Spinal Cord Injury Anaesthesia

Quick Answer

What are the critical anaesthetic considerations in patients with chronic spinal cord injury?

Spinal cord injury (SCI) patients present unique challenges due to autonomic denervation, altered drug responses, and multisystem complications. Key principles:

1. Contraindications - Suxamethonium absolutely contraindicated after 24-72 hours up to 12 months+ post-injury (risk of fatal hyperkalaemia from upregulated acetylcholine receptors)
2. Cardiovascular instability - Neurogenic hypotension and bradycardia from sympathetic denervation; avoid hypotension aggressively
3. Autonomic dysreflexia - Life-threatening hypertensive crisis from noxious stimuli below injury level; prevention and rapid treatment essential
4. Temperature dysregulation - Poikilothermia (cannot regulate temperature); active warming mandatory
5. Respiratory compromise - Reduced vital capacity, weak cough, aspiration risk; careful extubation planning
6. Positioning - Careful spinal precautions; pressure injury risk
7. Thromboembolism - High risk; prophylaxis essential

Clinical Pearl: After SCI, denervation of muscle causes upregulation of acetylcholine receptors spreading beyond the neuromuscular junction. Suxamethonium depolarises all these receptors simultaneously, causing massive potassium efflux (up to 10-12 mmol/L rise) and cardiac arrest. Never use suxamethonium in SCI patients >24-72 hours old without specific ICU indication and preparation.

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Clinical Overview

Epidemiology

Global and Australian burden:

Aetiology:

Australian context:

• 350-400 new SCI cases annually
• Leading causes: transport (46%), falls (30%) [4]
• High rates in rural/remote areas (motor vehicle trauma)
• Average age increasing (older population falls)

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Pathophysiology of Spinal Cord Injury

Acute Phase (Spinal Shock)

Definition:

• Complete flaccid paralysis and areflexia below injury level
• Occurs immediately after injury
• Duration: Days to weeks (typically 7-20 days)
• Resolves as reflexes return (often exaggerated)

Cardiovascular effects:

Neurogenic shock vs hypovolaemic shock:

Duration of acute phase considerations:

• Complete injuries: Longer duration (weeks to months)
• Incomplete injuries: Shorter duration (days to weeks)
• Return of reflexes indicates end of spinal shock
• Autonomic dysreflexia cannot occur until reflexes return

Chronic Phase

Autonomic dysfunction:

• Sympathetic denervation below injury level
• Unopposed parasympathetic activity (vagal predominance)
• Loss of descending inhibitory control
• Exaggerated reflex responses

Muscle changes:

• Atrophy below injury level
• Upregulation of acetylcholine receptors (extrajunctional)
• Sensitivity to depolarising neuromuscular blockers (suxamethonium)
• Resistance to non-depolarising NMBAs

Cardiovascular adaptations:

• Chronic reduction in sympathetic tone
• Reduced plasma volume (venous pooling)
• Exercise-induced hypotension
• Autonomic dysreflexia capability returns

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Critical Anaesthetic Considerations

1. Suxamethonium Contraindication

Pathophysiology:

Mechanism of hyperkalaemia:

1. Denervation causes upregulation of nicotinic acetylcholine receptors
2. Receptors spread across entire muscle membrane (not just junction)
3. Suxamethonium depolarises ALL receptors simultaneously
4. Massive efflux of potassium from muscle cells
5. Serum potassium can rise by 5-10 mmol/L
6. Cardiac arrest from hyperkalaemia

Evidence:

• Case reports of cardiac arrest with suxamethonium in SCI [5,6]
• Upregulation documented within 48 hours of denervation [7]
• Risk persists for at least 12 months, possibly lifelong in complete injuries

Safe alternatives:

• Rocuronium (rapid onset with sugammadex reversal)
• Atracurium/cisatracurium
• Vecuronium
• High-dose rocuronium (1.2 mg/kg) for RSI

If absolutely necessary (rare scenarios):

• Defibrillation pads applied
• Calcium gluconate/chloride available
• Insulin/glucose, salbutamol for K+ management
• Haemodialysis capability
• NOT recommended unless life-threatening airway emergency with no alternatives

2. Autonomic Dysreflexia (AD)

Definition:

