Spinal Cord Injuries 

Updated: Nov 01, 2018
Author: Lawrence S Chin, MD, FACS, FAANS; Chief Editor: Brian H Kopell, MD 

Overview

Practice Essentials

Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or permanent, in the cord’s normal motor, sensory, or autonomic function. Patients with SCI usually have permanent and often devastating neurologic deficits and disability. The most important aspect of clinical care for the SCI patient is preventing complications related to disability. Supportive care has shown to decrease complications related to mobility. Further, in the future our increasing fund of knowledge of the brain-computer interface might mitigate some of the disabilities associated with SCI.

Signs and symptoms

The extent of injury is defined by the American Spinal Injury Association (ASIA) Impairment Scale (modified from the Frankel classification), using the following categories:[1, 2]

  • A = Complete: No sensory or motor function is preserved in sacral segments S4-S5[3]

  • B = Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5

  • C = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade of less than 3

  • D = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade that is greater than or equal to 3

  • E = Normal: Sensory and motor functions are normal

Definitions of complete and incomplete spinal cord injury, as based on the above ASIA definition, with sacral-sparing, are as follows:[1, 2, 3]

  • Complete: Absence of sensory and motor functions in the lowest sacral segments

  • Incomplete: Preservation of sensory or motor function below the level of injury, including the lowest sacral segments

Respiratory dysfunction

Signs of respiratory dysfunction include the following:

  • Loss of ventilatory muscle function from denervation and/or associated chest wall injury

  • Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion

  • Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs

A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction, as follows:

  • With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent

  • With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective

  • With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak

  • With lower cord injuries, respiratory function improves

  • With injuries at T11, respiratory dysfunction is minimal; vital capacity is essentially normal, and cough is strong

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

The following laboratory studies can be helpful in the evaluation of spinal cord injury:

  • Arterial blood gas (ABG) measurements - May be useful to evaluate adequacy of oxygenation and ventilation

  • Lactate levels - To monitor perfusion status; can be helpful in the presence of shock

  • Hemoglobin and/or hematocrit levels - May be measured initially and monitored serially to detect or monitor sources of blood loss

  • Urinalysis - Can be performed to detect any associated genitourinary injury

Imaging studies

Imaging techniques in spinal cord injury include the following:

  • Plain radiography - Radiographs are only as good as the first and last vertebrae seen, therefore, radiographs must adequately depict all vertebrae

  • Computed tomography (CT) scanning - Reserved for delineating bony abnormalities or fracture; can be used when plain radiography is inadequate or fails to visualize segments of the axial skeleton

  • Magnetic resonance imaging (MRI) - Used for suspected spinal cord lesions, ligamentous injuries, and other soft-tissue injuries or pathology

See Workup for more detail.

Treatment

Emergency department care

  • Airway management - The cervical spine must be maintained in neutral alignment at all times; clearing of oral secretions and/or debris is essential to maintaining airway patency and preventing aspiration

  • Hypotension - Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury; a diligent search for occult sources of hemorrhage must be made

  • Neurogenic shock - Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 L is the initial treatment of choice; maintain adequate oxygenation and perfusion of the injured spinal cord; supplemental oxygenation and/or mechanical ventilation may be required[4, 5]

  • Head injuries - Amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, or a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning

  • Ileus - Placement of a nasogastric (NG) tube is essential; antiemetics should be used aggressively

  • Pressure sores - To prevent pressure sores, turn the patient every 1-2 hours, pad all extensor surfaces, undress the patient to remove belts and back pocket keys or wallets, and remove the spine board as soon as possible

Pulmonary management

Treatment of pulmonary complications and/or injury in patients with spinal cord injury includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax.

Surgical decompression

Emergent decompression of the spinal cord is suggested in the setting of acute spinal cord injury with progressive neurologic deterioration, facet dislocation, or bilateral locked facets. The procedure is also suggested in the setting of spinal nerve impingement with progressive radiculopathy, in patients with extradural lesions such as epidural hematomas or abscesses, and in the setting of the cauda equina syndrome.

See Treatment and Medication for more detail.

Background

Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or permanent, in its normal motor, sensory, or autonomic function. Patients with spinal cord injury usually have permanent and often devastating neurologic deficits and disability. According to the National Institutes of Health (NIH), "among neurological disorders, the cost to society of automotive SCI is exceeded only by the cost of mental retardation."[6]

After a suspected SCI, the goals are to establish the diagnosis and initiate treatment to prevent further neurologic injury from either mechanical instability secondary to injury from the deleterious effects of cardiovascular instability or respiratory insufficiency.

SCI terminology and classification

The International Standards for Neurological and Functional Classification of Spinal Cord Injury (ISNCSCI) is a widely accepted system describing the level and extent of injury based on a systematic motor and sensory examination of neurologic function.[1, 2] The following terminology has developed around the classification of spinal cord injuries:

  • Tetraplegia (replaces the term quadriplegia): Injury to the spinal cord in the cervical region, with associated loss of muscle strength in all 4 extremities

  • Paraplegia: Injury in the spinal cord in the thoracic, lumbar, or sacral segments, including the cauda equina and conus medullaris

The percentage of spinal cord injuries as classified by the American Spinal Injury Association (ASIA) is as follows:

  • Incomplete tetraplegia: 29.5%

  • Complete paraplegia: 27.9%

  • Incomplete paraplegia: 21.3%

  • Complete tetraplegia: 18.5%

The most common neurologic level of injury is C5. In paraplegia, T12 and L1 are the most common level. The following image depicts the ASIA classification by neurologic level.

American Spinal Injury Association (ASIA) method f American Spinal Injury Association (ASIA) method for classifying spinal cord injury (SCI) by neurologic level.

See also Hypercalcemia and Spinal Cord Injury, Spinal Cord Injury and Aging, Rehabilitation of Persons With Spinal Cord Injuries, Central Cord Syndrome, Brown-Sequard Syndrome, and Cauda Equina and Conus Medullaris Syndromes.

Historical information in SCI classification

In 1982, ASIA first published standards for neurologic classification of patients with spinal injury, followed by further refinements to definitions of neurologic levels, identification of key muscles and sensory points corresponding to specific neurologic levels, and validation of the Frankel scale. In 1992, the International Medical Society of Paraplegia (IMSOP) adopted these guidelines to create true international standards, followed by further refinements. A standardized ASIA method for classifying spinal cord injury (SCI) by neurologic level was developed (see the image above).

Anatomy

The spinal cord is divided into 31 segments, each with a pair of anterior (motor) and dorsal (sensory) spinal nerve roots. On each side, the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neuroforamina. The spinal cord extends from the base of the skull and terminates near the lower margin of the L1 vertebral body. Thereafter, the spinal canal contains the lumbar, sacral, and coccygeal spinal nerves that comprise the cauda equina. As a result, injuries below L1 are not considered spinal cord injuries (SCIs), because they involve the segmental spinal nerves and/or cauda equina. Spinal injuries proximal to L1, above the termination of the spinal cord, often involve a combination of spinal cord lesions and segmental root or spinal nerve injuries.

