Spinal Cord Injuries Emedicine

8/2/2019 Spinal Cord Injuries Emedicine

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Spinal Cord Injuries Medication

Author: Donald Schreiber, MD, CM; Chief Editor: Rick Kulkarni, MDUpdated: Dec 15, 201

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-threateningconditions. Assessment of airway, breathing, and circulation (ABCs) takes precedence. A spinal

cord injury must be considered concurrently.[23, 24, 25]

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 alsoimportant in identifying the potential for spinal injury.

The axial skeleton should be examined to identify and provide initial treatment of potentiallyunstable spinal fractures from both a mechanical and a neurologic basis. The posterior cervicalspine 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 areespecially 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 ofspinal cord injury:

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

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

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 shockmay 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 signconfusion may falsely reassure the emergency physician. 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 anassessment of autonomic function be routinely used, along with American Spinal InjuryAssociation (ASIA) assessment, in the neurologic evaluation of patients with spinal cord

injury.[26]

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.
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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 findingsassociated 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 ofassociated 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 tendonreflexes, 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 isevidence 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 motorrecovery. 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 cordinjury 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 absentreflexes indicates a nerve root lesion.

ASIA has established pertinent definitions (see the following image). The neurologic level ofinjury 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.


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American Spinal Injury Association (ASIA) method for classifying spinalcord 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
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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 ofa 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 thepatient supine.

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

Motor index scoring uses the 0-5 scoring of each key muscle, with total points being 25 perextremity 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 communityambulator.

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


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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 mucocutaneousjunction. 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 Frankelclassification), using the following categories[2, 3] :

A = Complete: No sensory or motor function is preserved in sacral segments S4-S5 [27] 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 keymuscles below the neurologic level have muscle grade less than 3

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

E = Normal: Sensory and motor functions are normalThus, definitions of complete and incomplete spinal cord injury, as based on the above ASIAdefinition, with sacral-sparing, are as follows[2, 3, 27] :


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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 indefining the type of spinal cord injury (eg, "C8 ASIA A with zone of partial preservation of

pinprick to T2").


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Background

Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary orpermanent, 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 ofautomotive SCI is exceeded only by the cost of mental retardation."[1]

The goals for the physician, in particular emergency physicians, are to establish the diagnosis

and initiate treatment to prevent further neurologic injury from either pathologic motion of the

injured vertebrae or secondary 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 asystematic motor and sensory examination of neurologic function.

[2, 3]The following terminology

has developed around the classification of spinal cord injuries:

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

Paraplegia: Injury in the spinal cord in the thoracic, lumbar, or sacral segments, includingthe 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 is the most common level.

The following image depicts the ASIA classification by neurologic level.


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

See alsoHypercalcemia and Spinal Cord Injury,Spinal Cord Injury and Aging,Rehabilitation of

Persons With Spinal Cord Injuries,Central Cord Syndrome,Brown-Sequard Syndrome, andCauda Equina and Conus Medullaris Syndromes.

Historical information re 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 keymuscles 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 standardizedASIA method for classifying spinal cord injury (SCI) by neurologic level was developed (see theimage 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 cordextends 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 anatomically

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
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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 usuallydecussate 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, injuryto 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 incompleteloss 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 nervesexit 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 vesselresults 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 dorsalcolumns. 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 highcervical 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 alsoTopographic and Functional Anatomy of the Spinal Cord.

Pathophysiology


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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 intomore 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 spinalcord 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 peripheralvasodilation 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 consideredhemorrhagic 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, andsometimes 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


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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 occurswith 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 orabscesses cause acute cord compression and injury. Spinal cord compression frommetastatic

diseaseis 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 injurywithout 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 epiduralhematoma, 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 thanpatients with spinal cord injury and radiologic evidence of traumatic injury.[4, 5, 6]

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 orhypoxic 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 clinicalscenarios, 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, theBrown-Squard syndrome, and the central cordsyndrome.

Anterior cord syndrome involves a lesion causing variable loss of motor function and pain and/ortemperature sensation, with preservation of proprioception.
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Brown-Squard syndrome, which is often associated with a hemisection lesion of the cord,

involves a relatively greater ipsilateral loss of proprioception and motor function, withcontralateral 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 motorweakness 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 temperaturesensation 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

Theconus 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 lumbarnerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesserdegree, 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 spinalcord that fully recovers without any apparent structural damage.