• Life-threatening hypertensive emergency
• Occurs in injuries at T6 and above
• Triggered by noxious stimuli below injury level
• Results in paroxysmal hypertension, bradycardia, headache, sweating

Pathophysiology:

1. Noxious stimulus below lesion (bladder distension, bowel distension, pressure sore, uterine contraction, surgery)
2. Reflex sympathetic activation below lesion (intact spinal reflex arc)
3. Vasoconstriction and hypertension below lesion
4. Baroreceptors detect hypertension above lesion
5. Brain attempts to inhibit sympathetic outflow (via damaged cord - ineffective below lesion)
6. Brain increases vagal outflow (intact vagus) causing bradycardia and vasodilation above lesion
7. Result: Severe hypertension below, normal/low pressure above, pounding headache, nasal congestion, sweating above lesion, pale cool skin below

Triggers:

Clinical features:

Management:

Prevention:

• Empty bladder preoperatively
• Bowel regimen optimised
• Adequate anaesthesia/analgesia
• Preventive GTN patch
• Spinal/epidural anaesthesia (blocks reflex arc)

Anaesthetic technique considerations:

Clinical Pearl: General anaesthesia does NOT prevent autonomic dysreflexia because the reflex arc is entirely within the spinal cord below the lesion. The patient may not feel pain, but the reflex sympathetic activation still occurs. Regional anaesthesia (spinal/epidural) is the most effective prevention as it blocks the reflex arc at the spinal level.

3. Cardiovascular Instability

Preoperative assessment:

Intraoperative management:

Hypotension management:

Bradycardia management:

Specific scenarios:

• Tracheal suctioning: Can provoke severe bradycardia (vagal) - pre-treat with atropine
• Laryngoscopy: Same risk - atropine 0.6 mg IV pre-intubation
• Peritoneal traction: Vagal response

4. Temperature Dysregulation

Pathophysiology:

• Loss of sympathetic innervation to skin below lesion
• Cannot vasoconstrict or vasodilate below lesion
• Cannot sweat or shiver below lesion
• Poikilothermia (body temperature tracks ambient temperature)
• "Quad belly" (paralysed abdominal muscles) - heat loss from large surface area

Consequences:

• Hypothermia in cold environments (theatre)
• Hyperthermia in warm environments
• Masked infection (cannot mount fever)
• Malignant hyperthermia difficult to diagnose (cannot increase temperature)

Management:

Anaesthetic implications:

• Propofol/volatiles impair thermoregulation further
• Neuromuscular blockade prevents shivering
• Warm theatre essential (24-26°C for SCI patients)
• Warm all IV fluids
• Bair Hugger/forced air warmer mandatory

5. Respiratory Considerations

Level of injury and respiratory function:

Specific respiratory risks:

Intubation/extubation considerations:

• Risk aspiration (gastric stasis)
• RSI with cricoid pressure may be needed
• Consider awake fibreoptic if difficult airway
• Extubate when fully awake, following commands
• Non-invasive ventilation (NIV) may be needed postoperatively
• Cough assist devices in ICU

6. Pharmacological Alterations

Drug responses altered:

Dosing recommendations:

• Rocuronium: 0.6-1.2 mg/kg (higher dose for faster onset)
• Atracurium: 0.5 mg/kg; normal dosing
• Neostigmine: Standard dose BUT give with glycopyrrolate (not atropine - lasts longer)
• Morphine/fentanyl: Reduced doses; careful monitoring

7. Thromboembolism Risk

High risk:

• DVT: 40-80% without prophylaxis
• PE: 5-10% without prophylaxis
• Peak risk: 7-14 days post-injury

Prophylaxis:

Perioperative management:

• Continue mechanical prophylaxis
• Timing of LMWH around surgery (discuss with surgeon)
• Early mobilisation when possible
• Pneumatic compression boots intraoperatively

8. Other Considerations

Pressure injuries:

• High risk (anaesthesia, reduced sensation, poor nutrition)
• Positioning: Padding at all pressure points
• Regular repositioning (intraoperative)
• Pressure-relieving mattress

Gastrointestinal:

• Gastric stasis common
• Reduced gastric emptying
• Aspiration risk - RSI with cricoid
• Consider nasogastric tube
• Stress ulcer prophylaxis

Urinary:

• Neurogenic bladder
• Intermittent catheterisation programme
• Ensure empty before surgery
• UTI common - check urine culture if febrile

