Total Spinal Anaesthesia - MD Anaesthesia Exam Notes

Definition

• Miller's Anesthesia, 10e: "Intracranial spread of local anesthetic distinguishes a total spinal from a high spinal block."

Incidence

• Exact incidence is unclear - not categorised separately in NAP3 or major retrospective case series
• High neuraxial block complicates approximately 1 in 4,000 obstetric neuraxial anaesthetics (Barash 9e)
• More common context: accidental intrathecal injection during epidural/caudal anaesthesia, where drug volumes are 5-10x higher than spinal doses

Causes / Mechanisms

1. Spinal Anaesthesia (Primary Total Spinal)

• Excessive dose of intrathecal local anaesthetic
• Exaggerated spread of a standard dose due to patient/positional factors
• Use of wrong drug/concentration (medication error)

2. Epidural Anaesthesia - Accidental Intrathecal Injection

• Unrecognised dural puncture during epidural needle insertion
• Migration of an epidural catheter into the subarachnoid space (catheter migration)
• A full epidural dose injected intrathecally = 5-10x the spinal dose = catastrophic spread

3. Caudal Block

• Accidental subarachnoid injection during caudal block (especially in children)

4. Spinal After Failed Epidural ("Top-Up" Scenario)

• Drug already in epidural space from prior failed epidural adds to spread of subsequent spinal

5. Subdural Injection (related, but distinct)

• The subdural space extends intracranially; epidural volumes here can spread unpredictably - onset delayed 15-30 min, patchy block, may ascend to total spinal level

Risk Factors

Pathophysiology and Clinical Progression

Stage 1 - High Thoracic (T1-T4 block)

• Sympathetic blockade (T1-L2 fibres) -> profound hypotension (loss of vasoconstriction)
• Cardiac accelerator fibres (T1-T4) blocked -> bradycardia
• Risk of cardiac arrest (Bezold-Jarisch reflex + sympathectomy)

Stage 2 - Lower Cervical (C5-T1 block)

• Intercostal muscle paralysis -> reduced chest wall movement
• Tingling/weakness of hands and arms (patient can report this as warning sign)
• Dyspnoea, inability to take deep breath

Stage 3 - Upper Cervical (C3-C5 block)

• Phrenic nerve (C3-5) blocked -> diaphragmatic paralysis -> respiratory arrest
• Patient can only whisper (reduced vocal cord function)
• Inability to phonate/swallow

Stage 4 - Brainstem involvement (intracranial spread)

• Loss of consciousness
• Brainstem respiratory centre depression
• This is what makes it "total" spinal rather than just high spinal

Clinical Features Summary

Prevention

A. Technical Measures (During Spinal)

1. Use the minimum effective dose of local anaesthetic - avoid excessive volumes/concentrations
2. Baricity control - use isobaric solutions when sitting position needed; avoid inadvertent hyperbaric spread
3. Correct patient positioning - avoid Trendelenburg immediately after hyperbaric spinal (cephalad spread)
4. Avoid high injection level - use lower lumbar interspaces (L3-L4 or L4-L5)
5. Gentle, slow injection - reduces turbulence and erratic spread

B. Prevention During Epidural (Critical - most preventable cause)

1. Test dose - inject 3 mL of 1.5-2% lidocaine with 15 mcg adrenaline (epinephrine) before full epidural dose
   • Positive intrathecal test dose: rapid dense motor block within 2-3 minutes
   • Positive intravascular test dose: HR increase >20 bpm within 30-60 seconds
2. Aspiration before every injection - check for CSF or blood; "if in doubt, aspirate"
3. Incremental dosing - inject in 3-5 mL aliquots every 90-120 seconds
   • Morgan & Mikhail 7e: "Every dose is a test dose"
4. Confirm epidural catheter position - advance no more than 4-6 cm into space; single-orifice catheters
5. Recognise accidental dural puncture immediately and convert plan accordingly
6. After accidental dural puncture - if converting to spinal, use reduced spinal dose
7. Avoid re-dosing epidural without reassessment if patient returns from theatre to recovery

