Spinal Shock

Overview[edit | edit source]

Also known as spinal shock syndrome, spinal shock is the loss of muscle tone and spinal reflexes below the level of a severe spinal cord lesion[1]. This "shock" does not imply a state of circulatory collapse but of surpressed spinal reflexes below the level of cord injury[2]. 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[3]. It usually is consequent to severe spinal cord injury (SCI) that is either traumatic or ischaemic, with traumatic spinal shock occuring more in young people and mostly among males than females[4]. Spinal shock is characterized by a temporary rise in blood pressure that is proceeded by hypotension, flaccid paralysis, urinary retention and faecal incontinence[4]. If reversal of symptoms does not occur within 24hrs, it may call for protracted recovery time and lengthened stay in rehabilitation[4].

Differential Diagnoses of Spinal Shock[edit | edit source]

These include:

Complications of Spinal Shock[edit | edit source]

Differences between Neurogenic Shock and Spinal Shock[edit | edit source]

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[5]
  • Consequent to SCI with associated autonomic dysregulation[5]
  • 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[5], but may also occur in non-traumatic cord lesions[6]
  • 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[7]

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[8]
  • 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[9]
  • When reflexes return, they follow a pattern where superficial ones show up before deep tendon reflexes[8].
  • Characterized by:
    • Flaccid paralysis
    • Anaesthesia
    • Areflexia or hyporeflexia[7]
  • Lasts between days to months
  • Most often resolves on its own

[10]

Stages of Spinal Shock[edit | edit source]

The resolution of spinal shock does not occur abruptly but in phases. Ditunno et al (2004)[11] proposed a four-phase model of the syndrome.

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

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.

References[edit | edit source]

  1. Smith PM, Jeffery ND. Spinal Shock-Comparative Aspects and Clinical Relevance. Journal of Verterinary Int Med 2008; 19(Iss 6)
  2. Singhal V, Aggarwal R. Spinal Shock. In: Prabhakar H. Complications in Neuroanesthesia. Academic Press: Science Direct, 2016. p89-94.
  3. Ko HY. Spinal Shock. In Management and Rehabilitation of Spinal Cord Injuries. Singapore: Springer, 2019. pg123-134.
  4. 4.0 4.1 4.2 4.3 4.4 Ziu E, Mesfin FB. Spinal Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. p1-11.
  5. 5.0 5.1 5.2 Dave S, Cho JJ. Neurogenic Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020; p1-10.
  6. 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.
  7. 7.0 7.1 Volski A, Ackerman DJ, Neurogenic Shock. In: Stawicki SP, Swaroop M editors. The Science and Art of Physiological Restoration. IntechOpen, 2019.
  8. 8.0 8.1 Singhal V, Aggarwal R, Spinal Shock. In: Prabhakar H editor. Complications in Neuroanaesthesia. Academic: Science Direct, 2016. p89-94.
  9. Graells XS, Benato ML, del Santoro PG, et al. Spinal Cord Injury. In: Nasr A, Saavedra TF, Collaço I, Abreu P, Namias N, Marttos. The Trauma Golden Hour. Cham: Springer, 2020. p65-72.
  10. ACLS Certification Association. Neurogenic shock vs. Spinal shock. Available from: https://youtu.be/nPu7RW2JBkw [last accessed 10/1/2021]
  11. Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord. 2004; 42:383-395.