High spinal / total spinal

Surgical approach (context)

Not an operation: this is a neuraxial anaesthetic complication.
Typical setting: obstetric (labour epidural top-up for CS), orthopaedic/vascular/lower abdominal surgery under spinal, or epidural analgesia with accidental intrathecal/intravenous dosing.

Anaesthetic management (context of cases where it occurs)

Type of anaesthesia: neuraxial (spinal/epidural/CSE); may convert to GA if high/total spinal develops.
Airway: may require rapid airway support; often ETT if apnoea/unconsciousness or for controlled ventilation; SGA may be a temporising option in selected fasted, low aspiration-risk patients but obstetrics usually ETT.
Duration: depends on local anaesthetic dose and baricity; severe symptoms can occur within minutes; recovery typically parallels spinal regression (often 30–120+ min). In inadvertent intrathecal epidural dose, may be prolonged (hours).
How painful: the problem is physiological collapse rather than pain; patient may be comfortable but frightened/dyspnoeic; surgery may be painless but awareness can occur if sedation/GA not managed carefully.

Definition and spectrum

High spinal: excessive cephalad spread of neuraxial block causing significant hypotension ± bradycardia, dyspnoea, upper limb/hand paraesthesia/weakness.
Total spinal: profound sympathetic, motor and sensory block with severe hypotension, bradycardia/asystole, respiratory insufficiency/apnoea, loss of consciousness.
Mechanisms: high intrathecal dose, unrecognised intrathecal catheter, subdural injection, rapid epidural top-up with unrecognised intrathecal placement, patient factors and positioning affecting spread.

Aetiology / risk factors

Drug/dose factors: excessive intrathecal dose; high concentration/volume; rapid epidural top-up; opioid adjuncts may worsen respiratory depression but primary issue is neuraxial block.
Technique errors: unrecognised intrathecal epidural catheter; accidental intrathecal injection during epidural top-up; subdural placement (patchy, delayed, unexpectedly high sensory level).
Patient factors: pregnancy (reduced CSF volume, engorged epidural veins), short stature, obesity, spinal deformity, extremes of age, hypovolaemia.
Positioning: head-down tilt after spinal; supine position with aortocaval compression in pregnancy; rapid changes in position soon after injection.

Pathophysiology (what causes collapse)

Sympathetic block: vasodilation (venous > arterial) → reduced venous return/preload → hypotension; reduced SVR; reduced coronary perfusion.
Cardiac accelerator fibres (T1–T4): blockade → bradycardia, reduced contractility; vagal predominance; can progress to asystole.
Respiratory effects: intercostal paralysis (T1–T11) reduces chest wall mechanics; high block may impair accessory muscles; apnoea usually from brainstem hypoperfusion/unconsciousness rather than phrenic nerve block (C3–5) but very high spread can contribute.
Consciousness: cerebral hypoperfusion from severe hypotension → agitation, nausea, then LOC.

Clinical features and diagnosis

Early symptoms: nausea, dizziness, anxiety, dyspnoea, difficulty speaking, tingling/numb hands, weakness in arms.
Signs: rapidly falling BP, bradycardia, pallor, diaphoresis; high sensory level; upper limb weakness; reduced tidal volume; desaturation late.
Total spinal: profound hypotension, severe bradycardia/asystole, apnoea, unresponsiveness, dilated pupils may occur (hypoperfusion).
Differentiate from: local anaesthetic systemic toxicity (tinnitus, metallic taste, seizures, ventricular arrhythmias), anaphylaxis (bronchospasm, rash, angioedema), pulmonary embolus/amniotic fluid embolism (sudden hypoxia, RV strain), haemorrhage, high block vs panic/hyperventilation.
- Key discriminator: high/total spinal usually follows neuraxial dosing with rapidly rising sensory/motor block and predominant hypotension/bradycardia.

Immediate management (structured approach)

Call for help early: senior anaesthetist, ODP, obstetric/ICU support; declare emergency.
A: Airway: reassure; jaw thrust; prepare for intubation if reduced consciousness, apnoea, or inability to protect airway.
B: Breathing: high-flow O2; assist ventilation with bag-mask; early controlled ventilation if deteriorating; consider capnography once ventilating.
C: Circulation: left uterine displacement in pregnancy; stop neuraxial dosing; rapid IV fluids (crystalloid bolus) while preparing vasopressors; treat bradycardia and hypotension aggressively.
Vasopressors: phenylephrine for hypotension with tachycardia; ephedrine if hypotension with bradycardia; adrenaline for severe bradycardia/hypotension or impending arrest.
- Typical bolus dosing (adult): phenylephrine 50–100 micrograms IV; ephedrine 3–6 mg IV; atropine 500 micrograms IV for bradycardia; adrenaline 10–100 micrograms IV titrated for peri-arrest hypotension/bradycardia.
If cardiac arrest: start ALS immediately; treat as reversible cause (high neuraxial block); early adrenaline 1 mg IV per ALS; high-quality CPR; consider early intubation; in obstetrics follow maternal ALS with LUD and consider perimortem CS if indicated.
D: Disability: assess level of block; manage agitation; avoid heavy sedation without airway control; consider GA if surgery ongoing or patient distressed/ventilatory failure.
E: Exposure/monitoring: continuous ECG, NIBP (cycle frequently), SpO2; consider arterial line if unstable; temperature; document times, drugs, sensory level.

Airway/anaesthesia strategy once stabilising

Indications to intubate: apnoea/hypoventilation, reduced consciousness, inability to speak, persistent severe hypotension requiring high-dose vasopressors, ongoing surgery requiring immobility/controlled ventilation.
Induction: treat hypotension first where possible; use reduced induction doses; ketamine or etomidate may be haemodynamically favourable; consider RSI in obstetrics (aspiration risk).
Maintenance: volatile/TIVA with caution (vasodilation); opioid sparing may be possible due to dense neuraxial block; ensure amnesia/analgesia if converting to GA to avoid awareness.
Ventilation: controlled ventilation with capnography; anticipate low ventilatory requirements initially; monitor for return of spontaneous effort as block regresses.