Musculoskeletal:

• Osteoporosis (immobility) - fracture risk with positioning
• Heterotopic ossification (spasticity)
• Contractures - careful positioning
• Spasticity - may continue antispasmodics (baclofen, tizanidine)

Psychological:

• Depression common
• Anxiety about surgery
• Body image concerns
• Sexual dysfunction (discuss if relevant to surgery)
• Previous negative experiences with healthcare

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Regional Anaesthesia in SCI

Advantages:

• Blocks autonomic dysreflexia reflex arc
• Excellent analgesia
• Reduces opioid requirements
• Spasticity reduction
• May improve postoperative ileus

Considerations:

• Difficult to assess block level (sensory loss already present)
• Risk of hypotension (may be profound)
• Spinal deformity may make technique difficult
• Autonomic dysreflexia already risk
• Pre-existing back surgery (hardware)

Technique:

• Spinal or epidural
• Reduced local anaesthetic dose (sensory loss already present)
• Careful haemodynamic monitoring
• Treat hypotension promptly
• Caudal block for perineal procedures

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Patients

Disproportionate injury burden:

Challenges in chronic SCI management:

Cultural considerations:

Practical strategies:

1. Travel support - PATS funding; accommodation for family
2. Equipment provision - Ensure discharge with appropriate equipment
3. Remote care planning - Telehealth where possible; visiting specialist services
4. Cultural liaison - ALO involvement in rehabilitation planning
5. Community follow-up - Coordinate with remote health services for catheter care, pressure area monitoring

Māori Health (Aotearoa New Zealand)

Epidemiology:

• Higher rates of traumatic SCI in Māori population
• Younger age at injury
• Higher proportion from transport accidents and violence

Whānau considerations:

• Extended whānau involvement in care
• Marae-based rehabilitation in some regions
• Whānau ora approach to holistic care

Cultural safety:

• Māori Health Worker involvement
• Karakia offered
• Recognition of te reo Māori as official language
• Whānau accommodation near spinal unit (Burwood, Auckland)

Te Tiriti obligations:

• Equity of access to SCI services
• Culturally appropriate rehabilitation
• Māori workforce development
• Address disparities in injury rates and outcomes

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ANZCA Final Examination Focus

High-Yield Topics

Written examination:

Viva scenarios:

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Assessment Content

SAQ 1: Suxamethonium in Spinal Cord Injury (20 marks)

Question:

A 35-year-old man with a T4 complete spinal cord injury sustained 6 months ago presents for emergency appendicectomy. He is haemodynamically stable. The anaesthetic registrar suggests using suxamethonium for rapid sequence induction.

a) Why is suxamethonium contraindicated in this patient, and what is the pathophysiological mechanism? (8 marks)

b) What alternatives would you recommend for rapid sequence induction? (4 marks)

c) What other specific anaesthetic considerations are relevant for this patient undergoing general anaesthesia? (8 marks)

Model Answer:

a) Suxamethonium Contraindication (8 marks):

Contraindication status (2 marks):

• Absolutely contraindicated in this patient
• Injury >6 months old - well within high-risk period
• Risk period: 24-72 hours post-injury up to 12+ months (possibly lifelong for complete injuries)

Pathophysiological mechanism (6 marks):

• Denervation of skeletal muscle below T4 causes upregulation of nicotinic acetylcholine receptors
• Receptors proliferate across the entire muscle membrane (extrajunctional receptors)
• Normally receptors concentrated at neuromuscular junction only
• Suxamethonium (depolarising NMBA) binds to ALL upregulated receptors simultaneously
• Causes massive depolarisation of muscle membrane
• Potassium efflux from cells into circulation (normally 0.5 mmol/L rise)
• In SCI: Potassium rise 5-10 mmol/L (to potentially fatal levels >8-10 mmol/L)
• Risk of ventricular arrhythmia, cardiac arrest, death
• Evidence: Multiple case reports of cardiac arrest with suxamethonium in SCI patients

b) Alternatives for RSI (4 marks):

Preferred option (2 marks):

• Rocuronium 1.2 mg/kg (high-dose RSI dose)
• Sugammadex 16 mg/kg available for immediate reversal if needed
• Onset comparable to suxamethonium (60-90 seconds)
• No hyperkalaemia risk

