Spinal shock
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This term is often used in two completely different senses:
- 1st SENSE: hypotension (shock) that follows spinal cord injury (SBP usually ~ 80 mm Hg). Caused by multiple factors:
- interruption of sympathetics: implies spinal cord injury above T1
- loss of vasoconstrictors → vasodilatation (loss of vascular tone) below the level of injury
- leaves parasympathetics relatively unopposed causing bradycardia
- loss of muscle tone due to skeletal muscle paralysis below level of injury results in venous pooling and thus a relative hypovolemia
- blood loss from associated wounds → true hypovolemia
- interruption of sympathetics: implies spinal cord injury above T1
- 2nd SENSE: transient loss of all neurologic function (including segmental and polysynaptic reflex activity and autonomic function) below the level of the SCI → flaccid paralysis and areflexia
- duration: may abate in as little as 72 hours, but typically persists 1-2 weeks, occasionally several months
- accompanied by loss of the bulbocavernosus reflex
- spinal cord reflexes immediately above the injury may also be depressed on the basis of the Schiff-Sherrington phenomenon (primarily described in animal models)
- when spinal shock resolves, there will be spasticity below the level of the lesion and return of the bulbocavernosus reflex
- a poor prognostic sign