Neuropathways

The spinal cord itself is organized into a series of tracts or neuropathways that carry motor (descending) and sensory (ascending) information. These tracts are organized somatotopically within the spinal cord. The corticospinal tracts are descending motor pathways located anteriorly within the spinal cord. Axons extend from the cerebral cortex in the brain as far as the corresponding segment, where they form synapses with motor neurons in the anterior (ventral) horn. They decussate (cross over) in the medulla before entering the spinal cord.

The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and vibration information to the sensory cortex. They do not decussate until they reach the medulla. The lateral spinothalamic tracts transmit pain and temperature sensation. These tracts usually decussate within 3 segments of their origin as they ascend. The anterior spinothalamic tract transmits light touch. Autonomic function traverses within the anterior interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1, whereas parasympathetic system pathways exit between S2 and S4.

Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensation. Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation. Anterior cord injury causes paralysis and incomplete loss of light touch sensation.

Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous system fibers exit from the spinal cord between C7 and L1. The parasympathetic system nerves exit between S2 and S4. Therefore, progressively higher spinal cord lesions or injury causes increasing degrees of autonomic dysfunction.

Vascular supply

The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature sensation, and autonomic dysfunction. The posterior spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in the neck and descend from the base of the skull. Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow.

The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. For example, a lower cervical spine fracture may result in disruption of the vertebral artery that ascends through the affected vertebra. The resulting vascular injury may cause an ischemic high cervical cord injury. At any given level of the spinal cord, the central part is a watershed area. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome.

See also Topographic and Functional Anatomy of the Spinal Cord.

Pathophysiology

Spinal cord injury (SCI), as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the spinal cord injury.

Spinal cord injury can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage:

  • Destruction from direct trauma

  • Compression by bone fragments, hematoma, or disk material

  • Ischemia from damage or impingement on the spinal arteries

Edema could ensue subsequent to any of these types of damage.

Neurogenic shock

Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of sympathetic nervous system control in acute spinal cord injury. Hypothermia is also characteristic. This condition does not usually occur with spinal cord injury below the level of T6 but is more common in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance, with the associated vascular dilatation. Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.

Spinal shock

Shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. That is, spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions.

An initial increase in blood pressure due to the release of catecholamines, followed by hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. These symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [MSR]).

Primary vs secondary SCIs

Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary spinal cord injury. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.

Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas or abscesses cause acute cord compression and injury. Spinal cord compression from metastatic disease is a common oncologic emergency.

Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary spinal cord injury without spinal fracture or dislocation. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in spinal cord injury without radiologic abnormality (SCIWORA).

SCIWORA was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or computed tomography (CT) scanning evidence of fracture or dislocation. However with the advent of magnetic resonance imaging (MRI), the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury. SCIWORA should now be more correctly renamed as "spinal cord injury without neuroimaging abnormality" and recognize that its prognosis is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury.[7, 8, 9]

Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or hypoxic effects compound the extent of spinal cord injury.

Complete vs incomplete spinal cord syndrome

One of the goals of the physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete. In most clinical scenarios, physicians should use a best-fit model to classify the spinal cord injury syndrome.

A complete cord syndrome is characterized clinically as complete loss of motor and sensory function below the level of the traumatic lesion. Incomplete cord syndromes have variable neurologic findings with partial loss of sensory and/or motor function below the level of injury; these include the anterior cord syndrome, the Brown-Séquard syndrome, and the central cord syndrome.

Anterior cord syndrome involves a lesion causing variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception.

Brown-Séquard syndrome, which is often associated with a hemisection lesion of the cord, involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.

Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities, with sacral sensory sparing. The pattern of motor weakness shows greater distal involvement in the affected extremity than proximal muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in the upper extremities (eg, sensation of burning in the hands or arms), are common.

Other cord syndromes

The conus medullaris syndrome, cauda equina syndrome, and spinal cord concussion are briefly discussed below.

Conus medullaris syndrome is a sacral cord injury, with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs, whereas the sacral segments occasionally may show preserved reflexes (eg, bulbocavernosus and micturition reflexes). Motor and sensory loss in the lower limbs is variable.

Cauda equina syndrome involves injury to the lumbosacral nerve roots in the spinal canal and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true spinal cord injury, the affected limbs are areflexic. Cauda equina syndrome is usually caused by a central lumbar disk herniation.

A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage.

Etiology

Since 2005, the most common causes of spinal cord injury (SCI) remain: (1) motor vehicle accidents (40.4%); (2) falls (27.9%), most common in those aged 45 y or older. Older females with osteoporosis have a propensity for vertebral fractures from falls with associated SCI; (3) interpersonal violence (primarily gunshot wounds) (15.0%), which is the most common cause in some US urban settings. Among patients who had suffered an assault, spinal cord injury from a penetrating injury tended to be worse than that from a blunt injury[10] ; (4) and sports (8.0%), in which diving is the most common cause).[11] Spinal cord injury (SCI) due to trauma has major functional, medical, and financial effects on the injured person, as well as an important effect on the individual's psychosocial well-being.[12, 13, 14]

Other causes of spinal cord injury include the following:

  • Vascular disorders

  • Tumors[15]

  • Infectious conditions

  • Spondylosis

  • Iatrogenic injuries, especially after spinal injections and epidural catheter placement

  • Vertebral fractures secondary to osteoporosis

  • Developmental disorders

Injuries often associated with traumatic spinal cord injury also include bone fractures (29.3%), loss of consciousness (17.8%), and traumatic brain injury affecting emotional/cognitive functioning (11.5%).

The rate of alcohol intoxication among individuals who sustain spinal cord injuries is 17–49%.

Epidemiology

The incidence of spinal cord injury in the United States is approximately 40 cases per million population, or about 12,000 patients, per year based on data in the National Spinal Cord Injury database.[11] However, this estimate is based on older data from the 1990s as there has not been any new overall incidence studies completed.[11] Estimates from various studies suggest that the number of people in the United States alive in 2010 with spinal cord injury was about 265,000 persons (range, 232,000-316,000).[11]

Spinal cord injuries occur most frequently in July and least commonly in February. The most common day on which these injuries occur is Saturday. Spinal cord injuries also occur more frequently during daylight hours, which may be due to the increased frequency of motor vehicle accidents and of diving and other recreational sporting accidents during the day.

Racial, sexual, age-related differences in incidence

A significant trend over time has been observed in the racial distribution of persons with spinal cord injury. Since 2005, 66.5% are white, 26.8% are black, 8.3% are Hispanic, and 2.0% are Asian.[11]

Males are approximately 4 times more likely than females to have spinal cord injuries. Overall, males account for 80.7% of reported injuries in the national database.[11]

Since 2005, the average age at injury is 40.7 years, reflecting the rise in the median age of the general population in the United States.[11] About 50% of spinal cord injuries occur between the ages of 16 and 30 years, 3.5% occur in children aged 15 years or younger, and about 11.5% in those older than 60 years (11.5%). Greater mortality is reported in older patients with spinal cord injury.