Etiology

Since 2005, the most common causes of spinal cord injury (SCI) remain: (1) motor vehicleaccidents (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 apenetrating injury tended to be worse than that from a blunt injury[7] ; (4) and sports (8.0%), in

which diving is the most common cause).[8] Spinal cord injury (SCI) due to trauma has majorfunctional, medical, and financial effects on the injured person, as well as an important effect on

the individual's psychosocial well-being.[9, 10, 11]

Other causes of spinal cord injury include the following:

Vascular disorders Tumors[12]


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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/cognitivefunctioning (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 millionpopulation, or about 12,000 patients, per year based on data in the National Spinal Cord Injury

database.[8] However, this estimate is based on older data from the 1990s as there has not beenany new overall incidence studies completed.

[8]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).[8]

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 vehicleaccidents 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.[8]

Males are approximately 4 times more likely than females have spinal cord injuries, overallcomprising 80.7% of reported injuries in the national database.[8]

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.[8]

About 50% of spinal cord injuries occur between theages 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 cordinjury.

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 andcolleagues found that, with regard to the annual pediatric incidence rate a significantly greater


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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 (0.87case 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).[13]

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).

[13]

The overall incidence of pediatric SCI is 1.99 cases per 100,000 US children. As estimated fromthe 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[13]

, 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 notwearing a seatbelt.[13] 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 15years 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 yearsfollowing 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


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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 Dare 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. Individualswho 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.[14]

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 severeinjury, 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 moreelapsed 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 regainindependence.


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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 toreach 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,[15, 16]

subsequent trauma, suicide, and alcohol-relateddeaths are also major causes of death in these patients.[17, 18] 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 lifeexpectancy 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).[8] 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 withparaplegia).

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 between1973 and 2004.[19]

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.[20, 21]

Rehabilitation

Patients younger than 65 years with muscle grade of 3 or greater in the myotome L3 and S1, andlight touch sensation in the dermatome L3 and S1 within 15 days of injury (all within AmericanSpinal Injury Association [ASIA] impairment scale D), are more likely to be independent indoor

walkers within a year of injury.[22]

Rehabilitation goals in this group should therefore be geared

toward functional capacity and within expected independent walking.


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Patient Education

As part of inpatient therapy, patients with spinal cord injury (SCI) should receive acomprehensive 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 orinadequate safety precautions, are potentially preventable causes. Unfenced, shallow, or empty

swimming pools are known hazards.


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Approach Considerations

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

Arterial blood gas (ABG)measurements may be useful to evaluate adequacy ofoxygenation 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 injuryDiagnostic 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.[28, 29]

In many

centers, CT scanning has supplanted plain radiographs.

A properly performed lateral radiograph of the cervical spine that includes the C7-T1 junctioncan provide sufficient information to allow the multiple trauma victim to proceed emergently tothe 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.[23, 30, 31]

Plain RadiographyIn 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 ofinjury 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 respiratorycompromise. 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
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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 obtainadequate 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 insymptomatic trauma patients with neck pain. The NEXUS (National Emergency X-Radiography

Utilization Study) criteria and the Canadian C-spine rules were validated in large clinicaltrials.[32, 33, 34] These algorithms may be used to guide physicians to determine whether or not

imaging of the cervical spine is required.[32, 33, 34]

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 seriousconsequences if they are not detected.

Dynamic flexion/extension views are safe and effective for detecting occult ligamentous injuryof 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 inthe setting of normal findings on cervical spine radiography and CT scanning is low, so clinicaljudgment 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%.[28]

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.[28, 35]

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.


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To provide further evaluation when radiography depicts suspicious and/or indeterminateabnormalities

When radiography depicts fracture or displacement, CT scanning provides bettervisualization of the extent and displacement of the fracture

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is best for suspected spinal cord lesions, ligamentousinjuries, 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.


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Approach Considerations

Admit all patients with an acute spinal cord injury (SCI). Depending on the level of neurologicdeficit 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 ofinjury 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 areusually 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, assessmentand treatment of airway, respiration, and circulation (ABCs) takes precedence.


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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 supineposition 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 tomaintain 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 thevital 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 shockfocuses 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 distresssyndrome (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 thisrange are typical for patients with complete cord lesions. Compelling animal and humanstudies recommend maintenance of systolic BP above 90 mm Hg and to avoid any

hypotensive episodes[25, 36]

The most important treatment consideration is to maintain adequate oxygenation andperfusion of the injured spinal cord; supplemental oxygenation and/or mechanicalventilation may be required[25, 36]

Heart rate should be 60-100 beats per minute (bpm) in normal sinus rhythm


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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 bereserved 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 aresufficient

Prevent hypothermiaHead injuries and neurologic evaluation

Associated head injury occurs in about 25% of patients with spinal cord injury. A carefulneurologic 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 usedaggressively.