C. Obstetric-Specific Prevention

• Use lateral rather than sitting position for epidural placement (reduces epidural vein cannulation)
• Flush epidural needle with saline before catheter insertion
• Avoid catheter advancement >6 cm
• Recognise that epidural veins are more dilated in pregnancy (higher risk of vascular/intrathecal placement)
• Careful management of "top-up" doses for Caesarean section

Management

Immediate (0-2 minutes)

1. Call for help - activate emergency response, get senior anaesthetist + team
2. Reassure the conscious patient - psychological support is important (patient may be awake and terrified)
3. 100% oxygen by facemask immediately
4. Position - supine with left lateral tilt (if pregnant), or supine; avoid Trendelenburg (worsens hypotension and cerebral hypoperfusion) and avoid reverse Trendelenburg (reduces cerebral blood flow)
5. Flex patient's neck (Barash 9e) - may limit further cephalad spread of hyperbaric LA

Airway and Breathing

1. Assist ventilation with bag-mask if respiratory effort reduced
2. Rapid sequence intubation (RSI) if:
   • Loss of consciousness
   • Respiratory arrest
   • Unable to maintain airway
   • Inability to phonate (imminent respiratory failure)
3. Mechanical ventilation until block resolves

Circulation

1. IV fluid bolus - rapid crystalloid/colloid administration for preload
2. Vasopressors:
   • Phenylephrine 50-100 mcg IV boluses (or infusion) - vasopressor of choice in obstetrics
   • Ephedrine 6-12 mg IV boluses - mixed alpha/beta, useful if bradycardia co-exists
   • Norepinephrine 6 mcg IV bolus - alternative to phenylephrine (Barash 9e)
   • Epinephrine (adrenaline) - for cardiac arrest or refractory hypotension; Barash notes that delayed epinephrine administration in arrest cases led to uniformly poor neurological outcomes - give early if arrest occurs
3. Atropine 0.5-1 mg IV for bradycardia
4. Leg elevation - increases venous return
5. Left uterine displacement (obstetric patients) - relieves aortocaval compression

Cardiac Arrest (if occurs)

1. Commence CPR immediately
2. Epinephrine 1 mg IV as per ALS protocol - do not delay
3. If refractory - consider cardiopulmonary bypass (CPB)
4. Continue resuscitation: block is reversible - local anaesthetic effect will wear off (typically within 1-2 hours for bupivacaine, shorter for lidocaine)

Ongoing

1. Maintain anaesthesia if for surgery - patient needs general anaesthesia/sedation once intubated
2. Monitor - invasive arterial line if time permits, SpO2, ETCO2, ECG, urine output
3. ICU transfer post-resuscitation
4. Block will resolve - supportive care is the mainstay; no antidote exists

Duration and Resolution

• Resolution depends on the local anaesthetic used:
  • Lidocaine: 1-2 hours
  • Bupivacaine: 2-4+ hours
• All effects are reversible once drug dissipates from neural tissue

Key Differentials (Exam Point)

Memory Aid for Management - "ABCDE + P"

• Airway - RSI if LOC or respiratory failure
• Breathing - BVM assist, then ventilate
• Circulation - fluids + vasopressors (ephedrine/phenylephrine/adrenaline)
• Drugs - atropine for bradycardia, epinephrine for arrest
• Elevate legs + left tilt (obstetrics)
• Psychological support + reassure if conscious

Sources

• Miller's Anesthesia, 10e - "Total Spinal" (p. 6127)
• Morgan & Mikhail's Clinical Anesthesiology, 7e - "C. Total Spinal Anesthesia" (p. 1850)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9e - "High Block/Total Subarachnoid Spinal Block" (p. 2865)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9e - "Total Spinal Anesthesia" (p. 3504)

Recent evidence note: A 2026 prospective national observational study (Lucas et al., Anaesthesia, PMID 40991953) on high neuraxial block in UK obstetric practice provides the latest incidence and risk factor data - worth citing in a viva context. OAA 2024 guidelines (PMID 39327940) address intrathecal catheter management after inadvertent dural puncture.