Pediatric SCI data

The pediatric data parallels that of the adult data on spinal cord injuries. Using information from the Kids' Inpatient Database (KID) and the National Trauma Database (NTDB), Vitale and colleagues found that, with regard to the annual pediatric incidence rate a significantly greater incidence of spinal cord injuries was found in black children (1.53 cases per 100,000 children) than in Native American children (1.0 case per 100,000 children) and Hispanic children (0.87 case per 100,000 children), and the frequency in Asian children was significantly lower than that in all other races (0.36 per 100,000 children).[16] In addition, the likelihood that boys would suffer spinal cord injuries (2.79 cases per 100,000)was found to be more than twice that of girls (1.15 cases per 100,000).[16]

The overall incidence of pediatric SCI is 1.99 cases per 100,000 US children. As estimated from the above data, 1455 children are admitted to US hospitals annually for treatment of spinal cord injuries.

Vitale et al also looked at the major causative factors of pediatric cases, reporting the following incidences[16] , again paralleling adult data:

  • Motor vehicle accidents - 56%

  • Accidental falls - 14%

  • Firearm injuries - 9%

  • Sports injuries - 7%

Among children in the study, 67.7% of those injured in a motor vehicle accident were not wearing a seatbelt.[16] Alcohol and drugs were found to have played a role in 30% of all pediatric cases of spinal cord injuries.

Other epidemiologic data

Marital, educational, and employment status of patients with spinal cord injuries are discussed below.

Marital status

Single persons sustain spinal cord injuries more commonly than do married persons. Research has indicated that among persons with spinal cord injuries whose injury is approximately 15 years old, one third will remain single 20 years postinjury. The marriage rate after SCI is annually about 59% below that of persons in the general population of comparable gender, age, and marital status.

Marriage is more likely if the patient is a college graduate, previously divorced, paraplegic (not tetraplegic), ambulatory, living in a private residence, and independent in the performance of activities of daily living (ADL).

The divorce rate annually among individuals with spinal cord injury within the first 3 years following injury is approximately 2.5 times that of the general population, whereas the rate of marriages contracted after the injury is about 1.7 times that of the general population.

The divorce rate in those who were married at the time of their injury is higher if the patient is younger, female, black, without children, nonambulatory, and previously divorced. The divorce rate among those who were married after the spinal cord injury is higher if the individual is male, has less than a college education, has a thoracic level injury, and was previously divorced.

Educational status

The rate of injury differs according to educational status, as follows:

  • Less than a high school degree: 39.8%

  • High school degree: 49.9%

  • Associate degree: 1.6%

  • Bachelors degree: 5.9%

  • Masters or doctorate degree: 2.1%

  • Other degree: 0.7%.

Employment status

Patients with spinal cord injury classified as American Spinal Injury Association (ASIA) level D are more likely to be employed than individuals with ASIA levels A, B, and C (see Neurologic level and extent of injury under Clinical). Persons employed tend to work full-time. Individuals who return to work within 1 year of injury tend to return to the same job. Those individuals who return to work after 1 year of injury tend to work for a different employer at a different job requiring retraining.[17]

The likelihood of employment after injury is greater in patients who are younger, male, and white and who have more formal education, higher reported intelligence quotient (IQ), greater functional capacity, and less severe injury. Patients with greater functional capacity, less severe injury, history of employment at the time of injury, greater motivation to return to work, nonviolent injury, and ability to drive are more likely to return to work, especially after more elapsed time following injury.

Prognosis

Patients with a complete spinal cord injury (SCI) have a less than 5% chance of recovery. If complete paralysis persists at 72 hours after injury, recovery is essentially zero. In the early 1900s, the mortality rate 1 year after injury in patients with complete lesions approached 100%. Much of the improvement since then can be attributed to the introduction of antibiotics to treat pneumonia and urinary tract infection (UTI).

The prognosis is much better for the incomplete cord syndromes.

If some sensory function is preserved, the chance that the patient will eventually be able walk is greater than 50%.

Ultimately, 90% of patients with spinal cord injury return to their homes and regain independence.

Providing an accurate prognosis for the patient with an acute SCI usually is not possible in the emergency department (ED) and is best avoided.

Life expectancy and mortality

Approximately 10-20% of patients who have sustained a spinal cord injury do not survive to reach acute hospitalization, whereas about 3% of patients die during acute hospitalization.

Originally the leading cause of death in patients with spinal cord injury who survived their initial injury was renal failure, but, currently, the leading causes of death are pneumonia, pulmonary embolism, or septicemia. Heart disease,[18, 19] subsequent trauma, suicide, and alcohol-related deaths are also major causes of death in these patients.[20, 21] In persons with spinal cord injury, the suicide rate is higher among individuals who are younger than 25 years.

Among patients with incomplete paraplegia, the leading causes of death are cancer and suicide (1:1 ratio), whereas among persons with complete paraplegia, the leading cause of death is suicide, followed by heart disease.

Life expectancies for patients with spinal cord injury continues to increase but are still below the general population. Patients aged 20 years at the time they sustain these injuries have a life expectancy of approximately 35.7 years (patients with high tetraplegia [C1-C4]), 40 years (patients with low tetraplegia [C5-C8]), or 45.2 years (patients with paraplegia).[11] Individuals aged 60 years at the time of injury have a life expectancy of approximately 7.7 years (patients with high tetraplegia), 9.9 years (patients with low tetraplegia), and 12.8 years (patients with paraplegia).

A 2006 study by Strauss and colleagues reported that among patients with spinal cord injury, during the critical first 2 years following injury, a 40% decline in mortality occurred between 1973 and 2004.[22] During that same 31-year period, there had been only a small, statistically insignificant reduction in mortality in the post 2-year period for these patients.

Life satisfaction

Studies have found that patients with spinal cord injury who suffer from pain have less life satisfaction than do patients in whom pain is well controlled; this may also affect the patients' general outlook on life.[23, 24]

Rehabilitation

Patients younger than 65 years with muscle grade of 3 or greater in the myotome L3 and S1, and light touch sensation in the dermatome L3 and S1 within 15 days of injury (all within American Spinal Injury Association [ASIA] impairment scale D), are more likely to be independent indoor walkers within a year of injury.[25] Rehabilitation goals in this group should therefore be geared toward functional capacity and within expected independent walking.

Brain-computer interface for SCI

SCI can leave patients with severe or complete permanent paralysis. Brain-computer interface (BCI) can potentially restore or substitute for motor behaviors in patients with a high-cervical SCI.[26] Recent studies have shown that patients with SCI are able to control virtual keyboards,[27] a computer cursor,[26] and a limb prosthetic device[28] using BCI technologies. The BCI outputs are accomplished by acquiring neurophysiological signals associated with a motor process in the cerebral cortex, analyzing these signals in real time, and subsequently translating them into commands for a limb prosthesis. These are promising findings; in the future, BCI may provide a permanent solution for restoration of motor functions in SCI patients.

Walking assistance systems

In 2014, the FDA approved a wearable, motorized device to help individuals with paraplegia due to an SCI sit, stand, and walk with assistance from a companion.[29, 30]  The device, which is intended for patients with SCIs at levels T7-L5 and for those with level T4-T6 injuries when used only in rehabilitation institutions, consists of the following:

  • Fitted metal brace that supports the legs and part of the upper body
  • Motors that provide movement to the hips, knees, and ankles
  • Tilt sensor
  • Computer and power supply worn on the back

Before using the device, caregivers and patients are required to undergo extensive training.

Patient Education

As part of inpatient therapy, patients with spinal cord injury (SCI) should receive a comprehensive program of physical and occupational therapy.

