Spinal cord injury

9 min read Last updated April 8, 2026

Surgical approach (typical)

  • Depends on level, stability, neurology, and imaging (CT/MRI): aims are decompression, stabilisation, and alignment
    • Cervical: anterior cervical discectomy/corpectomy + fusion (ACDF), posterior laminectomy, lateral mass/pedicle screw fixation
    • Thoracolumbar: posterior decompression (laminectomy), pedicle screw-rod fixation; occasionally anterior corpectomy/strut graft
    • Open reduction of fracture-dislocation; may use traction (e.g. Gardner-Wells tongs) pre/intra-op
    • May require staged procedures; prone positioning common; neuromonitoring (SSEPs/MEPs) may be used
  • Associated injuries often addressed: chest drains, laparotomy, pelvic fixation, long bone fixation

Anaesthetic management (typical for decompression/fixation)

  • Type of anaesthesia: usually GA (often with arterial line ± central access); regional techniques rarely primary in acute SCI surgery
    • Consider TIVA (propofol/remifentanil) if MEP/SSEP monitoring required; avoid/limit volatile and long-acting NMB
  • Airway: ETT (cuffed). Anticipate difficult airway + full stomach + need to minimise cervical movement
    • Manual in-line stabilisation (MILS); videolaryngoscopy often preferred; awake fibreoptic if unstable/high-risk airway
    • If >24–48 h post-injury: avoid suxamethonium (hyperkalaemia risk); use rocuronium + sugammadex if needed
  • Duration: variable (often 2–6+ hours; longer if multilevel/staged/combined approach)
  • How painful: moderate–severe (posterior instrumentation particularly painful)
    • Analgesia: multimodal (paracetamol/NSAID if appropriate), opioids; consider ketamine infusion; consider wound infiltration/erector spinae plane catheter in selected cases
  • Key intra-op goals: maintain spinal cord perfusion (avoid hypotension), normoxia/normocapnia, normothermia, careful positioning/pressure care, blood conservation
    • MAP targets often 85–90 mmHg for first 5–7 days in acute traumatic SCI (local protocol dependent; balance against bleeding/cardiac risk)

Definition and classification

  • SCI = impairment of spinal cord function due to trauma (most common), vascular, compressive, inflammatory, iatrogenic
  • Primary injury: immediate mechanical disruption; Secondary injury: oedema, ischaemia, excitotoxicity, inflammation, microvascular thrombosis
  • Neurological level and completeness: ASIA/ISNCSCI grading (A–E)
    • A = complete (no motor/sensory in S4–S5); B = sensory incomplete; C/D = motor incomplete; E = normal
  • Spinal shock (acute): transient loss of all neurological activity below lesion incl. reflexes; resolves over days–weeks (return of bulbocavernosus reflex often marks end)

Immediate priorities (ATLS + SCI-specific)

  • A: airway with cervical spine protection; high suspicion of C-spine injury in major trauma
  • B: ventilatory failure risk with high cervical lesions (C3–5 phrenic), intercostal weakness, atelectasis; treat pneumothorax/contusion
  • C: distinguish neurogenic shock from haemorrhagic shock; treat hypotension aggressively to preserve cord perfusion
    • Neurogenic shock: hypotension + relative bradycardia + warm peripheries (loss of sympathetic tone, usually injury above T6)
    • Haemorrhagic shock: tachycardia, cool clammy peripheries; assume bleeding until proven otherwise
  • D: document baseline neurology early (ASIA), check priapism (suggests complete cord injury), assess for concomitant head injury
  • E: prevent hypothermia; pressure area care; log-roll with spinal precautions

Neurogenic shock and haemodynamic management

  • Mechanism: loss of sympathetic outflow (T1–L2) → vasodilation/venous pooling + unopposed vagal tone → bradycardia
  • Treatment: cautious fluid resuscitation (avoid overload), early vasopressors; treat bradycardia if symptomatic
    • Vasopressor choice: noradrenaline often preferred (α + some β); phenylephrine may worsen bradycardia; consider adrenaline if severe bradycardia/low output
    • Bradycardia: atropine/glycopyrrolate; consider pacing if refractory/high cervical injury
  • Perfusion targets: avoid hypotension; many protocols target MAP 85–90 mmHg early after acute traumatic SCI (balance risks; discuss with spinal/neuro ICU team)

Respiratory physiology and ventilatory management

  • Lesion level effects
    • Above C3: apnoea (loss of phrenic drive) → immediate ventilation
    • C3–5: diaphragmatic weakness; high risk of ventilatory failure
    • C5–T1: intercostal weakness; reduced cough; atelectasis; secretion retention
    • Above T6: impaired sympathetic tone → bronchoconstriction, increased secretions; neurogenic pulmonary oedema can occur
  • Ventilation: lung-protective strategy, aggressive chest physiotherapy, early tracheostomy may be required in high cervical injuries

