Spinal cord injury

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