Prevention

Many spinal cord injuries result from incidents involving drunk driving, assaults, and alcohol or drug abuse. Spinal cord injuries from industrial hazards, such as equipment failures or inadequate safety precautions, are potentially preventable causes. Unfenced, shallow, or empty swimming pools are known hazards.

 

Presentation

History and Physical Examination

As with all trauma patients, initial clinical evaluation of a patient with suspected spinal cord injury (SCI) begins with a primary survey. The primary survey focuses on life-threatening conditions. Assessment of airway, breathing, and circulation (ABCs) takes precedence. A spinal cord injury must be considered concurrently.[31, 32, 4]

Perform careful history taking, focusing on symptoms related to the vertebral column (most commonly pain) and any motor or sensory deficits. Ascertaining the mechanism of injury is also important in identifying the potential for spinal injury.

The axial skeleton should be examined to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. The posterior cervical spine and paraspinal tissues should be evaluated for pain, swelling, bruising, or possible malalignment. Logrolling the patient to systematically examine each spinous process of the entire axial skeleton from the occiput to the sacrum can help identify and localize injury. The skeletal level of injury is the level of the greatest vertebral damage on radiograph.

Complete bilateral loss of sensation or motor function below a certain level indicates a complete spinal cord injury.

Pulmonary evaluation

The clinical assessment of pulmonary function in acute spinal cord injury begins with careful history taking regarding respiratory symptoms and a review of underlying cardiopulmonary comorbidity such as chronic obstructive pulmonary disease (COPD) or heart failure.

Carefully evaluate respiratory rate, chest wall expansion, abdominal wall movement, cough, and chest wall and/or pulmonary injuries. Arterial blood gas (ABG) analysis and pulse oximetry are especially useful, because the bedside diagnosis of hypoxia or carbon dioxide retention may be difficult.

The degree of respiratory dysfunction is ultimately dependent on preexisting pulmonary comorbidity, the level of the spinal cord injury, and any associated chest wall or lung injury. Any or all of the following determinants of pulmonary function may be impaired in the setting of spinal cord injury:

  • Loss of ventilatory muscle function from denervation and/or associated chest wall injury

  • Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion

  • Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs

A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction, as follows:

  • With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent

  • With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective

  • With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak

  • With lower cord injuries, respiratory function improves

  • With injuries at T11, respiratory dysfunction is minimal; vital capacity is essentially normal, and cough is strong.

Other findings of respiratory disfunction include the following:

  • Agitation, anxiety, or restlessness

  • Poor chest wall expansion

  • Decreased air entry

  • Rales, rhonchi

  • Pallor, cyanosis

  • Increased heart rate

  • Paradoxic movement of the chest wall

  • Increased accessory muscle use

  • Moist cough

Hemorrhage, hypotension, and hemorrhagic and neurogenic shock

Hemorrhagic shock may be difficult to diagnose, because the clinical findings may be affected by autonomic dysfunction. Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure. In addition, occult internal injuries with associated hemorrhage may be missed.

In a study showing a high incidence of autonomic dysfunction, including orthostatic hypotension and impaired cardiovascular control, following spinal cord injury, it was recommended that an assessment of autonomic function be routinely used, along with American Spinal Injury Association (ASIA) assessment, in the neurologic evaluation of patients with spinal cord injury.[33]

In all patients with spinal cord injury and hypotension, a diligent search for sources of hemorrhage must be made before hypotension is attributed to neurogenic shock. In acute spinal cord injury, shock may be neurogenic, hemorrhagic, or both.

The following are clinical "pearls" useful in distinguishing hemorrhagic shock from neurogenic shock:

  • Neurogenic shock occurs only in the presence of acute spinal cord injury above T6; hypotension and/or shock with acute spinal cord injury at or below T6 is caused by hemorrhage

  • Hypotension with a spinal fracture alone, without any neurologic deficit or apparent spinal cord injury, is invariably due to hemorrhage

  • Patients with a spinal cord injury above T6 may not have the classic physical findings associated with hemorrhage (eg, tachycardia, peripheral vasoconstriction); this vital sign confusion attributed to autonomic dysfunction is common in spinal cord injury

  • The presence of vital sign confusion in acute spinal cord injury and a high incidence of associated injuries requires a diligent search for occult sources of hemorrhage

Cord syndromes and nerve root injury

A careful neurologic assessment, including motor function, sensory evaluation, deep tendon reflexes, and perineal evaluation, is critical and required to establish the presence or absence of spinal cord injury and to classify the lesion according to a specific cord syndrome.

The presence or absence of sacral sparing is a key prognostic indicator. Sacral-sparing is evidence of the physiologic continuity of spinal cord long tract fibers (with the sacral fibers located more at the periphery of the cord). Indication of the presence of sacral fibers is of significance in defining the completeness of the injury and the potential for some motor recovery. This finding tends to be repeated and better defined after the period of spinal shock.

Determine the level of injury and try to differentiate nerve root injury from spinal cord injury, but recognize that both may be present. Differentiating a nerve root injury from spinal cord injury can be difficult. The presence of neurologic deficits that indicate multilevel involvement suggests spinal cord injury rather than a nerve root injury. In the absence of spinal shock, motor weakness with intact reflexes indicates spinal cord injury, whereas motor weakness with absent reflexes indicates a nerve root lesion.

ASIA has established pertinent definitions (see the following image). The neurologic level of injury is the lowest (most caudal) level with normal sensory and motor function. For example, a patient with C5 quadriplegia has, by definition, abnormal motor and sensory function from C6 down.

American Spinal Injury Association (ASIA) method f American Spinal Injury Association (ASIA) method for classifying spinal cord injury (SCI) by neurologic level.

Sensory function testing

Assessment of sensory function helps to identify the different pathways for light touch, proprioception, vibration, and pain. Use a pinprick to evaluate pain sensation.

Sensory level is the most caudal dermatome with a normal score of 2/2 for pinprick and light touch.

Sensory index scoring is the total score from adding each dermatomal score with a possible total score of 112 each for pinprick and light touch.

Sensory testing is performed at the following levels:

  • C2: Occipital protuberance

  • C3: Supraclavicular fossa

  • C4: Top of the acromioclavicular joint

  • C5: Lateral side of antecubital fossa

  • C6: Thumb

  • C7: Middle finger

  • C8: Little finger

  • T1: Medial side of antecubital fossa

  • T2: Apex of axilla

  • T3: Third intercostal space

  • T4: Fourth intercostal space at nipple line

  • T5: Fifth intercostal space (midway between T4 and T6)

  • T6: Sixth intercostal space at the level of the xiphisternum

  • T7: Seventh intercostal space (midway between T6 and T8)

  • T8: Eighth intercostal space (midway between T6 and T10)

  • T9: Ninth intercostal space (midway between T8 and T10)

  • T10: 10th intercostal space or umbilicus

  • T11: 11th intercostal space (midway between T10 and T12)

  • T12: Midpoint of inguinal ligament

  • L1: Half the distance between T12 and L2

  • L2: Midanterior thigh

  • L3: Medial femoral condyle

  • L4: Medial malleolus

  • L5: Dorsum of the foot at third metatarsophalangeal joint

  • S1: Lateral heel

  • S2: Popliteal fossa in the midline

  • S3: Ischial tuberosity

  • S4-5: Perianal area (taken as 1 level)

Sensory scoring is for light touch and pinprick, as follows:

  • 0: Absent; a score of zero is given if the patient cannot differentiate between the point of a sharp pin and the dull edge

  • 1: Impaired or hyperesthesia

  • 2: Intact

Motor strength testing

Muscle strength always should be graded according to the maximum strength attained, no matter how briefly that strength is maintained during the examination. The muscles are tested with the patient supine.

