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Acute & Chronic Spinal Cord Injury (SCI)

Pathophysiology

Primary Injury

• Mechanical insult–traction, compression, shear or laceration destroys grey/white-matter tracts.

Secondary Injury (minimise intra-theatre)

• Within minutes–weeks: spinal cord ischaemia, glutamate excitotoxicity, inflammatory cytokine surge, oedema, free-radical formation and delayed apoptosis

Phases after Injury

Phase	Timing	Key features	Anaesthetic relevance
Initial	Seconds–minutes	Transient extreme sympathetic discharge → severe hypertension, arrhythmia, APO	Treat as hypertensive crisis; invasive BP if unstable
Spinal-shock	~30 min–8 weeks	Areflexia, flaccidity, paralytic ileus; variable hypotension/bradycardia	Expect haemodynamic lability; avoid high PEEP which ↓ venous return
Neurogenic-shock	Usually cervical/high-thoracic injuries within first 24 h	Triad: hypotension, relative bradycardia, peripheral vasodilation	Maintain MAP ≥ 85 mmHg for 5–7 days with fluids + noradrenaline/phenylephrine
Reflex/Spastic	≥ 3 weeks	Return of reflex arcs, spasticity; risk of autonomic dysreflexia (AD) above T6	Anticipate severe peri-operative hypertension/tachy-/brady-arrhythmias

Key Distinctions between Spinal Shock and Neurogenic Shock

Aspect	Spinal shock	Neurogenic shock
Primary phenomenon	Neurological: transient loss of all motor, sensory and reflex activity below the level of injury	Haemodynamic: distributive shock from loss of sympathetic tone (vasodilatation ± bradycardia)
Typical cord level	Any; severity ↑ with high cervical injuries	Almost always lesions above T6 (loss of splanchnic sympathetic outflow)
Pathophysiology	Sudden interruption of descending facilitatory pathways → flaccid areflexia; gradual synaptic re-organisation leads to hyper-reflexia/spasticity	Loss of vasomotor tone + unopposed vagal cardiac influence → ↓ SVR, venous pooling, relative bradycardia
Onset	Immediate (seconds–minutes) after injury	Usually within hours of injury (can be delayed)
Duration	Hours → weeks (resolution heralded by bulbocavernosus reflex & return of deep-tendon reflexes)	Days → up to 6 weeks; resolves with sympathetic re-adaptation or after vasopressor support
Cardiovascular signs	BP normal or ↓ (if coincident neurogenic shock), heart rate often normal or tachycardic initially	Hypotension with relative bradycardia (HR < 60–80 bpm), warm peripheries, wide pulse pressure
Neurological signs	Flaccid paralysis, areflexia, sensory loss below lesion	May have motor/sensory loss (from SCI) but reflexes unaffected by the shock state
Temperature regulation	Usually normal initially; later poikilothermia as reflexes return	Impaired–patient tends to assume ambient temperature owing to vasodilatation
Core management	Supportive; prevent secondary cord injury (MAP ≥ 85 mmHg, oxygenation)	Fluid resuscitation + vasopressor (noradrenaline/phenylephrine); atropine/isoprenaline for severe bradycardia; treat hypothermia
Prognosis marker	Return of reflexes → phase-2 recovery; eventual spasticity/hyper-reflexia	Responds rapidly to haemodynamic optimisation; mortality increases if unrecognised

Classification

American Spinal Injury Association (ASIA) Impairment Scale (AIS)

Grade	Description
A–Complete	No motor/sensory function in S4–S5
B–Sensory incomplete	Sensory but no motor below lesion incl. S4–S5
C–Motor incomplete	< 50 % key muscles below lesion grade ≥ 3
D–Motor incomplete	≥ 50 % key muscles below lesion grade ≥ 3
E–Normal	Normal exam; prior deficits present

The neurological level = lowest level with intact motor and sensory bilaterally.

Key Syndrome Patterns

Syndrome	Typical cause	Ipsilateral loss	Contralateral loss
Brown-Séquard	Penetrating hemi-cord injury	Motor, vibration, proprioception	Pain & temperature
Anterior cord	Anterior spinal artery occlusion	Motor, pain, temperature	—
Central cord	Hyper-extension in spondylotic neck	Upper-limb > lower-limb weakness, +/- bladder retention	Variable
Posterior cord	Posterior spinal artery / B12	Proprioception & vibration	—
Conus medullaris	L1 fracture, tumour	Mixed UMN/LMN; early sphincter dysfunction	—
Cauda equina	Large central disc, fracture	LMN pattern; patchy	—

Respiratory Consequences

Injury level	Vital capacity (% predicted)	Cough	Ventilatory support
C1–C2	< 10 %	Absent	Permanent invasive ventilation
C3–C5 (phrenic)	10–30 %	Ineffective	80 % need ventilation within 48 h; consider NIV wean
Above T8	30–80 %	Weak	May require short-term ventilation/assisted cough
Below T8	80–100 %	± weak	Rarely ventilated

Early chest physiotherapy, cough assist and physiologic PEEP reduce pneumonia and atelectasis

Anaesthetic Management

Pre-operative Assessment (ATLS framework)

1. Airway–anticipate difficult intubation (rigid collar, limited jaw movement, chronic spasm).
2. Breathing–evaluate FVC, peak cough flow; baseline ABG.
3. Circulation–exclude haemorrhage; recognise neurogenic shock.
4. Disability–document motor level (medico-legal).
5. Exposure–pressure-area check, temperature, spasm trigger survey.