Airway management in suspected/confirmed cervical spine injury

  • Principles: oxygenation first; minimise cervical movement; anticipate difficult airway and aspiration
  • Techniques: MILS with videolaryngoscopy; awake fibreoptic for unstable injuries/anticipated difficulty; consider intubating LMA as rescue
  • RSI: use modified RSI if needed; cricoid pressure may worsen view and is controversial—apply only if it helps and release if impedes
  • Neuromuscular blockade: suxamethonium acceptable in first 24 h post-injury (many use up to 48 h), then avoid due to hyperkalaemia from receptor upregulation
    • Non-depolariser sensitivity may be increased in acute phase; later spasticity may increase requirements—titrate with nerve stimulator

Anaesthesia for spinal surgery after SCI (key considerations)

  • Monitoring: arterial line (beat-to-beat BP), large-bore IV access; consider central line if vasoactive infusions/poor access; urinary catheter
  • Positioning: prone risks—ETT security, eye protection (ischaemic optic neuropathy risk with long prone cases), pressure points, abdomen free to reduce venous bleeding, avoid brachial plexus stretch
  • Blood loss: can be significant (posterior multilevel). Use cell salvage if appropriate, TXA per trauma/spine protocol, maintain normothermia and calcium
  • Neuromonitoring: MEPs/SSEPs affected by hypotension, anaesthetic agents, temperature, anaemia
    • MEPs: avoid/limit neuromuscular blockade; prefer TIVA; maintain MAP and normothermia
    • SSEPs: more tolerant of NMB but depressed by volatile agents and hypotension
  • Post-op destination: HDU/ICU if high cervical lesion, respiratory compromise, ongoing vasopressors, major blood loss, or polytrauma

Autonomic dysreflexia (AD)

  • Occurs in chronic SCI typically above T6 after spinal shock resolves (weeks onward). Trigger below lesion → massive sympathetic discharge → severe hypertension
  • Triggers: bladder distension/blocked catheter (commonest), bowel impaction, skin irritation, surgery, labour, sexual activity
  • Features: hypertension, pounding headache, flushing/sweating above lesion, pallor below, bradycardia (or tachycardia), arrhythmias; risk of ICH, seizures, MI
  • Management: sit patient up, remove trigger (drain bladder, check catheter), deepen anaesthesia/analgesia; treat BP with short-acting agents
    • Drugs: GTN (spray/IV), nicardipine, sodium nitroprusside, hydralazine; beta-blocker cautiously if bradycardic
    • Prevention for procedures below lesion: adequate anaesthesia (GA or neuraxial). Spinal/epidural can be very effective if feasible

Steroids in acute traumatic SCI

  • High-dose methylprednisolone is not routinely recommended in many modern guidelines due to limited benefit and increased complications (infection, GI bleed, hyperglycaemia)
  • Know local policy; if already given, anticipate hyperglycaemia, infection risk, and stress ulcer prophylaxis considerations

Other perioperative issues in SCI

  • DVT/PE: high risk—early mechanical prophylaxis; pharmacological prophylaxis when safe (coordinate with surgeons re bleeding/epidural)
  • Temperature: poikilothermia (impaired autonomic control) → active warming/cooling
  • GI: ileus, stress ulceration; aspiration risk; consider NG tube if significant ileus
  • Bladder: urinary retention; catheter care; UTIs can precipitate autonomic dysreflexia
  • Pressure sores and positioning injuries: meticulous padding; frequent checks, especially long prone cases
  • Late: chronic pain, spasticity, respiratory infections, osteoporosis, anaemia, renal impairment; consider drug interactions and altered pharmacodynamics
You are called to ED for a 25-year-old with suspected cervical spine injury after an RTC. How will you manage the airway?

Structure your answer around priorities: oxygenation, aspiration risk, and minimising cervical movement.

  • Preparation: full monitoring, suction, 2 IV lines, vasopressors drawn up; difficult airway plan + help; preoxygenate thoroughly
  • C-spine protection: collar loosened/removed for intubation with MILS; avoid excessive traction
  • Technique: videolaryngoscopy commonly first-line; consider awake fibreoptic if unstable fracture, anticipated difficulty, or need to maintain spontaneous ventilation
  • RSI: modified RSI as needed; gentle mask ventilation if desaturation risk; cricoid only if helpful and release if obstructing view
  • Drugs: induction titrated to haemodynamics; ketamine may support BP; paralysis with rocuronium (especially if >24–48 h post-injury) ± sugammadex
  • Post-intubation: confirm with capnography, secure tube, maintain MAP to support cord perfusion, analgesia/sedation, CXR and definitive imaging
Explain neurogenic shock. How do you diagnose and treat it, and how is it different from haemorrhagic shock?