Motor level is determined by the most caudal key muscles that have muscle strength of 3 or above while the segment above is normal (= 5).

Motor index scoring uses the 0-5 scoring of each key muscle, with total points being 25 per extremity and with the total possible score being 100.

Lower extremities motor score (LEMS) uses the ASIA key muscles in both lower extremities, with a total possible score of 50 (ie, maximum score of 5 for each key muscle [L2, L3, L4, L5, and S1] per extremity). A LEMS of 20 or less indicates that the patient is likely to be a limited ambulator. A LEMS of 30 or more suggests that the individual is likely to be a community ambulator.

ASIA recommends use of the following scale of findings for the assessment of motor strength in spinal cord injury:

  • 0: No contraction or movement

  • 1: Minimal movement

  • 2: Active movement, but not against gravity

  • 3: Active movement against gravity

  • 4: Active movement against resistance

  • 5: Active movement against full resistance

Neurologic level and extent of injury

Neurologic level of injury is the most caudal level at which motor and sensory levels are intact, with motor level as defined above and sensory level defined by a sensory score of 2.

Zone of partial preservation is all segments below the neurologic level of injury with preservation of motor or sensory findings. This index is used only when the injury is complete.

The key muscles that need to be tested to establish neurologic level are as follows:

  • C5: Elbow flexors (biceps, brachialis)

  • C6: Wrist extensors (extensor carpi radialis longus and brevis)

  • C7: Elbow extensors (triceps)

  • C8: Long finger flexors (flexor digitorum profundus)

  • T1: Small finger abductors (abductor digiti minimi)

  • L2: Hip flexors (iliopsoas)

  • L3: Knee extensors (quadriceps)

  • L4: Ankle dorsiflexors (tibialis anterior)

  • L5: Long toe extensors (extensor hallucis longus)

  • S1: Ankle plantar flexors (gastrocnemius, soleus)

Perform a rectal examination to check motor function or sensation at the anal mucocutaneous junction. The presence of either is considered sacral-sparing.

The sacral roots may be evaluated by documenting the following:

  • Perineal sensation to light touch and pinprick

  • Bulbocavernous reflex, S3 or S4

  • Anal wink, S5

  • Rectal tone

  • Urine retention or incontinence

  • Priapism

The extent of injury is defined by the ASIA Impairment Scale (modified from the Frankel classification), using the following categories[1, 2] :

  • A = Complete: No sensory or motor function is preserved in sacral segments S4-S5[3]

  • B = Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5

  • C = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade less than 3

  • D = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade greater than or equal to 3

  • E = Normal: Sensory and motor functions are normal

Thus, definitions of complete and incomplete spinal cord injury, as based on the above ASIA definition, with sacral-sparing, are as follows[1, 2, 3] :

  • Complete: Absence of sensory and motor functions in the lowest sacral segments

  • Incomplete: Preservation of sensory or motor function below the level of injury, including the lowest sacral segments

With the ASIA classification system, the terms paraparesis and quadriparesis have become obsolete. Instead, the ASIA classification uses the description of the neurologic level of injury in defining the type of spinal cord injury (eg, "C8 ASIA A with zone of partial preservation of pinprick to T2").

 

DDx

Diagnostic Considerations

Attributing hypotension to neurogenic shock in the setting of spinal cord injury (SCI) is a potentially devastating error. As noted under Clinical, before hypotension can be attributed to neurogenic shock, a diligent search for sources of hemorrhage must be completed. Shock may be hemorrhagic, neurogenic, or both in patients with acute spinal cord injury.

The presence of vital sign confusion in acute spinal cord injury coupled with the limitations of the physical examination can make the diagnosis of hemorrhage from associated injuries challenging.

Also consider other conditions in patients with suspected spinal cord injury, such as transverse myelitis, acute intervertebral disk herniation, and extradural spinal cord compression.

Differential Diagnoses

 

Workup

Approach Considerations

With regard to laboratory studies, the following may be helpful:

  • Arterial blood gas (ABG) measurements may be useful to evaluate adequacy of oxygenation and ventilation

  • Lactate levels to monitor perfusion status can be helpful in the presence of shock

  • Hemoglobin and/or hematocrit levels may be measured initially and monitored serially to detect or monitor sources of blood loss

  • Urinalysis can be performed to detect any associated genitourinary injury

Diagnostic imaging traditionally begins with the acquisition of standard radiographs of the affected region of the spine. Investigators have shown that computed tomography (CT) scanning is exquisitely sensitive for the detection of spinal fractures and is cost effective.[34, 35] In many centers, CT scanning has supplanted plain radiographs.

A properly performed lateral radiograph of the cervical spine that includes the C7-T1 junction can provide sufficient information to allow the multiple trauma victim to proceed emergently to the operating room if necessary without additional intervention other than maintenance of full spinal immobilization and a hard cervical collar.

Noncontiguous spinal fractures are defined as spinal fractures separated by at least 1 normal vertebra. Noncontiguous fractures are common and occur in 10-15% of patients with spinal cord injury. Therefore, once a spinal fracture is identified, the entire axial skeleton must be imaged, preferably by CT scanning, to assess for noncontiguous fractures.[31, 36, 37]

Plain Radiography

In many emergency departments (EDs), radiology support is limited. If unsure of a finding, request a formal interpretation or immobilize the patient appropriately, pending formal review of the studies.

In addition, note that the failure to adequately immobilize the spine when the mechanism of injury is consistent with the diagnosis is a pitfall.

Agitated, intoxicated patients are often the most difficult to manage properly. Pharmacologic restraint may be required to allow proper assessment. Haldol and intravenous (IV) droperidol have been used successfully, even in large doses, without hemodynamic or respiratory compromise. Occasionally, rapid-sequence intubation and pharmacologic paralysis is required to manage these patients.

Physical examination and radiographic studies could be delayed until the patient is more cooperative, if his or her overall condition permits.

Radiographic views

Radiographs are only as good as the first and last vertebrae seen, therefore, radiographs must adequately depict all vertebrae. A common cause of missed injury is the failure to obtain adequate images (eg, cervical spine radiograph that incompletely depicts the C7-T1 junction). However, be aware that radiography is insensitive to small fractures of the vertebra.

Published clinical criteria have established guidelines for cervical spine radiography in symptomatic trauma patients with neck pain. The NEXUS (National Emergency X-Radiography Utilization Study) criteria and the Canadian C-spine rules were validated in large clinical trials.[38, 39, 40] These algorithms may be used to guide physicians to determine whether or not imaging of the cervical spine is required.[38, 39, 40]

The standard 3 views of the cervical spine are recommended in patients with suspected spinal cord injury (SCI): anteroposterior (AP), lateral, and odontoid.

