Spine trauma: Difference between revisions

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{{NoteBox|secondary}}<strong>Related pages</strong>
* [[Spinal shock]]
{{NoteBoxEnd}}
= Pathophysiology =
= Pathophysiology =
{| class="wikitable" style=width:100%
{| class="wikitable" style=width:100%
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The max total score for each sensory modality (light touch or pinprick, adding up scores from left & right sides) is 112.
The max total score for each sensory modality (light touch or pinprick, adding up scores from left & right sides) is 112.


== Frankel/ASIA impairment scale ==
=== Frankel/ASIA impairment scale ===
{| class="wikitable"
{| class="wikitable"
!Grade
!Grade
Line 100: Line 103:
|Sensory and motor functions are normal.
|Sensory and motor functions are normal.
|}
|}
{{NoteBox|warn}}
{{NoteBox|warn w-50}}<html><center><a href="https://asia-spinalinjury.org/wp-content/uploads/2019/10/ASIA-ISCOS-Worksheet_10.2019_PRINT-Page-1-2.pdf" target="_blank" rel="noreferrer noopener">ASIA ISCOS Worksheet</a></center></html>{{NoteBoxEnd}}
 
= Clinical Features =
 
== Neurogenic Shock vs. Spinal Shock ==
{| class="wikitable"
!
!Neurogenic Shock
![[Spinal shock]]
|-
|Definition
|Sudden loss of the descending sympathetic tracts after severe central nervous system damage
|Immediate loss of reflexes, bladder function, and muscle tone below the level of injury
|-
|Blood pressure
|Hypotension
|Hypotension
|-
|Pulse
|Bradycardia
|Bradycardia
|-
|Motor palsy
|Variable
|Flaccid
|-
|Mechanism
|Excessive pooling of blood in the organs caused by loss of descending sympathetic tracts and loss of the reflex vasoconstrictor effect of arterial baroreceptors
|Venous pooling caused by lack of counteracting muscular effects of the lower extremities resulting from unresponsiveness of peripheral nerves to brain stimulation
|}
 
= Management =
{{NoteBox|secondary}}<strong>Key articles</strong><hr>
{| style="border-collapse: collapse; width: 100%;"
|-
| style="width: 15%; vertical-align: top;" | [[NASCIS I]]
| style="width: 85%; vertical-align: top;" | Efficacy of high-dose vs. standard-dose steroids in acute SCI ⇒ <span style="background-color:#fff2cc;">no difference in neuro. recovery</span>; <span style="background-color:#ea9999;">high-dose steroids had ↑ early mortality & wound infx rates.</span> <i>(JAMA 1984)</i>
|-
| style="width: 15%; vertical-align: top;" | [[NASCIS II]]
| style="width: 85%; vertical-align: top;" | Efficacy of high-dose steroids & naloxone in acute SCI ⇒ <span style="background-color:#fff2cc;">high-dose steroids significantly ↑ neuro. recovery if Rx w/i 8 hrs of injury</span>; naloxone showed no significant benefits. <i>(N Engl J Med 1990)</i>
|-
| style="width: 15%; vertical-align: top;" | [[NASCIS III]]
| style="width: 85%; vertical-align: top;" | Efficacy of 24 hrs vs 48 hrs Rx of steroids and 48 hrs Rx of tirilazad mesylate in acute SCI ⇒ <span style="background-color:#fff2cc;">48 hrs steroids ↑ neuro. recovery for pts Tx 3-8 hrs post-injury</span>, while tirilazad showed no superior benefits. <i>(JAMA 1997)</i>
|}{{NoteBoxEnd}}


{{NoteBoxEnd}}
[[Category:Neurotrauma]]
[[Category:Neurotrauma]]
[[Category:Spine]]

