Shock Clarification

Neurogenic Shock

Disruption of sympathetic outflow from T1-L2
- Unopposed vagal tone
  - Decreased SVR -> vasodilation
Cannot Dx NS unless SS r/o (Bulbocavernosus absent = SS)
Cervical/ upper thoracic SCI (usually not below T6)
- 8% of all SCI
- 24% of cervical SCI
Features (stereotypic hypotension with bradycardia is actually not common)
- Hypotension (peripheral vasodilation)
- Relative bradycardia
- Hypothermia with warm peripheries
- Variable/ independent changes in motor/ bulbocavernosu
Mechanism
- Disruption of Autonomic Pathway within the cord
- Pre-ganglionic nerves of sympathetic nervous system
  - Injuries above midthoracic can cause loss of sympathetic tone (neurogenic shock – vasodilation and hypotension)
Timeline: Usually lasts 48-72h following SCI
Overall – circulatory collapse, potentially fatal
Mx
- Vasopressors
- Swan-Ganz monitoring for careful fluid management

Spinal Shock

Temporary loss of spinal cord function and reflex below level of SCI
Flaccid areflexic paralysis
- Absent bulbocavernosus +/- sustained priapism
- +/- hypotension – initial hypertension (release catecholamines)
- +/- bradycardia
ONCE SPINAL SHOCK ENDS, You can classify your SCI
Blocks
- Corticospinal and Spinothalamic Pathway
- Autonomic Pathway
Mechanism
- Temporary loss of spinal cord function and reflex activity below the level of SCI
  - Neurophysiologic in nature – neurons become hyperpolarized and lose the ability to respond to stimuli from brain
Timeline: 48-72h
Ditunno et al. review the basic physiologic mechanism of spinal shock. They discuss it as a four-phased process. Phase 1 occurs in the first 24 hours and consists of absent motor function and sensation distal to the spinal injury. Distal reflexes, including the bulbocavernosus, are absent. Phase 2 occurs from days 1-3 and is characterized by the initial return of the cutaneous reflexes (bulbocavernosus and cremasteric). Phase 3 occurs between days 4-30 and is characterized by hyperreflexia, and phase 4 occurs after 1 month and is characterized by spasticity.

Hypovolemic Shock

Hypotension, TACHYcardia
Mechanism – decreased preload -> decreased cardiac output -> Tissue hypoperfusion -> shock

Hemorrhagic Shock