The cervical spine radiographs must include the C7-T1 junction to be considered adequate. Subtle findings (eg, increased prevertebral soft tissue swelling or widening of the C1-C2 preodontoid space) indicate potentially unstable cervical spine injuries that could have serious consequences if they are not detected.

Dynamic flexion/extension views are safe and effective for detecting occult ligamentous injury of the cervical spine in the absence of fracture. The negative predictive value of a normal 3-view cervical spine series and flexion/extension views exceeds 99%. The incidence of occult injury in the setting of normal findings on cervical spine radiography and CT scanning is low, so clinical judgment and the mechanism of injury should be used to guide the decision to order flexion/extension views.

Anteroposterior and lateral views of the thoracic and lumbar spine are recommended for suspected injuries to the thoracolumbar spine.

Adequate spinal radiography supplemented by computed tomography (CT) scanning through areas that are difficult to visualize or are suspicious detects the vast majority of fractures with a reported negative predictive value between 99% and 100%.[34]

Computed Tomography Scanning

Computed tomography (CT) scanning is reserved for delineating bony abnormalities or fracture. Some studies have suggested that CT scanning with sagittal and coronal reformatting is more sensitive than plain radiography for the detection of spinal fractures.[34, 41]

Perform CT scanning in the following situations:

  • When plain radiography is inadequate or fails to visualize segments of the axial skeleton

  • Convenience and speed: If a CT scan of the head is required, then it is usually simpler and faster to obtain a CT of the cervical spine at the same time. Similarly, CT images of the thoracic or lumbar spine might be easier and faster to obtain than plain radiographs.

  • To provide further evaluation when radiography depicts suspicious and/or indeterminate abnormalities

  • When radiography depicts fracture or displacement, CT scanning provides better visualization of the extent and displacement of the fracture

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is best for suspected spinal cord lesions, ligamentous injuries, or other soft-tissue injuries or pathology. This imaging modality should be used to evaluate nonosseous lesions, such as extradural spinal hematoma; abscess or tumor; disk rupture; and spinal cord hemorrhage, contusion, and/or edema.

Neurologic deterioration is usually caused by secondary injury, resulting in edema and/or hemorrhage. MRI is the best diagnostic image to depict these changes.

 

Treatment

Approach Considerations

Admit all patients with an acute spinal cord injury (SCI). Depending on the level of neurologic deficit and associated injuries, the patient may require admission to the intensive care unit (ICU), neurosurgical observation unit, or general ward.

The most common levels of injury on admission are C4, C5 (the most common), and C6, whereas the level for paraplegia is the thoracolumbar junction (T12). The most common type of injury on admission is American Spinal Injury Association (ASIA) level A (see Neurologic level and extent of injury under Clinical).

Transfer

Depending on local policy, patients with acute spinal cord injury are best treated at a regional spinal cord injury center. Therefore, once stabilized, early referral to a regional spinal cord injury center is best. The center should be organized to provide ongoing definitive care.

Other reasons to transfer the patient include the lack of appropriate diagnostic imaging (computed tomography [CT] scanning or magnetic resonance imaging [MRI]) and/or inadequate spine consultant support (orthopedist or neurosurgeon).

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 as well as other specialists may also be required.

Prehospital Management

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 emergency department (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° while the patient remains fully immobilized in a neutral position. Spinal immobilization protocols should be standard in all prehospital care systems.

Emergency Department Management

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

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.

Airway management

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, hemorrhage, and shock

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 sources of occult hemorrhage are injuries to the chest, abdomen, and retroperitoneum and fractures of the pelvis or long-bones. Appropriate investigations, including radiography or computed tomography (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.

Neurogenic shock management and treatment goals

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 L 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 (ARDS).

The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters:

  • A systolic blood pressure (BP) of 90-100 mm Hg should be achieved; systolic BPs in this range are typical for patients with complete cord lesions. Compelling animal and human studies recommend maintenance of systolic BP above 90 mm Hg and to avoid any hypotensive episodes[4, 5]

  • The most important treatment consideration is to maintain adequate oxygenation and perfusion of the injured spinal cord; supplemental oxygenation and/or mechanical ventilation may be required[4, 5]

  • Heart rate should be 60-100 beats per minute (bpm) 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 and to decompress the neurogenic bladder is essential

  • Rarely, inotropic support with dopamine or norepinephrine is required; this 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

Head injuries and neurologic evaluation

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

Ileus is common. Placement of a nasogastric (NG) tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function (see Treatment of Pulmonary Complications and Injury). Antiemetics should be used aggressively.

Pressure sores

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.

Steroid Therapy in SCI and Controversies

The National Acute Spinal Cord Injury Studies (NASCIS) II and III,[42, 43] a Cochrane Database of Systematic Reviews article of all randomized clinical trials,[44] 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.

NASCIS II and III trials

High doses of steroids or tirilazad are thought to minimize the secondary effects of acute SCI. The NASCIS II study evaluated a 30-mg/kg bolus of methylprednisolone administered within 8 hours of injury, whereas 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.)

Between the 2 studies, it was determined that: (1) in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 hours was best; (2) in patients treated 3-8 hours after injury, the use of methylprednisolone for 48 hours was best; (3) Tirilazad was equivalent to methylprednisolone for 24 hours.[43]

Both NASCIS studies evaluated the patients' neurologic status at baseline on enrollment into the study, at 6 weeks, and at 6 months and found absolutely no evidence 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 concluded that there was only a benefit if methylprednisolone or tirilazad were given within 8 hours of injury.[43]

Controversy re results of NASCIS studies

Following the NASCIS trials, the use of high-dose methylprednisolone in nonpenetrating acute SCI had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned the validity of the results.[45] These authors cited concerns about the statistical analysis, randomization, and clinical endpoints used in the study. In addition, the investigators noted that even if the benefits of steroid therapy were valid, the clinical gains were questionable. Other reports have also 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.

Revised recommendations

As a result of the controversy over the NACSIS II and III studies, a number of professional organizations have revised their recommendations pertaining to steroid therapy in SCI.[46, 47]

The Congress of Neurological Surgeons (CNS) 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."[48] The American College of Surgeons (ACS) has modified their advanced trauma life support (ACLS) guidelines to state that methylprednisolone is "a recommended treatment" rather than "the recommended treatment." The Canadian Association of Emergency Physicians (CAEP) is no longer recommending high-dose methylprednisolone as the standard of care.

In a survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids in SCI, but only 24% believed that they were of any clinical benefit.[49] Note that the investigators not only discovered that approximately 7% of spine surgeons do not recommend or use steroids at all in acute SCI, but that most centers were following the NASCIS II trial protocol.

Updated guidelines issued in 2013 by the CNS and the American Association of Neurological Surgeons (AANS) recommend against the use of steroids early after an acute SCI. The guidelines recommend that methylprednisolone not be used for the treatment of acute SCI within the first 24-48 hours following injury. The previous standard was revised because of a lack of medical evidence supporting the benefits of steroids in clinical settings and evidence that high-dose steroids are associated with harmful adverse effects.[50, 51]

GM-1

Two North American studies have addressed the administration of monosialotetrahexosyl ganglioside (GM-1) 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.[5, 52]

Summary

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 spinal cord injury is practiced by most physicians.