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 backpocket 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,[37, 38] a Cochrane Database

of Systematic Reviews article of all randomized clinical trials,[39] and other published reports,

have verified significant improvement in motor function and sensation in patients with completeor 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 spinal

cord injury (SCI). The NASCIS II study evaluated a 30-mg/kg bolus of methylprednisolone

administered within 8 hours of injury, whereas the NASCIS III study evaluatedmethylprednisolone 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.)


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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 3-8hours after injury, the use of methylprednisolone for 48 hours was best; (3) Tirilazad was

equivalent to methylprednisolone for 24 hours.[38]

Both NASCIS studies evaluated the patients' neurologic status at baseline on enrollment into thestudy, 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, betweenhours 7 and 8). The authors concluded that there was only a benefit if methylprednisolone or

tirilazad were given within 8 hours of injury.[38]

Controversy re results of NASCIS studies

Following the NASCIS trials, the use of high-dose methylprednisolone in nonpenetrating acutespinal cord injury had become the standard of care in North America. Nesathurai and Shanker

revisited these studies and questioned the validity of the results.[40]

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 andavascular necrosis has been documented.

Revised recommendations

As a result of the controversy over the NACSIS II and II studies, a number of professional

organizations have revised their recommendations pertaining to steroid therapy in spinal cordinjury.[41, 42]

The Canadian Association of Emergency Physicians (CAEP) is no longer recommending high-

dose methylprednisolone as the standard of care. The Congress of Neurological Surgeons (CNS)

has stated that steroid therapy "should only be undertaken with the knowledge that the evidencesuggesting harmful side effects is more consistent than any suggestion of clinical benefit."[43] 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 "therecommended treatment."

In a survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids inspinal cord injury, but only 24% believed that they were of any clinical benefit .[44]

Note that theinvestigators not only discovered that approximately 7% of spine surgeons do not recommend or

use steroids at all in acute spinal cord injury, but that most centers were following the NASCIS II

trial protocol.

GM-1


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Two North American studies have addressed the administration of monosialotetrahexosyl

ganglioside (GM-1) following acute spinal cord injury. The available medical evidence does notsupport a significant clinical benefit. It was evaluated as a treatment adjunct after the

administration of methylprednisolone.[36, 45]

In summary

Overall, the benefit from steroids is considered modest at best, but for patients with complete orincomplete 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 ofinjury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutesand 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 fiberopticintubation 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 necessaryexperience 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 ofconsciousness (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 bepreventive. Atropine may be required as an adjunct. Topical lidocaine spray can minimize or

prevent this reaction.


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Surgical Intervention

Orthopedic and/or neurosurgical consultants should determine the need for and timing of anysurgical intervention.

Currently, there are no defined standards existing regarding the timing of decompression andstabilization 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 injurywith progressive neurologic deterioration, facet dislocation, or bilateral locked facets.

Emergent decompression is also suggested in the setting of spinal nerve impingement withprogressive 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 in progress. The hope is that this

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 orbenefits could be made.[46]

Previous studies from the 1960s and 1970s showed that the patients experienced no improvementwith 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.[47]

Mirza et al reported that stabilization within 72 hours of injury in

cervical spinal cord injury improved neurologic outcomes.[48]

Unfortunately, both the above studies and others were not prospectively controlled orrandomized. 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.[49]

Complications

Neurologic deterioration, pressure sores, aspiration and pulmonary complications, and othercomplications 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 daysfollowing acute injury, despite optimal treatment.


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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 2segments. 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 askeys and wallets.

Try to remove the patient from the backboard as soon as possible. Some patients may requirespinal 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 thestomach 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. Pulmonarycomplications of spinal cord injury include the following:

Atelectasis secondary to decreased vital capacity and decreased functional residualcapacity

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 fatigueOther complications

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

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


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Medication Summary

The goal of pharmacotherapy is to improve motor function and sensation in patients with spinalcord 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.

View full drug information

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

Methylprednisolone is used to reduce the secondary effects of acute spinal cord injury (SCI).
http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746http://reference.medscape.com/drug/medrol-medrol-dosepak-methylprednisolone-342746

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