SPINAL SHOCK 
By: Dr Ismah, Ortho department 
1
Contents 
 Definition 
 Anatomy 
 Pathophysiology 
 Phases 
 Vs. neurogenic shock 
 Management 
2
Definition 
3 
 Immediate temporary loss of total power, 
sensation and reflexes below the level of injury 
 + Loss of bulbo-cavernous reflex 
 Usually recover within 24-48 hrs 
-oxford handbook-
4 
bulbo-cavernous reflex
Anatomy 
5 
http://www.radiologyassistant.nl/ 
en/p4906c8352d8d2/spine-thoracolumbar- 
injury.html 
Dennis three 
column 
-spine stability
6 
Walter B. Greene. Netter's Orthopaedics 1st ed. 2006
Pathophysiology 
7 
TRAUMA -- > SCI 
- causes a concussion like injury to spinal cord 
- total sensory and motor power loss and loss of all reflexes for 
initial some period 
- followed by then gradual recovery of reflexes 
 Reflexes in the SC caudal to the SCI are depressed 
(areflexia) 
 This state of sensory and motor loss along with total loss of 
reflexes following trauma is known as spinal shock 
 The 'shock' in spinal shock does not refer to circulatory 
collapse
Phases 
Phase Time Physical exam 
findings 
Underlying physiological 
event 
1 0-1 days Areflexia Loss of descending 
facilitation 
2 1-3 days Initial reflex return Denervation 
supersensitivity 
3 1-4 weeks Hyperreflexia Axon-supported synapse 
growth 
4 1-12 months Hyperreflexia, 
Spasticity 
Soma-supported synapse 
growth 
http://www.nature.com/sc/journal/v42/n7/full/3101603a.html 
8
Phase 1: 
 A complete loss or weakening of all reflexes below 
the level of spinal cord injury 
 Spinal concussion caused the neurons involved in 
various reflex arcs and the neural input from the 
brain become hyperpolarized and unresponsive. 
9
Phase 2 
 Characterized by the return of some reflexes. The 
first reflexes to reappear is the bulbocavernosus 
reflex 
 The reason reflexes return is the hypersensitivity of 
reflex muscles following denervation; more 
receptors for neurotransmitters are expressed and 
are therefore they are easier to stimulate. 
10
Phases 3 and 4 
 Characterized by hyperreflexia 
 Neurons below the injury attempt to reestablish 
the synapses 
11
Spinal vs neurogenic shock 
12 
Spinal shock Neurogenic shock 
Definition Immediate temporary loss 
of total power, sensation 
and reflexes below the level 
of injury 
Sudden loss of the 
sympathetic nervous 
system signals 
BP Hypotension Hypotension 
Pulse Bradycardia Bradycardia 
Bulbocaverno 
Absent Variable 
sus reflex 
Motor Flaccid paralysis Variable 
Time 48-72 hrs immediate after SCI 
Mechanism Peripheral neurons become 
temporarily unresponsive to 
brain stimuli 
Disruption of autonomic 
pathways  loss of 
sympathetic tone and 
vasodilation 
http://www.orthobullets.com/spine/2006/spinal-cord-injuries
13 
MANAGEMENT 
Immobilisation 
-Spinal board 
-Cervical collar 
1) Monitor 
neurological status 
2) Cord/cauda-equina 
Sx 
Methylprednisolone 
-given as bolus of 30 mg 
/ kg body wt 
-followed by infusion at 
5.4 mg / kg / hour for 24 
hours 
Symtomatic 
medication: 
-Pain relief 
-Constipation 
DVT prophylaxis
The National Spinal Cord Injury Study 
(NASCIS) 
14 
 NASCIS 3 USA, 1997 
 High dose methylprednisolone 
 Prevent secondary injury of SCI 
 Rx start within 3 hrs for 24 hrs 
 Side effects: immunosuppression, GIT bleeding, 
hyperglycemia and ARDS
15
16 Thank you