Latest revision as of 03:40, 20 July 2024

Related pages

Pathophysiology

Injury Phase Time Relative to Primary Injury Key Processes and Events
Immediate <2 hours
  • Primary mechanical injury (severing of axons)
  • Gray matter hemorrhage and ischemia
  • Microglial activation
  • Release of pro-inflammatory factors (IL-1β, TNFα, IL-6)
Early acute <48 hours
  • Vasogenic and cytotoxic edema
  • ROS production, lipid peroxidation
  • Glutamate-mediated excitotoxicity
  • Continued hemorrhage, ischemia, and necrosis
  • Neutrophil invasion
  • Peak BSCB permeability
  • Early demyelination (oligodendrocyte death)
  • Neuronal death
  • Axonal swelling
  • Systemic events (systemic shock, spinal shock, hypotension, hypoxia)
Subacute <14 days
  • Macrophage infiltration
  • Initiation of astroglial scar (reactive astrogliosis)
  • BSCB repair and resolution of edema
Intermediate <6 months
  • Continued formation of glial scar
  • Cyst formation
  • Lesion stabilization
Chronic >6 months
  • Prolonged Wallerian degeneration
  • Persistence of spared, demyelinated axons
  • Potential structural and functional plasticity of spared spinal cord tissue

Classification

ASIA Classification

Motor Function:

Motor fnx is ✓ at five levels in UE & LE (20 stations) on scale from 0-5. The scale is as follows:

  • 0: No movement
  • 1: Muscle twitch, but no movement
  • 2: Movement, but not against gravity
  • 3: Movement against gravity, but not against resistance
  • 4: Movement against resistance, but weaker than normal
  • 5: Normal strength

The max total score for motor fnx (adding up scores from left & right sides) is 100.

Sensory Function:

Sensory fnx is ✓ for light touch and pinprick (sharp/dull discrimination) in 28 different dermatomes (56 stations), on a scale from 0-2:

  • 0: Absent (no sensation)
  • 1: Impaired (some sensation)
  • 2: Normal (full sensation)

The max total score for each sensory modality (light touch or pinprick, adding up scores from left & right sides) is 112.

Frankel/ASIA impairment scale

Grade Degree of Impairment Definition
A Complete No sensory or motor function is preserved in sacral segments S4-5.
B Incomplete Sensory, but not motor, function is preserved below the neurological level and extends through sacral segments S4-5.
C Incomplete Sensory and motor functions are preserved below the neurological level. Most key muscles below the neurological level have a muscle grade of <3.
D Incomplete Sensory and motor functions are preserved below the neurological level. Most key muscles below the neurological level have a muscle grade of ≥3.
E Normal Sensory and motor functions are normal.

Clinical Features

Neurogenic Shock vs. Spinal Shock

Neurogenic Shock Spinal shock
Definition Sudden loss of the descending sympathetic tracts after severe central nervous system damage Immediate loss of reflexes, bladder function, and muscle tone below the level of injury
Blood pressure Hypotension Hypotension
Pulse Bradycardia Bradycardia
Motor palsy Variable Flaccid
Mechanism Excessive pooling of blood in the organs caused by loss of descending sympathetic tracts and loss of the reflex vasoconstrictor effect of arterial baroreceptors Venous pooling caused by lack of counteracting muscular effects of the lower extremities resulting from unresponsiveness of peripheral nerves to brain stimulation

Management

Key articles
NASCIS I Efficacy of high-dose vs. standard-dose steroids in acute SCI ⇒ no difference in neuro. recovery; high-dose steroids had ↑ early mortality & wound infx rates. (JAMA 1984)
NASCIS II Efficacy of high-dose steroids & naloxone in acute SCI ⇒ high-dose steroids significantly ↑ neuro. recovery if Rx w/i 8 hrs of injury; naloxone showed no significant benefits. (N Engl J Med 1990)
NASCIS III Efficacy of 24 hrs vs 48 hrs Rx of steroids and 48 hrs Rx of tirilazad mesylate in acute SCI ⇒ 48 hrs steroids ↑ neuro. recovery for pts Tx 3-8 hrs post-injury, while tirilazad showed no superior benefits. (JAMA 1997)