Spinal and neurogenic shock

The axial skeleton

consists of 33 vertebrae:

• 7 Cervical
• 12 Thoracic
• 5 Lumbar
• 5 (fused) Sacrum
• 4 (fused) Coccyx

Between each of the

vertebral body is
intervertebral disc.
Except between
• C1-C2
• Sacrum-Coccyx
• Cervical spine(C1-C7) Is particulary vulnerable to injury due to its mobility
and exposure.
• Cervicothoracic junction(C7-T1) is one of the transitional zone of spinal
column where vertebral morphology changes its sustain greatest amount of
stress during motion thus most vulnerable to injury.
• Thoracolumbar junction(T11-L2) is a fulcrum between highly fixed thoracic
and relatively mobile lumbar spine thus more prone to inury
• Thoracic spine (T1-T10) is a rigid segment, its stiffness enhanced by
articulation with rib cage therefore injury less common than other region but
this also mean that the present of thoracic spine injury indicates severe
traumatic forces and higher risk for intrathoracic injury.
• Lumbar spine(L3-L5) more wider of spinal canal isolated fracture rarely injury
the cord to result in neurologic deficit unless central canal are involved.
 Spinal injury
Mode of injury
• Fall from height
• Road traffic accident
• Direct contact/penatrating injury to the back/spine
• Sports injury
Criteria of unstable spinal injury

• Increase gap between two spinous process

• Neurological deficit
• Vertebral body compression >1/3
• Vertebral body displacement >1/3
• Vertebral canal compromisation > 1/3
• Bilateral facet joints fracture dislocation
• More than one column involved (concept of Denis)
• Anterior column- anterior longitudinal ligament to anterior half of
vertebral body
• Middle column – posterior half of vertebral body , posterior longitudinal
ligament
• Posterior column – neural arch and posterior ligament complex
Spinal cord injury
Cord concussion
• Functional loss without demonstrable anatomical lesion.
• motor paralysis, sensory loss, visceral paralysis below the level of affected
segment. Recovery begins within 8 hours, patient eventually recover fully
Cord transection( complete neurologic lesion)
• Cord and its surrounding tissues are transected. The injury are anatomical and
irreparable. Present of BCR, anal reflex, plantar reflex without recovery of motor
power, sensation and autonomic functions.
• Few days or weeks later below the level of injury become spastic paralysis.
Incomplete neurologic lesion
• if sensory, motor, both functions are partially present below the level of injury.
Patient are expected to have at least some degree of recovery.
Mechanism of injury
Flexion injury
Flexion rotation injury
• highly unstable spine and neurologic damage
• Force toward one shoulder causing trunk in flexion and rotation to opposite side
or fall/blow on the postero-lateral aspect of the head.
Vertical compression injury
• Falling object on the head or fall from height in erect position
Extension injury
• Commonly seen in cervical spine
• As result of forehead striking against windscreen force the neck into
hyperextension
Flexion distraction injury
• commonly cause chance fracture
• Logroll maneuver
• Access the whole spine for spinal bony tenderness
• Step deformity
• Per rectal examination for perianal and inner thigh
sensation, anal sphincter reflex, bulbocarvenosus reflex
• Priapism- implies complete cord injury
• Neurological examinations- motor, sensory(dermatomes),
deep tendon reflex, Babinski sign
Spinal shock
• Period of complete flaccid motor paralysis recovered with
reappearance of bulbo-carvenosus reflex(BCR), anal reflex, plantar
reflex without recovery of motor power and sensation.
• Spinal shock usually involves a 24- to 72-hour period of paralysis,
hypotonia, and areflexia.
• Return of the bulbocavernosus reflex (anal sphincter contraction in
response to squeezing the glans penis or tugging on the Foley
catheter) signifies the end of spinal shock.
• Injuries at or below the thoracolumbar level (conus or cauda equina)
may permanently interrupt the bulbocavernosus reflex.
• In complete injuries, further neurologic improvement is minimal.
Phases of spinal shock (variable)

Phase 1—areflexic/hyporeflexic phase

• Typically first 24 to 48 hours
• Loss of reflexes below level of SCI
• Due to loss of basal level of excitatory
stimulation from brain to neurons involved in the reflex arc
• As a result, there is less responsiveness to stimuli and therefore
hyporeflexia or areflexia.
Phase 2—initial reflex return

• Next 1 or 2 days
• Return of some but not all reflexes below level of SCI
• First reflexes to return are polysynaptic;
bulbocavernosus is polysynaptic and typically the first reflex
to return.
• Monosynaptic reflexes such as deep tendon reflexes (DTRs)
typically do not return until phase 3.
Phase 3—initial hyperreflexia
• Next 1 to 4 weeks
• Abnormal strong reflexes
Increased expression of neurotransmitter receptors results in
increased reflex response with minimal stimulation.

