• Annually 15,000 permanent spinal cord injuries
• Commonly men 16–30 years old
• Mechanism of Injury
Vehicle crashes: 48%
Penetrating trauma: 15%
Sports injury: 14%
• 25% of all spinal cord injuries occur from improper handling of the spine
and patient after injury.
– ASSUME based upon MOI that patients have a spinal injury.
– MANAGE ALL spinal injuries with immediate and continued care.
• Best form of care is public safety and prevention programs.
• Skeletal support structure
• Major portion of axial skeleton
• Protective container for spinal cord
• Vertebral Body
• Major weight-bearing component
• Anterior to other vertebrae components
• The lumbar and low thoracic vertebrae are larger and
• The spinous processes are more horizontal.
• Thoracolumber junction is more susceptible to injury
because there is a fulcrum of increased motion.
• Cauda equina begins at L1-L2. Lesions below L1 have a
better prognosis as nerve roots , not cord are affected.
• Dura mater
• Pia mater
• Cover entire spinal cord and peripheral nerve roots
• CSF fills the subarachnoid space
• Exchange of nutrients and waste products
• Absorbs shocks of sudden movement
Transmits sensory input from body to the brain
Conducts motor impulses from brain to muscles and organs
• Intercepts sensory signals and initiates a reflex signal
• Entire cord fills entire spinal foramen
– The lower tip of the spinal cord (conus medullaris) is usually at the
level of the L1 vertebra.
– Spinal nerves below this level comprise the cauda equina.
Subdivision of ANS
– Parasympathetic, “Feed
• Controls rest and
• Peripheral nerve roots
from the sacral and
• Major Functions
– Slows heart rate
– Increases digestive
– Plays a role in sexual
– Sympathetic, “Fight or
• Increases metabolic rate
• Branches from nerves in the
thoracic and lumbar regions
• Major Functions
– Decreases organ and
digestive system activity
– Release of epinephrine and
» Reduces venous blood
» Increases peripheral
– Increases heart rate
– Increases cardiac output
Upper Motor Neurons
Originate in cerebral cortex
Result in skeletal muscle
• Injury = SPASTIC paralysis
• Lower Motor Neurons
• Originate at each vertebral
• Project to specific parts of the
• Result in movement
• Injury = FLACCID paralysis
– 31 pairs of nerves that originate
along the spinal cord from anterior
and posterior nerve roots
Sensory & motor functions
Travel through intervertebral
Each pair has 2 dorsal and 2 ventral
Ventral roots: motor impulses from
– Topographical region of
the body surface
innervated by one nerve
Key locations are :-
Mechanisms of Spinal Injury
– Extremes of Motion
• Common in the neck
• Anterior ligaments and disc may be damaged.
• If posterior ligament is intact , wedging of vertebral body occurs.If torn , may
• Causes burst fractures. Bony fragments may be pushed into spinal canal.
Flexion with rotation:
• Causes dislocation with or without fracture.
Flexion with posterior distraction:
• May disrupt middle and posterior column
The 3-column concept of the spine as defined by Denis is widely used as the
conceptual framework for diagnosing acute overt spinal instability.
The anterior column consists of the anterior vertebral body (usually anterior twothirds), the anterior annulus, and the anterior longitudinal ligament.
The middle column refers to the posterior wall of the vertebral body, the posterior
annulus, and the posterior longitudinal ligament.
The posterior column refers to the posterior ligamentous complex that connects
adjacent neural arches, consisting of facet capsules, ligamentum flavum,
interspinous ligament, and supraspinous ligament.
Failure of two or more columns generally results in instability.
• Stable Injuries
• Vertebral components won’t be displaced by normal movement.
• An undamaged spinal cord is not in danger.
• There is no development of incapacitating deformity or pain.
• Unstable Injuries
Further displacement of the injury may occur.
Loss of 50% of vertebral height.
Angulation of thoracolumbar junction of > 20 degrees.
Failure of at least 2 of Denis’s 3 columns.
Compression fracture of three sequential vertebrae can lead to post
• In this context, a simple compression wedge fracture occurs due to failure
of the anterior column with preservation of the middle column (stable).
• On the other hand, a burst fracture occurs due to compression failure of
both anterior and middle columns (usually unstable), often resulting in
bone retropulsion into spinal canal.
• A seat-belt type injury is attributed to distraction failure of the posterior
and middle columns with hinging of an intact anterior column (unstable).