Physiological Changes After Initiating Epidural Anaesthesia

MS Anaesthesia Exam Notes

Overview - The Fundamental Mechanism

• Sympathetic preganglionic fibres (T1-L2) are the smallest, most sensitive fibres - they are blocked first and at the lowest local anaesthetic concentrations
• Parasympathetic efferents exit via cranial nerves (especially vagus, CN X) and sacral nerves (S2-S4) - the vagus nerve is NOT blocked by neuraxial anaesthesia
• Therefore all effects = decreased sympathetic tone + unopposed parasympathetic tone

Key Epidural vs. Spinal Difference (Exam Favourite)

• In spinal anaesthesia: there is a "zone of differential sympathetic blockade" extending 2-6 segments above the sensory level
• In epidural anaesthesia: no such zone exists - the sympathetic block level approximates the sensory block level (Goodman & Gilman)
• Therefore epidural cardiovascular effects develop more gradually as drug spreads, allowing compensatory responses

Differential Blockade Order (Exam Favourite)

• Sympathetic block extends 2 segments above sensory level
• Sensory block (pinprick) extends 2 segments above motor block

1. CARDIOVASCULAR SYSTEM

A. Hypotension

1. Venodilation (dominant effect) - sympathetic block relaxes venous capacitance vessels (T5-L1) -> blood pools in splanchnic circulation and lower limbs -> decreased venous return -> decreased preload -> decreased cardiac output
2. Arterial vasodilation - loss of arteriolar tone -> decreased systemic vascular resistance (SVR)
3. Compensatory vasoconstriction fails if block is high (T4+) - normally unblocked segments above the block constrict to compensate; with high block this compensation is lost

• Pregnancy (aortocaval compression, high epidural vascularity)
• Hypovolaemia
• Advanced age
• Obesity
• Concurrent general anaesthesia
• Sensory level above T6
• Faster onset and more extensive block

B. Bradycardia

1. Cardiac accelerator fibre block (T1-T4): when block reaches upper thoracic levels, sympathetic fibres to the sinoatrial node are blocked -> vagal predominance -> HR falls
2. Bezold-Jarisch reflex: decreased venous return (from venodilation) -> decreased ventricular filling -> activates 5-HT3 receptors in ventricular myocardium and vagus nerve -> efferent vagal signalling -> paradoxical bradycardia + worsened hypotension (a dangerous positive feedback loop)
3. Bradycardia (HR ≤45 bpm) is more common in males (Barash 9e)

C. Cardiac Output

• Complex: CO may increase initially due to reduced afterload (SVR falls)
• But if venous return falls severely (preload effect dominant), CO decreases
• Net effect depends on extent of block and fluid management

D. What is Preserved

• Compensatory vasoconstriction above the block level (if block is low/mid-thoracic)
• Autoregulation of coronary blood flow (largely maintained at normal perfusion pressures)

2. RESPIRATORY SYSTEM

A. Minimal effect in normal patients

• The diaphragm is innervated by the phrenic nerve (C3-C5) - not affected by lumbar or thoracic epidurals
• Tidal volume - unchanged even with high thoracic levels
• Vital capacity - only a small decrease, due to loss of abdominal muscle contribution to forced expiration (not inspiratory volume)

B. Effects that do occur

C. High epidural (cervical levels)

• If LA reaches C3-C5 -> phrenic nerve block -> diaphragmatic paralysis -> respiratory failure

D. Patients at risk

• Severe COPD/restrictive lung disease who rely on accessory muscles (intercostal, abdominal) for breathing - high epidurals can precipitate respiratory failure in these patients

E. Benefit in chronic lung disease patients (post-op)

• Thoracic epidural analgesia post upper abdominal/thoracic surgery: decreases incidence of pneumonia and respiratory failure, improves oxygenation, decreases duration of mechanical ventilation (Morgan & Mikhail 7e)