The current recommendation is to treat all patients with spinal cord injury 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.

Treatment of Pulmonary Complications and 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 spinal cord injury 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 spinal cord injury are acute respiratory failure, decreased level of consciousness (Glasgow score < 9), increased respiratory rate with hypoxia, partial pressure of carbon dioxide (PCO2) greater than 50 mm Hg, 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.

Surgical Intervention

Spine service consultants should determine the need for and timing of any surgical intervention. Currently, there are no defined standards existing regarding the timing of decompression and stabilization in spinal cord injury. The role of immediate surgical intervention is limited. Emergent decompression of the spinal cord is suggested in the setting of acute spinal cord injury with progressive neurologic deterioration, facet dislocation, or bilateral locked facets. Emergent decompression is also suggested in the setting of spinal nerve impingement with progressive radiculopathy and in those select patients with extradural lesions such as epidural hematomas or abscesses or in the setting of the cauda equina syndrome.

A prospective surgical trial, the Surgical Treatment for Acute Spinal Cord Injury Study (STASCIS) conducted by the Spine Trauma Study Group, is ongoing. Preliminary data from this study are showing that 24% of patients who receive decompressive surgery within 24 hours of their injury experience a 2-grade or better improvement on the ASIA scale, compared with 4% of those in the delayed-treatment group. Furthermore, the study found that cardiopulmonary and urinary tract complications were found to be 37% in the early surgery group compared with the delayed group rate of 48.6%. The hope is that the final data from STASCIS will better define the benefits and timing of early surgical decompression and stabilization.

A review article of spinal fixation surgery for acute traumatic spinal cord injury concluded that, in the absence of any randomized controlled studies, no recommendations regarding risks or benefits could be made.[53]

Previous studies from the 1960s and 1970s showed that the patients experienced no improvement with emergent surgical decompression, although 2 studies in the late 1990s appeared to show improved neurologic outcomes with early stabilization. Gaebler et al reported that early decompression and stabilization procedures within 8 hours of injury allowed for a higher rate of neurologic recovery.[54] Mirza et al reported that stabilization within 72 hours of injury in cervical spinal cord injury improved neurologic outcomes.[55]

Unfortunately, both the above studies and others were not prospectively controlled or randomized. In the only prospective, randomized, controlled study to determine whether functional outcome is improved in patients with cervical spinal cord injury, Vaccaro et al reported no significant difference between early (< 3 d, mean 1.8 d) or late (>5 d, mean 16.8 d) surgery.[56]

Complications

Neurologic deterioration, pressure sores, aspiration and pulmonary complications, and other complications following spinal cord injury (SCI) are briefly discussed in this section.

Neurologic deterioration

The neurologic deficit of spinal cord injury (SCI) often increases during the hours to days following acute injury, despite optimal treatment.

One of the first signs of neurologic deterioration is the extension of the sensory deficit cephalad. Careful repeat neurologic examination may reveal that the sensory level has risen 1 or 2 segments. Repeat neurologic examinations to check for progression are essential.

Pressure sores

Careful and frequent turning of the patient is required to prevent pressure sores. Denervated skin is particularly prone to this complication. Remove belts and objects from back pockets, such as keys and wallets.

Try to remove the patient from the backboard as soon as possible. Some patients may require spinal immobilization in a halo vest or a Stryker frame. Many patients with acute spinal cord injury have stable vertebral fractures yet needlessly spend hours on a hard backboard.

Aspiration and pulmonary complications

Patients with spinal cord injury are at high risk for aspiration. Nasogastric decompression of the stomach is mandatory.

Pulmonary complications in spinal cord injury are common. Such complications are directly correlated with mortality, and both are related to the level of neurologic injury. Pulmonary complications of spinal cord injury include the following:

  • Atelectasis secondary to decreased vital capacity and decreased functional residual capacity

  • Ventilation-perfusion (V/Q) mismatch due to sympathectomy and/or adrenergic blockade

  • Increased work of breathing because of decreased compliance

  • Decreased coughing, which increases the risk of retained secretions, atelectasis, and pneumonia

  • Muscle fatigue

Other complications

Severe sepsis or pneumonia frequently follows treatment with high-dose methylprednisolone that is frequently used in spinal cord injury.

Prevent hypothermia by using external rewarming techniques and/or warm humidified oxygen.

 

Guidelines

Guidelines Summary

Guidelines related to spinal cord injuries treatments are focused on avoidance of secondary injury from compressive lesions and hemodynamic instability.

American Association of Neurological Surgeons/Congress of Neurological Surgeons

The 2013 update of the AANS/CNS Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injury include the following recommendations.[57, 58]

Immobilization

Immobilization of trauma patients who are awake, alert, and are not intoxicated; who are without neck pain or tenderness; who do not have an abnormal motor or sensory examination; and who do not have any significant associated injury that might detract from their general evaluation is not recommended.

A combination of a rigid cervical collar and supportive blocks on a backboard with straps is effective in limiting motion of the cervical spine and is recommended.

The longstanding practice of attempted spinal immobilization with sandbags and tape is insufficient and is not recommended.

Spinal immobilization in patients with penetrating trauma is not recommended.

Radiographic assessment

In the awake, asymptomatic patient who is without neck pain or tenderness, who has a normal neurological examination, is without an injury detracting from an accurate evaluation, and who is able to complete a functional range of motion examination; radiographic evaluation of the cervical spine is not recommended.

In the awake, symptomatic patient, high-quality computed tomography (CT) imaging of the cervical spine is recommended.

In the obtunded or unevaluable patient, high-quality CT imaging is recommended as the initial imaging modality of choice. 

Pharmacological therapy

Administration of methylprednisolone (MP) for the treatment of acute spinal cord injury (SCI) is not recommended. Clinicians considering MP therapy should bear in mind that the drug is not Food and Drug Administration (FDA) approved for this application. 

Administration of GM-1 ganglioside (Sygen) for the treatment of acute SCI is not recommended.

 

Medication

Medication Summary

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

Glucocorticoids

Class Summary

Glucocorticoids are high-dose steroids, which 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 hours of injury.

Methylprednisolone (Solu-Medrol, A-Methapred, Depo-Medrol, Medrol)

Methylprednisolone is used to reduce the secondary effects of acute spinal cord injury (SCI).

Analgesics, Other

Class Summary

Various drugs are used for neuropathic pain. GABA analogs have been shown to be effective in treating neuropathic pain in spinal cord injuries. In June 2012, the FDA approved the use of pregabalin for the management of neuropathic pain associated with spinal cord injury. Approval was based on results of 2 randomized, double-blind phase 3 trials comparing flexibly dosed pregabalin (150-600 mg/d) with placebo in 357 patients. Studies showed pregabalin significantly reduced neuropathic pain between baseline and at 12 and 16 weeks in each study, respectively, compared with placebo. More patients taking pregabalin showed 30% and 50% reductions in pain than those taking placebo.[59, 60]

Pregabalin (Lyrica)

Indicated for neuropathic pain associated with spinal cord injury. The precise mechanism of action is unknown but is a GABA analog which binds to a subunit of voltage-gated calcium channels in CNS. It does not affect sodium channels, opiate receptors or cyclooxygenase enzyme activity. Its interactions with descending noradrenergic and serotonergic pathways originating from the brainstem appear to reduce neuropathic pain transmission from the spinal cord.

