Spinal shock syndrome, spinal shock is the loss of muscle tone and spinal reflexes below the level of a severe spinal cord lesion.
This "shock" does not imply a state of circulatory collapse but of suppressed spinal reflexes below the level of cord injury. It takes between days and months for spinal shock to completely resolve and when it does, the flaccidity that was once seen gradually becomes spasticity.
Spinal Shock
It usually is consequent to severe spinal cord injury (SCI) that is either traumatic or ischaemic, with traumatic spinal shock occurring more in young people and mostly among males than female.
Spinal shock is characterized by a temporary rise in blood pressure that is proceeded by hypotension, flaccid paralysis, urinary retention and fecal incontinence.
If reversal of symptoms does not occur within 24hrs, it may call for protracted recovery time and lengthened stay in rehabilitation.
Differential Diagnoses of Spinal Shock
- Vertebral fracture
- Spinal abscess
- Sepsis
- Cardiogenic shock
- Complications of Spinal Shock
- Neurological deterioration
- Pressure sores
- Fecal incontinence
- Urinary retention
- Deep vein thrombosis
- Aspiration pneumonitis
Differences between Neurogenic Shock and Spinal Shock
Neurogenic shock
- Also known as vasogenic shock
- Defined as systolic blood pressure less than 100 mm Hg with a heart rate less than 80 bpm[6]
- Consequent to SCI with associated autonomic dysregulation[6]
- Common with cord injuries above T6 level. In other words, it is associated with cervical and high thoracic spine injury.
- Occurs at anytime from the onset of injury
- Frequently follows a traumatic SCI, but may also occur in non-traumatic cord lesions
Characterized by:
- Systemic hypotension and bradycardia
- Respiratory insufficiency and pulmonary dysfunction
- Temperature dysregulation vis-à-vis hypothermia; flushed, warm skin
Lasts between 1 to 6 weeks post the initial injury
Managed by administering fluids and vasopressors with appropriate temperature monitoring.
Spinal shock
Defined as a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of sensorimotor functions.- Is a reversible reduction or loss in sensory and motor function after an acute SCI
- Rarely occurs in spinal cord lesions of gradual onset
- Involves reflex depression of cord function below the level of injury.
- When reflexes return, they follow a pattern where superficial ones show up before deep tendon reflexes.
Characterized by:
- Flaccid paralysis
- Anaesthesia
- Areflexia or hyporeflexia
- Lasts between days to months
- Most often resolves on its own
Stages of Spinal Shock
Phase 1
- Lasts between 0 to 1 day
- Characterized by loss of descending facilitation
- Presents as areflexia or hyporeflexia
Phase 2
- Occurs between 1 to 3 days post injury
- Shows as denervation supersensitivity
- Leads to initial re-emergence of reflexes
Phase 3
- Lasts between 4 days to 1 month
- Axon-supported synapse growth occurs at this stage
- Initial hyper-reflexia is elicited here
Phase 4
- Lasts between 1 to 12 months
- Soma-supported synapse growth occurs
- Presents as spasticity
- Autonomic Effects
In cervical and high thoracic SCI lesions, the synergy between sympathetic and parasympathetic system is lost but the parasympathetic system is preserved.
There may be sacral parasympathetic loss encountered in lesions below T6 or T7.
Cervical lesions cause total loss of sympathetic innervation. It leads to vasovagal hypotension and bradyarrhythmia's which resolve in 3–6 weeks.
Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It leading to extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.
 |
| Spinal Shock |
0Comments