Alternative options (2 marks):

• Rocuronium 0.6-1.0 mg/kg with continued mask ventilation until intubating conditions achieved
• Atracurium 0.5 mg/kg (slower onset - 3-4 minutes)
• If failed intubation: Continue mask ventilation, wake patient, proceed with awake fibreoptic

c) Specific Considerations (8 marks):

Cardiovascular (2 marks):

• Baseline BP likely low (90-100/60); maintain near baseline, not "normal" 120/80
• Risk of severe bradycardia with intubation/surgery - atropine 0.6 mg IV available
• Risk of autonomic dysreflexia (T4 injury susceptible) - ensure deep anaesthesia
• Treat hypotension promptly with fluids and vasopressors

Respiratory (2 marks):

• Reduced vital capacity (T4 level approximately 50-70% normal)
• Weak cough, poor respiratory reserve
• Aspiration risk from gastric stasis - RSI with cricoid pressure
• Extubation when fully awake, following commands
• Consider postoperative NIV if any respiratory compromise

Temperature (2 marks):

• Poikilothermia - cannot regulate temperature below T4
• Forced air warming essential; warm fluids; warm theatre
• Monitor core temperature

Other (2 marks):

• DVT prophylaxis - mechanical during surgery; LMWH postop
• Pressure care - careful padding; repositioning
• Reduced drug doses for some agents (opioids - respiratory depression)
• Ensure bladder emptied before surgery (prevents AD trigger)
• Continue home medications (antispasmodics)

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SAQ 2: Autonomic Dysreflexia (20 marks)

Question:

A 28-year-old man with a C6 complete spinal cord injury is undergoing cystoscopy under general anaesthesia. Ten minutes into the procedure, his blood pressure suddenly increases from 105/65 to 210/120 mmHg. His heart rate decreases from 72 to 42 bpm.

a) What is the diagnosis, and what is the underlying pathophysiology? (6 marks)

b) What are the immediate steps in management? (6 marks)

c) What preventive strategies could have been employed? (4 marks)

d) Why did the blood pressure and heart rate change in opposite directions? (4 marks)

Model Answer:

a) Diagnosis and Pathophysiology (6 marks):

Diagnosis (2 marks):

• Autonomic dysreflexia (AD)
• Occurs in spinal cord injury at T6 and above
• Medical emergency - can cause ICH, seizures, cardiac arrest if untreated

Pathophysiology (4 marks):

• Trigger: Noxious stimulus below C6 (likely bladder distension/instrumentation)
• Reflex sympathetic activation via intact spinal reflex arc below lesion
• Massive vasoconstriction and hypertension below C6 level
• Baroreceptors above lesion detect hypertension
• Brain attempts to inhibit sympathetic outflow via damaged cord (ineffective below lesion)
• Brain increases parasympathetic (vagal) outflow via intact cranial nerves
• Result: Hypertension below, normal/low pressure above, bradycardia, headache, sweating above lesion

b) Immediate Management (6 marks):

Immediate actions (3 marks):

1. Sit patient up immediately (reduces cerebral perfusion; promotes venous pooling)
2. Check and remove stimulus:
   • Check bladder (drain if distended)
   • Check bowel
   • Loosen tight clothing/tourniquets
   • Check for pressure areas
3. Ensure adequate depth of anaesthesia (deepen if light)

Pharmacological (2 marks):

• Rapid-acting antihypertensive:
  • Nifedipine 10 mg (bite and swallow/sublingual) OR
  • GTN spray 400 mcg sublingual OR
  • Hydralazine 10-20 mg IV OR
  • Labetalol 20 mg IV (avoid if bradycardic)
• Avoid long-acting agents (risk of hypotension when stimulus removed)

Monitoring (1 mark):

• Continuous BP monitoring (every 2-5 minutes)
• ECG (watch for arrhythmias)
• Target BP <160/90 initially, then normalise gradually

c) Preventive Strategies (4 marks):

Preoperative (2 marks):

• Ensure bladder empty (catheterise if needed)
• Optimise bowel regimen (constipation increases risk)
• Check for and treat UTI
• Check for pressure areas

Intraoperative (2 marks):