 

Questions & Answers

Overview

What is the focus of care for spinal cord injury (SCI)?

What are the categories of the American Spinal Injury Association (ASIA) Impairment Scale of spinal cord injury (SCI)?

What are the ASIA definitions for complete and incomplete spinal cord injury (SCI)?

What are signs of respiratory dysfunction in spinal cord injury (SCI)?

How does the level of spinal cord injury (SCI) affect the degree of respiratory dysfunction?

Which lab tests are performed in the workup of spinal cord injury (SCI)?

Which imaging studies are performed in the workup of spinal cord injury (SCI)?

What is included in emergency department (ED) care for spinal cord injury (SCI)?

How are pulmonary complications managed in spinal cord injury (SCI)?

When is surgical decompression indicated in the treatment of spinal cord injury (SCI)?

What is spinal cord injury (SCI)?

What is the ISNCSCI classification of spinal cord injuries?

What is the American Spinal Injury Association (ASIA) method for classifying spinal cord injury (SCI)?

What is the anatomy relevant to spinal cord injury (SCI)?

What is the neuropathway anatomy relevant to spinal cord injury (SCI)?

What is the vascular supply anatomy relevant to spinal cord injury (SCI)?

What is the pathophysiology of spinal cord injury (SCI)?

What is the role of neurogenic shock in the pathophysiology of spinal cord injury (SCI)?

What is the role of spinal shock in the pathophysiology of spinal cord injury (SCI)?

What is the pathophysiology of primary spinal cord injury (SCI)?

What is the pathophysiology of spinal cord injury without radiologic abnormality (SCIWORA)?

What is the pathophysiology of secondary spinal cord injury (SCI)?

What is the difference between a complete and incomplete spinal cord injury (PCI)?

What are the types of incomplete spinal cord injury (SCI)?

What is the pathophysiology of conus medullaris syndrome?

What is the pathophysiology of cauda equina syndrome?

What is the pathophysiology of a spinal cord concussion?

What causes spinal cord injury (SCI)?

What is the prevalence of spinal cord injury (SCI)?

Which patient groups are at highest risk for spinal cord injury (SCI)?

What is the prevalence of pediatric spinal cord injury (SCI)?

What are the most common causes of pediatric spinal cord injury (SCI)?

How does spinal cord injury (SCI) affect marital status?

What is the prevalence of spinal cord injury (SCI) according to educational status?

What is the effect of spinal cord injury (SCI) on employment status?

What is the prognosis of spinal cord injury (SCI)?

What is the life expectancy and mortality of spinal cord injury (SCI)?

How does pain management effect spinal cord injury (SCI) prognosis?

Which patient group is most likely to be indoor walkers after spinal cord injury (SCI)?

What is the role of a brain-computer interface (BCI) in spinal cord injury (SCI) management?

What is the role of walking assistance systems in spinal cord injury (SCI) management?

What is included in the impatient therapy for spinal cord injury (SCI)?

How is spinal cord injury (SCI) prevented?

Presentation

What is included in the initial clinical evaluation of spinal cord injury (SCI)?

What is included in the clinical assessment of pulmonary function in acute spinal cord injury (SCI)?

Which determinants of pulmonary function may be impaired in spinal cord injury (SCI)?

How does the level of spinal cord injury (SCI) affect the degree of respiratory dysfunction?

Which findings of respiratory dysfunction are characteristic of spinal cord injury (SCI)?

Which physical findings are characteristic of hemorrhagic shock in spinal cord injury (SCI)?

Which physical findings are characteristic of autonomic dysfunction in spinal cord injury (SCI)?

How is hemorrhagic shock differentiated from neurogenic shock in spinal cord injury (SCI)?

How is nerve root injury differentiated from spinal cord injury (SCI)?

How is sensory function testing performed in the evaluation of spinal cord injury (SCI)?

How is a sensory function test scored in the evaluation of spinal cord injury (SCI)?

How is motor strength assessed in spinal cord injury (SCI)?

How is the neurologic level of spinal cord injury (SCI) assessed?

How are sacral roots assessed in spinal cord injury (SCI)?

How are the American Spinal Injury Association (ASIA) Impairment Scale categories defined?

DDX

Which conditions should be included in the differential diagnoses of spinal cord injury (SCI)?

What are the differential diagnoses for Spinal Cord Injuries?

Workup

What is the role of lab testing in the workup of spinal cord injury (SCI)?

What is the role of imaging studies in the diagnosis of spinal cord injury (SCI)?

What is the role of plain radiography in the workup of spinal cord injury (SCI)?

What is the role of CT scanning in the workup of spinal cord injury (SCI)?

What is the role of MRI in the workup of spinal cord injury (SCI)?

Treatment

What is the initial approach to spinal cord injury (SCI) treatment?

When is patient transfer indicated in the treatment of spinal cord injury (SCI)?

Which specialist consultations are beneficial to patients with spinal cord injury (SCI)?

What is included in prehospital care for spinal cord injury (SCI)?

How should patient be positioned for the initial evaluation of spinal cord injury (SCI)?

What is the role of airway management in the ED treatment of spinal cord injury (SCI)?

How are hypotension, hemorrhage, and shock in spinal cord injury (SCI) assessed?

How is neurogenic shock managed in the treatment of spinal cord injury (SCI)?

How are head injuries assessed in patients with spinal cord injury (SCI)?

What is the ED treatment for ileus in spinal cord injury (SCI)?

How are pressure sores prevented during the ED treatment of spinal cord injury (SCI)?

What is the role of steroid therapy in the treatment of spinal cord injury (SCI)?

What is the efficacy of high dose steroids for the initial treatment of spinal cord injury (SCI)?

What are the possible adverse effects of steroid treatment for spinal cord injury (SCI)?

What are the guidelines on steroid therapy in the treatment of spinal cord injury (SCI)?

What is the role of GM-1 in the treatment of spinal cord injury (SCI)?

How are steroids administered in the treatment of spinal cord injury (SCI)?

How are the pulmonary complications of spinal cord injury (SCI) treated?

What is the role of surgery in the treatment of spinal cord injury (SCI)?

What are the possible complications of spinal cord injury (SCI)?

What are the signs of neurologic deterioration in spinal cord injury (SCI)?

What causes pressure sores in spinal cord injury (SCI)?

What is the role of a backboard in the initial treatment of spinal cord injury (SCI)?

What are the pulmonary complications relative to spinal cord injury (SCI)?

What causes sepsis in spinal cord injury (SCI)?

How is hypothermia prevented in spinal cord injury (SCI)?

Guidelines

What is the focus of guidelines on spinal cord injury (SCI)?

What are the AANS/CNS guidelines on immobilization of acute spinal cord injury (SCI)?

What are the AANS/CNS guidelines on the initial assessment of acute spinal cord injury (SCI)?

What are the AANS/CNS guidelines on the initial treatment of acute spinal cord injury (SCI)?

Medications

What are the goals of medical treatment of spinal cord injury (SCI)?

Which medications in the drug class Analgesics, Other are used in the treatment of Spinal Cord Injuries?

Which medications in the drug class Glucocorticoids are used in the treatment of Spinal Cord Injuries?