Spinal Shock
Original Editor - Cindy John-Chu
Top Contributors - Cindy John-Chu, Lucinda hampton, Chelsea Mclene, Kim Jackson, Vidya Acharya and Ahmed M Diab
Introduction[edit | edit source]
Spinal shock is often a sequel of severe spinal cord injury (SCI), usually resulting from high-impact, direct trauma, the patient with spinal shock typically being found at a trauma scene. Another cause of spinal shock is ischemia of the spinal cord.[1]
- With spinal shock there is loss of muscle tone and spinal reflexes below the level of a severe spinal cord lesion[2].
- "Shock" in this instance is not related to a state of circulatory collapse but of suppressed spinal reflexes below the level of cord injury[3].
Watch this informative 3 minute video titled "What is spinal shock?"
Spinal shock[edit | edit source]
Defined as a state of transient physiologic (rather than anatomic) reflex depression of spinal cord function below the level of injury, with associated loss of sensorimotor functions[5].
- 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.
- It is characterized by a temporary rise in blood pressure that is proceeded by hypotension, flaccid paralysis, urinary retention and fecal Urinary Incontinence.
- If reversal of symptoms does not occur within 24hrs, it may call for protracted recovery time and lengthened stay in rehabilitation.
- When reflexes return, they follow a pattern where superficial ones show up before deep tendon reflexes[5].
Characterized by:
- Flaccid paralysis
- Anaesthesia
- Areflexia or hyporeflexia[6]
Stages of Spinal Shock[edit | edit source]
The resolution of spinal shock does not occur abruptly but in phases. Ditunno et al (2004)[8] proposed a four-phase model of the syndrome. Phases:
- Lasts 0 to 1 day; loss of descending facilitation; areflexia or hyporeflexia
- Occurs 1 to 3 days post injury; denervation supersensitivity; initial re-emergence of reflexes
- Lasts 4 days to 1 month; axon-supported synapse growth occurs; initial hyper-reflexia
- Lasts 1 to 12 months; soma-supported synapse growth; spasticity
Autonomic Effects[edit | edit source]
- Neurogenic shock may occur in spinal cord injuries above T6, from the loss of autonomic innervation from the brain.
- 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.[8]
Differential Diagnoses[edit | edit source]
These include:
- Vertebral fracture
- Spinal abscess
- Sepsis
- Cardiogenic shock[9]
Differences between Neurogenic Shock and Spinal Shock[edit | edit source]
Neurogenic shock: Defined as systolic blood pressure less than 100 mm Hg with a heart rate less than 80 bpm[10]; consequent to SCI with associated autonomic dysregulation[10]; common with cord injuries above T6 level (associated with cervical and high thoracic spine injury); occurs at anytime from the onset of injury, frequently following a traumatic SCI[10], but may also occur in non-traumatic cord lesions[11]
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[6]
Complications[edit | edit source]
- Neurological deterioration
- Pressure sores
- Fecal incontinence
- Urinary retention
- Deep vein thrombosis
- Aspiration pneumonitis[9]
Conclusion[edit | edit source]
While spinal shock may not be easily prevented, it can be managed and often requires a multidisciplinary team effort to do so. Its understanding and that of its mechanisms will enable the application of interventions that will facilitate recovery.
Additional Information[edit | edit source]
Physiotherapy Management of Individuals with Spinal Cord Injury
Bed Mobility and Transfers in Spinal Cord Injury
Prognosis and Goal Setting in Spinal Cord Injury
References[edit | edit source]
- ↑ Ziu E, Mesfin FB. Spinal Shock.Available:https://www.ncbi.nlm.nih.gov/books/NBK448163/ (accessed 31.12.2022)
- ↑ Smith PM, Jeffery ND. Spinal Shock-Comparative Aspects and Clinical Relevance. Journal of Verterinary Int Med 2008; 19(Iss 6)
- ↑ Singhal V, Aggarwal R. Spinal Shock. In: Prabhakar H. Complications in Neuroanesthesia. Academic Press: Science Direct, 2016. p89-94.
- ↑ Em Quattrocchi. What is SPINAL SHOCK? Available from: https://www.youtube.com/watch?v=DlJWQOtLWnM [last accessed 24/3/2021]
- ↑ 5.0 5.1 Singhal V, Aggarwal R, Spinal Shock. In: Prabhakar H editor. Complications in Neuroanaesthesia. Academic: Science Direct, 2016. p89-94.
- ↑ 6.0 6.1 Volski A, Ackerman DJ, Neurogenic Shock. In: Stawicki SP, Swaroop M editors. The Science and Art of Physiological Restoration. IntechOpen, 2019.
- ↑ ACLS Certification Association. Neurogenic shock vs. Spinal shock. Available from: https://youtu.be/nPu7RW2JBkw [last accessed 10/1/2021]
- ↑ 8.0 8.1 Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal cord. 2004 Jul;42(7):383-95.
- ↑ 9.0 9.1 Ziu E, Mesfin FB. Spinal Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. p1-11.
- ↑ 10.0 10.1 10.2 Dave S, Cho JJ. Neurogenic Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020; p1-10.
- ↑ Flanagan EP, Pittock SJ, Diagnosis and Management of Spinal Cord Emergencies. In: Wijdicks EFM, Kramer AH editors. Handbook of Clinical Neurology. Elsevier, 2017. p319-335.