• Adequate depth of general anaesthesia
• Consider spinal or epidural anaesthesia (blocks reflex arc at spinal level - most effective prevention)
• Regional + GA combination
• Topical/injected local anaesthesia at surgical site
• GTN patch prophylaxis (5-10 mg)

d) Explanation of BP/HR Changes (4 marks):

Blood pressure rise (2 marks):

• Noxious stimulus below C6 triggers reflex sympathetic activation
• Intact spinal reflex arc below lesion causes massive noradrenaline release
• Vasoconstriction below lesion causes severe hypertension

Heart rate fall (2 marks):

• Baroreceptors (carotid, aortic arch) detect hypertension
• Signals to brain via glossopharyngeal and vagus nerves (intact above lesion)
• Brain responds by increasing vagal (parasympathetic) tone to heart
• Vagal stimulation slows heart rate (bradycardia)
• This is the normal baroreceptor reflex response to hypertension
• The apparent paradox (high BP, low HR) reflects intact vagal response above lesion and loss of descending sympathetic inhibition

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Viva Scenario: Anaesthesia for Chronic SCI Patient

Scenario:

You are assessing a 42-year-old man with a C5 complete spinal cord injury from a diving accident 5 years ago, scheduled for perineal pressure sore debridement. He is wheelchair-dependent with an indwelling catheter.

Examiner: "What are the key considerations for anaesthetising this patient?"

Candidate Response:

"I would approach this systematically, considering the multisystem effects of chronic spinal cord injury:

Airway and general anaesthesia considerations: The first critical point is that suxamethonium is absolutely contraindicated. At 5 years post-injury, this patient has upregulated acetylcholine receptors throughout his denervated muscle below C5. Suxamethonium would cause massive hyperkalaemia and potential cardiac arrest. I would use rocuronium if muscle relaxation needed, or preferably avoid NMBAs and use deep volatile or TIVA technique.

Autonomic dysreflexia risk: This is a C5 injury - well above T6 - so he's at high risk for autonomic dysreflexia. The stimulus from perineal surgery is exactly the type that triggers AD. General anaesthesia alone won't prevent it because the reflex arc is entirely within the spinal cord below the lesion. I would strongly recommend either spinal or epidural anaesthesia to block the reflex arc, or combined GA + regional. If using GA alone, I'd need deep anaesthesia and have immediate access to antihypertensives.

Cardiovascular instability: He likely has baseline hypotension from sympathetic denervation - perhaps 90-100 systolic. I need to maintain his normal pressure rather than aiming for 120. Bradycardia is common - atropine should be drawn up. Any noxious stimulus like laryngoscopy could trigger severe bradycardia.

Respiratory considerations: At C5, he has diaphragm function (C3-C5) but no intercostals. His vital capacity is probably 30-50% of predicted. I need to be careful with respiratory depressants and have a low threshold for postoperative ventilation if needed.

Temperature management: He'll be poikilothermic - can't regulate temperature below C5. I need active warming (forced air warmer), warmed fluids, warm theatre, and temperature monitoring.

Other considerations: His bladder catheter should be checked and emptied preoperatively - a distended bladder is a major AD trigger. DVT prophylaxis with mechanical methods intraoperatively. Positioning needs care for pressure areas. Gastric stasis means aspiration risk.

Technique: I'd prefer spinal anaesthesia for this case - it blocks the AD reflex arc, provides excellent operating conditions, and reduces systemic complications. If GA required, I'd use TIVA with careful haemodynamic management."

Examiner: "Why is general anaesthesia alone not sufficient to prevent autonomic dysreflexia?"

Candidate:

"General anaesthesia prevents the patient from perceiving pain, but autonomic dysreflexia is a spinal reflex that doesn't require brain involvement. The reflex arc consists of:

1. Afferent sensory input from below the lesion travels to the spinal cord
2. Integration at the spinal level (below C5 in this case)
3. Efferent sympathetic outflow causing vasoconstriction below the lesion

The brain is bypassed in this reflex. Even though the patient is unconscious, the spinal cord below C5 is intact and functional - it receives the sensory input and triggers the sympathetic response. The patient may not feel pain, but the hypertension, bradycardia, and sweating still occur.

Only regional anaesthesia (spinal or epidural) blocks this reflex at the spinal cord level by interrupting either the afferent input or the efferent sympathetic output. That's why regional is the gold standard for preventing AD in susceptible patients."

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