3. GASTROINTESTINAL SYSTEM

A. Gut motility

• Sympathetic block (T5-L1) -> unopposed vagal (parasympathetic) dominance -> increased peristalsis
• Gut is small, contracted, with active peristalsis - actually improves operative conditions for bowel surgery
• This is why epidural anaesthesia is used as an adjunct in colorectal surgery

B. Return of bowel function (Post-op)

• Postoperative epidural analgesia with local anaesthetics (not just opioids) hastens return of GI function after open abdominal procedures - key advantage over systemic opioids which suppress peristalsis

C. Hepatic blood flow

• Decreases proportionally with mean arterial pressure (MAP) reduction - not unique to epidural; applies to any hypotensive technique
• Liver autoregulation is limited compared to kidney

D. Nausea and vomiting

• Common with epidural anaesthesia, especially with hypotension
• Mechanism: gut hyperperfusion due to vasodilation + vagal dominance + brainstem effects

4. RENAL SYSTEM

• Renal blood flow is maintained by autoregulation within a wide MAP range (70-180 mmHg) - minimal effect on kidney function if normotension maintained
• Neuraxial block at lumbar and sacral levels (L1-S4) blocks both sympathetic and parasympathetic control of the bladder
• Result: urinary retention - loss of autonomic bladder tone until block wears off
• Patients unable to void post-neuraxial anaesthesia require urinary catheterisation

5. NEUROENDOCRINE / METABOLIC SYSTEM (Major Exam Topic)

A. Stress Response Attenuation

• ACTH and cortisol (HPA axis)
• Adrenaline and noradrenaline (adrenal medulla)
• Vasopressin (ADH)
• Renin-angiotensin-aldosterone system (RAAS)
• Growth hormone
• Glucagon

B. Conditions for maximum blunting:

• Block must precede incision AND continue postoperatively
• More effective for lower limb surgery (complete block of afferents) than upper abdominal/thoracic surgery (incomplete block of visceral afferents via vagus)

C. Glucose metabolism

• Epidural anaesthesia attenuates stress hyperglycaemia - beneficial in diabetic patients
• Avoids catecholamine-driven glycogenolysis and gluconeogenesis

6. THERMOREGULATION

• Sympathetic block causes peripheral vasodilation in blocked segments -> heat redistribution from core to periphery -> core temperature falls (redistribution hypothermia)
• Patients may feel warm (due to vasodilation) while their core temperature is actually dropping
• Shivering may occur (a thermoregulatory response to falling core temperature) - common complication during epidural
• Shivering mechanism: Blocked afferent thermal signals confuse hypothalamic thermoregulation; epidural opioids (pethidine) can treat shivering

7. COAGULATION / HAEMATOLOGICAL

• Reduced DVT/PE risk: epidural anaesthesia associated with decreased incidence of deep vein thrombosis and pulmonary embolism
• Mechanism: increased lower limb blood flow (vasodilation), reduced platelet aggregation, and reduced stress response-mediated coagulation activation
• Clinical benefit particularly demonstrated in lower limb joint replacement surgery

8. IMMUNOLOGICAL

• Partial attenuation of surgery-induced immunosuppression
• Reduced cortisol and catecholamine surges -> less suppression of NK cell function and cellular immunity
• May have implications for cancer surgery (area of ongoing research)

Summary Table for Exam Revision

Epidural-Specific vs. Spinal Differences (Exam Favourite Comparison)

Sources

• Morgan & Mikhail's Clinical Anesthesiology, 7e - "Cardiovascular Manifestations," "Pulmonary Manifestations," "Gastrointestinal Manifestations," "Urinary Tract Manifestations," "Metabolic & Endocrine Manifestations" (pp. 1802-1805)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9e - "Cardiovascular System," "Respiratory System," "Epidural" (pp. 2853-2858)
• Goodman & Gilman's Pharmacological Basis of Therapeutics - "Epidural Anaesthesia" - differential sympathetic blockade comparison