Phase 4—final hyperreflexia/spasticity

• Next 1 to 12 months
• In addition to hyperreflexia, this phase results in altered skeletal
muscle performance and hypertonia.
• Loss of inhibitory input to motor neuron below level of SCI
Spinal cord anatomy
Neurogenic shock (24-48 HOURS)
• A form of distributive shock occur with CNS or spinal cord injury
• Due to loss of peripheral sympathetic innervation results in generalized
vasodilatation secondary to absent of sympathetic arterial tone. This cause
blood pooling in distal circulation and hypotension.
• Most common in patients who sustain a cervical or upper thoracic spinal cord
injury
• If T1-T4 cord level are compromised, will be loss of sympathetic innervation to
the heart leaving unopposed vagal parasympathetic innervation results in
bradycardia or no reflex tachycardia.
• Patient with neurogenic shock are warm, flushing, hypotensive with relative
bradycardia. They tend to tolerate hypotension well as periphery oxygen
delivery is presumably normal. Later due to inability to redirect blood from
periphery to the core organ may cause heat loss and hypothermia.
• Neurogenic shock is the diagnosis of exclusion

• Hypotension in trauma patient can never be presumed to be

caused by neurogenic shock.

• The most common cause of hypotension in trauma patient is

haemorrhagic shock, though may coexist with neurogenic
shock thus patient should be treated as haemorrhagic shock
until specific etiologies can ne ruled out.
• General management of spine and spinal cord trauma includes restricting
spinal motion, intravenous fluids, medications and transfer.
Prehospital care
• Restrict the movement of the spine of patients before transporting them to
the ED.
• Laying the patient supine without rotating or bending the spinal column on a
firm surface with a properly sized and placed rigid cervical collar.
• Remember to maintain spinal motion restriction until injury excluded.
• Should not attempt to reduce an obvious deformity.
• A semirigid collar does not ensure complete motion restriction of the cervical
spine. Supplementation with head immobilizer and straps to the long spine
board is more effective in extrication, rapid patient movement and transfer.
Intravenous Fluids

• Overzealous fluid administration can cause pulmonary edema in

patients with neurogenic shock. If the patient’s fluid status is
uncertain, ultrasound estimation of volume status or invasive
monitoring may be helpful.
• Insert urinary catheter to monitor urinary output.
• If the patient’s blood pressure does not improve after a fluid
challenge, can consider inotrope support, dopamine or
norepinephrine is recommended.
• Atropine and vasopressor if hypotension remain refractory.
Medication
• Administration of high dose steroid remain controversial
treatment in acute blunt spinal cord injury and should not be
given routinely.

Urgent orthopaedic and/ or neurosurgical consult

Incomplete cord lesions

• Central cord lesion (most commonest)

• Anterior cord lesion
• Posterior cord lesion
• Brown sequard syndrome
Central cord syndrome : Commonest type
• Both white & gray matter of the cord are affected
• Preservation of bladder control & perianal sensation(sacral sparing)

• Characterized by a disproportionately greater loss of motor strength in the

upper extremities than in the lower extremities, with varying degrees of
sensory loss.

Anterior cord syndrome

• Results from injury to the motor and sensory pathways in the anterior part of
the cord.
• It is characterized by paraplegia and a bilateral loss of pain and temperature
sensation. However, sensation from the intact dorsal column is preserved.
Posterior cord syndrome
• Only vibration, proprioception and position sense are lost

Brown-Sequard syndrome
• Results from hemisection of the cord, usually due to a penetrating trauma.
• Consists of ipsilateral motor loss(corticospinal tract) and loss of position
sense (dorsal column), associated with contralateral loss of pain and
temperature sensation beginning one to two levels below the level of injury
(spino-thalamic tract).
Remember !!

1. Attend to life-threatening injuries first, restrict the movement of spinal

column until vertebral fractures and spinal cord injuries have been excluded.
As long as the patient’s spine is protected, a detailed neurology examination
can safely be deferred until the patient is stable.
2. Obtain images, when indicated, as soon as life threatening injuries are
managed.
3. Document the patient’s history and physical examination to establish a
baseline.
4. Obtain early consultation with a neurosurgeon and/or orthopedic surgeon
whenever a spinal injury is suspected or detected.
5. The most common cause of hypotension in trauma patient is haemorrhagic
shock.
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