Section: Trauma Curriculum: Curriculum, page 78

Spinal Shock

Metabolic derangement initially after any spinal cord injury
- Bleeding and inflammation at site of injury → Tissue damage
  - Releases chemical mediators
  - Cause vasoconstriction
  - Spinal cord ischaemia and hypoxia
  - Leads to spinal cord dysfunction
Clinical
- Paralysis | Hypotonia | Areflexia | Sensory Loss
Complete vs partial/compression
- So may regain function if partial/compression
Once resolved - do assessment to see what true functional impairment is
Return of Bulbocavernosus reflex usually means end of spinal shock (2 days)
- Feel for internal/external anal sphincter contraction in response to squeezing the glans penis or clitoris, or tugging on an IDC
Management of Spinal Shock
- Resuscitate - Volume load and pressors
- Ensure spinal cord perfusion
- Trendelenburg position
- Steroids

Neurogenic Shock

High level spinal cord injury (usually T6 and above)
Disruption of SNS from T1 to L2
- Loss of SNS stimulation
- Loss of Catecholamines (N/NA) and their effects
Effects
- Vasodilatation → Fluids
- Bradycardia → Atropine
- Target MAP over 80mmHg
- Hypotension | Bradycardia | Peripheral Vasodilation (loss of SNS tone) | Loss of all motor and sensory function below the injury level
Primary Injury (MECHANICAL)
- Direct injury due to mechanical disruption, transection or extradural
Secondary Injury (VASCULAR)
- Arterial disruption, thrombosis or hypoperfusion to spinal cord

Lateral Spinothalamic Pathway - Pain and Temperature
- Fibres decussate straight away
- Contralateral loss below lesion
Corticospinal Tract - Motor
- Decussate at midbrain
- Ipsilateral loss
Dorsal columns - Light touch and Proprioception
- Mixed?
Neurogenic = Nervous system is in shock
Spinal = Spinal cord in shock