Fracture-dislocations involve failure of all 3 columns and are considered
Spinal Cord Injury
• Similar to cerebral concussion
• Temporary and transient disruption of cord function
• Bruising of the cord
• Tissue damage, vascular leakage, and swelling
• Secondary to:
Displacement of the vertebrae
Herniation of intervertebral disk
Displacement of vertebral bone fragment
Swelling from adjacent tissue
– Bony fragments driven into the vertebral foramen
– Cord may be stretched to the point of tearing
• Associated with contusion, laceration, or stretching
Symptoms and Signs
Above the injury
Below the injury
absent or markedly diminished.
Specific manifestations depend on the exact level and whether cord injury
is complete or incomplete.
• Vertebral injury typically is painful, but patients who are distracted by
other painful injuries (eg, long bone fractures) or whose level of
consciousness is altered by intoxicants or head injury may not complain of
Location of Injury
At or above C5
Respiratory paralysis and quadriplegia
Paralysis of legs, wrists, and hands; weakened
shoulder abduction and elbow flexion; loss of
Paralysis of legs, wrists, and hands, but
shoulder movement and elbow flexion usually
possible; loss of biceps jerk reflex
Paralysis of legs and hands
With transverse lesions, Horner's syndrome
(ptosis, miotic pupils, facial anhidrosis),
paralysis of legs
Paralysis of leg muscles above and below the
At T12 to L1
Paralysis below the knee
Hyporeflexic or areflexic paresis of the lower
extremities, usually pain and hyperesthesia in
the distribution of the nerve roots, and usually
loss of bowel and bladder control
At S3 to S5 or
medullaris at L1
Complete loss of bowel and bladder control
Conus Medullaris Syndrome
Cauda Equina Syndrome
Presentatio Sudden and bilateral
Gradual and unilateral
Knee jerks preserved but ankle jerks affected
Both ankle and knee jerks affected
Numbness tends to be more localized to perianal area; Numbness tends to be more localized to saddle area;
symmetrical and bilateral; sensory dissociation occurs asymmetrical, may be unilateral; no sensory
dissociation; loss of sensation in specific dermatomes
in lower extremities with numbness and paresthesia;
possible numbness in pubic area, including glans penis
Typically symmetric, hyperreflexic distal paresis of
lower limbs that is less marked; fasciculations may be
Asymmetric areflexic paraplegia that is more marked;
fasciculations rare; atrophy more common
Less frequent; erectile dysfunction that includes
inability to have erection, inability to maintain
erection, lack of sensation in pubic area (including
glans penis or clitoris), and inability to ejaculate
Urinary retention and atonic anal sphincter cause
dysfunction overflow urinary incontinence and fecal incontinence;
Urinary retention; tends to present late in course of
Complete cord injury
Transection leads to immediate, complete, flaccid paralysis (including loss of anal sphincter
tone), loss of all sensation and reflex activity, and autonomic dysfunction below the level of
High cervical injury (at or above C5) , causing
Respiratory insufficiency especially in patients with injuries at or above C3.
Bradycardia and hypotension (neurogenic shock) .
Arrhythmias and BP instability may develop.
Flaccid paralysis gradually changes over hours or days to spastic paralysis with increased
deep tendon reflexes due to loss of descending inhibition.
Later, if the lumbosacral cord is intact, flexor muscle spasms appear and autonomic reflexes
Incomplete cord injury:
• Partial motor and sensory loss occurs, and deep tendon reflexes may be exuberant.
• Rapid swelling of the cord results in total neurologic dysfunction resembling
complete cord injury (spinal shock )
– Anterior Cord Syndrome
• Flexion Compression.
• Loss of motor function and
sensation of pain, light touch, and
temperature below injury site
• Retain positional, and vibration
• Poor prognosis
– Central Cord Syndrome(age > 50)
• Hyperextension injuries.
• Motor and sensory loss affecting
upper extremities more.
• Fair prognosis
– Brown-Sequard’s Syndrome
Penetrating injury that affects one side of the cord
Ipsilateral motor loss vibration and position sense.
Contralateral pain and temperature sensation loss
• Posterior Cord Syndrome
Least frequent syndrome
Injury to the posterior (dorsal) columns
Loss of proprioception
Pain, temperature, sensation and motor function below the level of the
lesion remain intact
Temporary insult to the cord
Affects body below the level of injury
Decr. Pain sensation
Decr. BP + Decr. Pluse rate = neurogenic
Decr. Body temp.
