Spinal Shock
Original Editor - Cindy John-Chu
Top Contributors - Cindy John-Chu, Lucinda hampton, Kim Jackson, Chelsea Mclene, Vidya Acharya and Ahmed M Diab
Introduction
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
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
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
- 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
These include:
- Vertebral fracture
- Spinal abscess
- Sepsis
- Cardiogenic shock[9]
Differences between Neurogenic Shock and Spinal Shock
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
- Neurological deterioration
- Pressure sores
- Fecal incontinence
- Urinary retention
- Deep vein thrombosis
- Aspiration pneumonitis[9]
Conclusion
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
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
- ↑ 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.