A common FRCA viva: define, physiology, clinical features, and management.

  • Definition: distributive shock due to loss of sympathetic tone after SCI (classically above T6)
  • Features: hypotension + relative bradycardia, warm peripheries, low SVR; may have hypothermia
  • Differentiate: haemorrhage usually causes tachycardia, cool clammy skin, narrow pulse pressure; assume bleeding until excluded in trauma
  • Treatment: cautious fluids; early vasopressors (often noradrenaline); treat bradycardia (atropine/glycopyrrolate) and consider pacing if refractory
  • Goal: maintain spinal cord perfusion—avoid hypotension; consider MAP augmentation protocols (e.g. 85–90 mmHg) with ICU/spinal team
When is suxamethonium contraindicated after spinal cord injury, and why?

This is frequently examined as a physiology/pharmacology crossover.

  • Mechanism: denervation → upregulation of extrajunctional ACh receptors → massive K+ efflux with suxamethonium
  • Timing: risk rises after ~24 h (many quote 48 h) and persists for months (and longer with ongoing denervation/spasticity)
  • Consequence: life-threatening hyperkalaemia → arrhythmias/cardiac arrest
  • Alternative: rocuronium (RSI dose) with sugammadex availability if appropriate
Describe autonomic dysreflexia: who gets it, what triggers it, and how do you manage it intra-operatively?

Focus on recognition, immediate actions, and short-acting antihypertensives.

  • Population: chronic SCI above T6, after spinal shock resolves
  • Triggers: bladder distension/blocked catheter (commonest), bowel impaction, surgical stimulation below lesion, labour
  • Signs: sudden severe hypertension, headache, sweating/flushing above lesion, bradycardia/arrhythmias
  • Immediate management: stop stimulus, deepen anaesthesia/analgesia, check/drain bladder, sit up if awake, treat BP with GTN/nicardipine/nitroprusside
  • Prevention: adequate anaesthesia; neuraxial (spinal/epidural) can prevent AD for procedures below lesion when feasible
A patient with acute cervical SCI is for posterior fixation in the prone position. What are your key anaesthetic concerns?

Think: airway security, haemodynamics, positioning, blood loss, neuromonitoring, and post-op ventilation.

  • Airway: secure cuffed ETT, robust fixation; plan for difficult re-intubation; avoid neck movement during turns
  • Haemodynamics: avoid hypotension; arterial line; vasopressors ready; consider MAP augmentation targets
  • Positioning: eyes/face pressure, abdomen free, pressure points, brachial plexus protection; temperature management
  • Bleeding: anticipate significant blood loss; TXA/cell salvage if appropriate; maintain Hb, Ca2+, temperature
  • Neuromonitoring: if MEPs—TIVA, avoid/limit NMB; maintain MAP and normothermia
  • Post-op: extubation decision based on level of injury, respiratory function, swelling, duration, and haemodynamics; low threshold for ICU
What is spinal shock and how is it different from neurogenic shock?

Examiners want clear definitions and timelines.

  • Spinal shock: neurological phenomenon—transient loss of motor, sensory, and reflex activity below lesion; flaccid areflexia; resolves days–weeks
  • Neurogenic shock: haemodynamic phenomenon—loss of sympathetic tone causing hypotension and bradycardia (distributive shock), often with lesions above T6
  • They can coexist early after injury but are conceptually distinct
What MAP/BP targets would you aim for after acute traumatic SCI, and what is the rationale?

Answer should acknowledge protocol variation and risk-benefit.

  • Rationale: secondary injury is worsened by hypoperfusion; maintaining perfusion pressure may improve neurological outcome
  • Common target: MAP 85–90 mmHg for ~5–7 days (institution-dependent; evidence moderate/limited)
  • How: arterial line, avoid hypoxia/anaemia, vasopressors (often noradrenaline), cautious fluids; balance against bleeding, cardiac ischaemia, pulmonary oedema
Discuss the effects of SCI on anaesthetic drug responses and perioperative physiology.

Cover autonomic changes, NMB issues, and chronic complications.

  • Autonomic: impaired sympathetic responses → hypotension with induction, blunted tachycardia; temperature dysregulation
  • NMB: suxamethonium hyperkalaemia risk after 24–48 h; altered sensitivity to non-depolarisers—titrate with monitoring
  • Respiratory: reduced FRC/cough, secretion retention; higher aspiration risk; consider post-op ventilation
  • Chronic SCI: autonomic dysreflexia, spasticity meds (baclofen), chronic opioids/neuropathic agents, osteoporosis/fragility

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