Spinal shock

  • 1.
    SPINAL SHOCK By:Dr Ismah, Ortho department 1
  • 2.
    Contents  Definition  Anatomy  Pathophysiology  Phases  Vs. neurogenic shock  Management 2
  • 3.
    Definition 3 Immediate temporary loss of total power, sensation and reflexes below the level of injury  + Loss of bulbo-cavernous reflex  Usually recover within 24-48 hrs -oxford handbook-
  • 4.
  • 5.
    Anatomy 5 http://www.radiologyassistant.nl/ en/p4906c8352d8d2/spine-thoracolumbar- injury.html Dennis three column -spine stability
  • 6.
    6 Walter B.Greene. Netter's Orthopaedics 1st ed. 2006
  • 7.
    Pathophysiology 7 TRAUMA-- > SCI - causes a concussion like injury to spinal cord - total sensory and motor power loss and loss of all reflexes for initial some period - followed by then gradual recovery of reflexes  Reflexes in the SC caudal to the SCI are depressed (areflexia)  This state of sensory and motor loss along with total loss of reflexes following trauma is known as spinal shock  The 'shock' in spinal shock does not refer to circulatory collapse
  • 8.
    Phases Phase TimePhysical exam findings Underlying physiological event 1 0-1 days Areflexia Loss of descending facilitation 2 1-3 days Initial reflex return Denervation supersensitivity 3 1-4 weeks Hyperreflexia Axon-supported synapse growth 4 1-12 months Hyperreflexia, Spasticity Soma-supported synapse growth http://www.nature.com/sc/journal/v42/n7/full/3101603a.html 8
  • 9.
    Phase 1: A complete loss or weakening of all reflexes below the level of spinal cord injury  Spinal concussion caused the neurons involved in various reflex arcs and the neural input from the brain become hyperpolarized and unresponsive. 9
  • 10.
    Phase 2 Characterized by the return of some reflexes. The first reflexes to reappear is the bulbocavernosus reflex  The reason reflexes return is the hypersensitivity of reflex muscles following denervation; more receptors for neurotransmitters are expressed and are therefore they are easier to stimulate. 10
  • 11.
    Phases 3 and4  Characterized by hyperreflexia  Neurons below the injury attempt to reestablish the synapses 11
  • 12.
    Spinal vs neurogenicshock 12 Spinal shock Neurogenic shock Definition Immediate temporary loss of total power, sensation and reflexes below the level of injury Sudden loss of the sympathetic nervous system signals BP Hypotension Hypotension Pulse Bradycardia Bradycardia Bulbocaverno Absent Variable sus reflex Motor Flaccid paralysis Variable Time 48-72 hrs immediate after SCI Mechanism Peripheral neurons become temporarily unresponsive to brain stimuli Disruption of autonomic pathways  loss of sympathetic tone and vasodilation http://www.orthobullets.com/spine/2006/spinal-cord-injuries
  • 13.
    13 MANAGEMENT Immobilisation -Spinal board -Cervical collar 1) Monitor neurological status 2) Cord/cauda-equina Sx Methylprednisolone -given as bolus of 30 mg / kg body wt -followed by infusion at 5.4 mg / kg / hour for 24 hours Symtomatic medication: -Pain relief -Constipation DVT prophylaxis
  • 14.
    The National SpinalCord Injury Study (NASCIS) 14  NASCIS 3 USA, 1997  High dose methylprednisolone  Prevent secondary injury of SCI  Rx start within 3 hrs for 24 hrs  Side effects: immunosuppression, GIT bleeding, hyperglycemia and ARDS
  • 15.
  • 16.

Editor's Notes

  • #5 - How to do it? Male & female with cbd Female without cbd Why it is important? Recovery of spinal shock Can comment on complete/incomplete sci Prognosis n mx for pt - Ths reflexes are LMN origin
  • #7 Explain more about dermatomes of LL C7 T12 L5 S5 Coccyx
  • #13 Hypotension and bradycardia in spinal shock  when the SCI at thoracic, area of sympathetic nerve origin
  • #14 Cauda equina syndrome: Characterized by Asymmetrical areflexia, numbness at saddle area, urinary/bowel incontinence Side effect of high dose steroid Reduced immunity  start abx Git bleeding  cover with ppi