Return of bulbocavernosus reflex = end of spinal shock
• Neurogenic Shock
– Signs and Symptoms
Cool, moist, and pale skin above the injury
Warm, dry, and flushed skin below the injury
• Autonomic Hyperreflexia Syndrome
– Associated with the body’s response of the effects of spinal
– Commonly associated with injuries at or above T-6
Sweating and flushing of skin above the point of injury
Spinal Injury Impairment Scale
American Spinal Injury Association
A = Complete
No motor or sensory function, including in the sacral
B = Incomplete
Sensory but not motor function is preserved below the
neurologic level and includes the sacral segments
C = Incomplete
Motor function is preserved below the neurologic level,
and > ⁄2 of key muscles below neurologic level have
a muscle grade < 3
D = Incomplete
Motor function is preserved below the neurologic level,
and at least ⁄2 of key muscles below the neurologic
level have a muscle grade > 3
E = Normal
Motor and sensory function are normal
Management of the
Spinal Injury Patient
Preserve neurological function.
Relieve reversible nerve or cord compression.
Stabilize the spine.
Rehabilitate the the patient.
DO NO HARM
An important goal is to prevent secondary injury to the spine or spinal
• An important goal is to prevent secondary injury to the
spine or spinal cord. In unstable injuries, flexion or extension of
the spine can contuse or transect the cord.
Which can result in paraplegia, quadriplegia, or even death from
Immobilize spine immediately.
A rigid collar should be used to immobilize the cervical spine.
Patients with thoracic or lumbar spine injuries should be shifted by
logroll technique on a flat ,firm padded back board in supine
Transfer to a trauma center Immediately.
Pre hospital medical care should be directed at avoiding hypoxia
and hypotension, both of which can further stress the injured cord.
Emergency department management
Intubation if needed.
Spinal s stabilization.
History – major accident , unconscious pt, fall from height , jerk to neck , head injury , facial injury.
Logroll – look for bruising , palpate for step and tenderness.
Look for associated injuries, such as brain, thoracic, or abdominal injuries.
Imaging; x-rays , CT , MRI.
repeated neurologic examination helps determine the presence of deficits its progression /resolution.
Hypotension and bradycardia may indicate neurogenic shock.
Maintain the systolic blood pressure at a value of at least 90 mm Hg with a heart rate of 60-100 beats
• Bradycardia may be treated by the use of atropine.
Attempt to maintain urine output at a minimum of 30 mL/h. If all of the above parameters are difficult
to maintain, consider support with inotropic agents.
These patients are also at risk for hypothermia and should be warmed to maintain a core temperature of
at least 96°F. Place a Foley catheter to help with voiding.
– Fluid Challenge
• Isotonic solution: 20 mL/kg
– 250 mL initially
– Monitor response and repeat as needed
• 2–20 mcg/kg/min titrated to blood pressure
• 0.5–1.0 mg q 3–5 min (maximum of 2.0 mg)
– Steroids (Methylprednisolone)
• Reduce swelling and pressure on cord
• Begin steroid therapy within 8 hours of the injury.
• The initial dose of methylprednisolone is 30 mg/kg administered over
• Start an infusion for the maintenance dose of 5.4 mg/kg/h at the
beginning of the first hour and continue it through the 23rd hour.
With no neurological deficit:
• If stable-pain relief , collar or brace.
• If unstable-reduce and hold secure until bone / ligaments heal with
surgery or traction.
With complete sensory or motor loss:
• Usually an unstable injury
• Only consider conservative management for high thoracic injuries.
• Early operative stabilization to help with nursing , prevent spinal
deformity and pain.
• Speeds up rehab.
With incomplete neurological loss:
• Stable injury-conservative bed rest , brace.
• Unstable injury-early reduction and stabilization.
The goals of operative treatment are to decompress the spinal cord canal and to stabilize the
disrupted vertebral column.
Three basic approaches are used for surgical management of the thoracolumbar spine:
(1) the posterior approach, (2) the posterolateral approach, and (3) the anterior approach.
Selection of the best approach is guided by the anatomy of the fracture and the location of
spinal canal encroachment.
Also consider the need for stabilization procedures.
Categories of procedures for spine stabilization
The 4 basic types of stabilization procedures are
(1) posterior lumbar interspinous fusion,
(2) posterior rods,
(3) cage, and
(4) the Z-plate anterior thoracolumbar plating system. Each has different advantages and
Highest morbidity in first 2 weeks
Most common cause of morbidity and motility are: