8.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.