Pharmacology Pearls

Drug/class	Evidence-based recommendation
Succinylcholine	Safe ≤ 48 h post-injury only; thereafter contra-indicated until ~9 months owing to lethal hyperkalaemia from ACh-receptor up-regulation
Non-depolarising NMB	Rocuronium 1 mg kg⁻¹ RSI; expect resistance in chronic phase (↑ dose/early sugammadex)
High-dose methyl-prednisolone	Not recommended–no neurological benefit, ↑ infection & GI bleeding risk
Vasopressors	Noradrenaline first-line; phenylephrine for episodic AD

Induction & Positioning

• Manual in-line stabilisation; avoid cricoid pressure unless gastric distension.
• If awake fibre-optic needed, lignocaine 4 mg kg⁻¹ nebuliser; maintain collar.
• Warm IV fluids & forced-air blankets–impaired thermoregulation.
• Confirm BP after every position change–drastic swings common.

Maintenance Goals (“MADE”)

• M: MAP ≥ 85 mmHg.
• A: Anaemia–keep Hb > 10 g dl⁻¹ (optimises DO₂).
• D: Dysreflexia–deep anaesthesia, α-blocker (phentolamine 5 mg IV) for crises.
• E: Euthermia–36–37 °C; treat pyrexia vigorously

Autonomic Dysreflexia (chronic ≥ T6)

• Triggers: bladder/kidney stones, distended colon, labour, surgical incision.
• Presentation: SBP ↑ > 20 %, pounding headache, sweating above lesion, reflex bradycardia.
• Immediate treatment: remove stimulus, deepen anaesthesia, give GTN 2 puffs SL / nicardipine 0.5 µg kg⁻¹ min⁻¹ infusion

Ventilation

• Vₜ 6 ml kg⁻¹, permissive hypercapnia avoided (↑ ICP in concomitant TBI).
• Assisted cough (MI-E device) before extubation.

Thromboprophylaxis

• Start LMWH within 24–72 h once haemostasis secure; continue ≥ 3 months or until ambulatory. Early initiation halves VTE risk
• Add intermittent pneumatic compression.

Post-operative Priorities

1. Haemodynamic monitoring for 24 h (invasive if high cervical).
2. Strict temperature charting–treat poikilothermia.
3. Early mobilisation/tilt-table.
4. Multimodal analgesia: paracetamol, ketamine 0.1 mg kg⁻¹ h⁻¹, gabapentinoids for neuropathic pain.
5. Pressure-area care checklist each nursing shift.

Elective / Chronic SCI Specifics

Issue	Practical tip
Respiratory failure risk	Pre-hab with inspiratory-muscle training; plan for NIV post-op if FVC < 50 % predicted
Difficult IV access & reduced blood volume (~20 %)	Ultrasound lines, preload 2 ml kg⁻¹ h⁻¹ balanced crystalloids
Spasm & contractures	Positioning aids, baclofen pre-med
Latex allergy (chronic IDC)	Use latex-free equipment
Thermoregulation	Active warming & ambient 24 °C
Neurological monitoring for regional	Sensory testing unreliable below lesion; use US guidance for neuraxial/plexus blocks.

• Minor procedures below the sensory level with low AD risk can occasionally proceed with local infiltration alone, provided IV access, standard monitors and an anaesthetist remain present throughout.

Disc Herniation

• Degenerative loss of proteoglycans → nucleus pulposus dehydration → annular tears.
• Lumbar L4/5 & L5/S1 90 %; Cervical C6/7 60 %.
• Lateral herniation → radiculopathy / cauda equina; central cervical → myelopathy.
• Anaesthetic relevance: optimise neurological exam pre-block; avoid excessive neck flexion.

American Spinal Injury (ASIA) Impairment Scale

Links

• Autonomic hyperreflexia
• Traumatic brain injury
• Spine surgery

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References:

1. Dooney N, Dagal A. Anesthetic considerations in acute spinal cord trauma. Int J Crit Illn Inj Sci. 2011 Jan;1(1):36-43. doi: 10.4103/2229-5151.79280. PMID: 22096772; PMCID: PMC3210001.
2. Bonner, S. and Smith, C. (2013). Initial management of acute spinal cord injury. Continuing Education in Anaesthesia Critical Care &Amp; Pain, 13(6), 224-231. https://doi.org/10.1093/bjaceaccp/mkt021
3. Badhiwala JH et al. A clinical practice guideline for acute SCI: haemodynamic management. Global Spine J 2022. PMC
4. Levi AD. Mean arterial pressure targets and neurologic recovery after SCI. Neurosurgery 2020. PubMed
5. StatPearls. Succinylcholine Chloride (update 2025). OpenAnesthesia
6. Yang J et al. Peri-operative autonomic dysreflexia review. J Anaesth Crit Care 2024. PMC
7. OpenAnesthesia. Spinal cord injury–key points (2023). OpenAnesthesia
8. SurgicalCriticalCare.net guideline: High-dose methylprednisolone NOT recommended (2023). Surgical Critical Care
9. Medscape Reference. Corticosteroids in acute SCI (2023 update). Medscape
10. PVA Consortium. Early acute management in adults with SCI (2019). Paralyzed Veterans of America
11. Cardenas DD et al. Anticoagulant thromboprophylaxis after SCI. Global Spine J 2020. College of Medicine
12. West CR et al. Respiratory complications in chronic SCI. BJA 2019. OpenAnesthesia
13. FRCA Mind Maps. (2024). Retrieved June 5, 2024, from https://www.frcamindmaps.org/
14. Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/

Summaries:

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© 2025 Francois Uys. All Rights Reserved.

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