Obstetric specifics

Aortocaval compression worsens hypotension: immediate left uterine displacement; consider manual displacement if tilt inadequate.
Fetal considerations: maternal resuscitation is priority; inform obstetric/neonatal team; prepare for urgent delivery if maternal instability persists.
Vasopressor choice: phenylephrine commonly first-line for spinal hypotension; in severe high/total spinal with bradycardia, adrenaline may be required.

Prevention

Correct dosing: use appropriate intrathecal dose; adjust for pregnancy, height, age; avoid unnecessary head-down tilt.
Epidural top-ups: fractionate doses; aspirate before dosing; use test dose where appropriate; observe closely after each increment; be cautious after recent spinal/CSE.
Catheter safety: label neuraxial catheters; clear documentation; avoid IV misconnections; consider dedicated neuraxial connectors; staff education.
Monitoring: continuous monitoring after neuraxial dosing; frequent BP cycling (e.g., every 1–2 min initially in high-risk situations).
Prophylaxis for spinal hypotension: left uterine displacement, vasopressor infusion (e.g., phenylephrine) and co-load with crystalloid in obstetrics as per local policy.

Aftercare and follow-up

Post-event monitoring: HDU/ICU if significant cardiovascular/respiratory compromise, high vasopressor requirement, or prolonged ventilation.
Documentation and communication: clear explanation to patient; duty of candour; incident reporting; debrief team; consider anaesthetic chart review and governance learning.
Exclude alternative diagnoses if atypical: ECG/troponin if ischaemia suspected; consider LAST/anaphylaxis/PE depending on presentation; check neuraxial catheter position if relevant.

You are called to theatre: 2 minutes after a spinal for CS the patient says she can’t breathe and feels sick. BP 60/30, HR 45. What is your diagnosis and immediate management?

Treat as high spinal until proven otherwise; prioritise oxygenation and circulation, and address aortocaval compression.

Diagnosis: high spinal causing sympathetic block ± block of cardiac accelerator fibres; dyspnoea may be from high block/intercostal weakness and/or cerebral hypoperfusion.
Immediate actions: call for help; high-flow O2; reassure; left uterine displacement; check block level; increase BP cycling frequency.
Treat hypotension/bradycardia: IV fluid bolus; atropine 500 micrograms IV; vasopressor boluses (ephedrine 3–6 mg IV or phenylephrine 50–100 micrograms IV depending on HR); if severe/rapidly deteriorating use adrenaline 10–100 micrograms IV titrated.
Prepare for airway support: bag-mask ventilation if needed; early RSI and intubation if reduced consciousness/apnoea or ongoing instability.

How do you distinguish high/total spinal from local anaesthetic systemic toxicity (LAST) in theatre?

Use timing, neurological features, cardiovascular pattern, and evidence of rising neuraxial block.

High/total spinal: rapidly rising sensory/motor block; predominant hypotension with bradycardia; upper limb weakness; symptoms follow neuraxial injection/positioning.
LAST: CNS prodrome (tinnitus, metallic taste, circumoral numbness) → seizures; cardiovascular toxicity often tachyarrhythmias/wide complexes then collapse; may follow intravascular injection of LA (e.g., epidural).
Both can coexist in epidural mishaps; if uncertain, manage ABCs and consider lipid emulsion if LAST possible while treating neuraxial-induced hypotension.

A labour epidural is topped up for category 2 CS. After 5 minutes the patient becomes profoundly hypotensive, apnoeic and unresponsive. What has happened and what are your next steps?

Likely inadvertent intrathecal dosing via epidural catheter (or subdural with rapid progression). Treat as total spinal with immediate resuscitation and conversion to GA.

Stop further neuraxial dosing; call for help; commence high-flow O2; bag-mask ventilation; prepare RSI and intubation (obstetric aspiration risk).
Circulation: LUD; rapid IV fluids; immediate vasopressors—adrenaline boluses 10–100 micrograms IV titrated for peri-arrest state; treat bradycardia with atropine; prepare infusion (e.g., adrenaline/phenylephrine/noradrenaline) depending on response and local practice.
If arrest: ALS; early adrenaline 1 mg; consider perimortem CS if no ROSC promptly and gestation viable (follow local maternal arrest algorithm).
After stabilisation: continue anaesthesia to prevent awareness; inform obstetric/neonatal teams; document and plan post-op critical care.

Explain why a patient with a high spinal may say they cannot breathe even if oxygen saturation is normal.

Dyspnoea is multifactorial and not synonymous with hypoxia.

Intercostal and abdominal muscle paralysis reduces chest wall sensation and ability to generate a forceful breath/cough; patient feels they cannot breathe.
Loss of chest wall proprioception and numbness can be interpreted as breathlessness.
Cerebral hypoperfusion from hypotension causes air hunger, anxiety, and can progress to LOC.
Diaphragm often preserved initially (phrenic nerve C3–5), so SpO2 may remain normal with supplemental oxygen until ventilation fails or consciousness is lost.

What are the key immediate drug treatments for severe bradycardia and hypotension due to high spinal?

Treat preload, vagal predominance, and loss of sympathetic tone; escalate early if severe.

Fluids: rapid crystalloid bolus (co-load); consider additional boluses guided by response.
Atropine: 500 micrograms IV (repeat to 3 mg) for bradycardia.
Vasopressors: phenylephrine 50–100 micrograms IV for hypotension with adequate HR; ephedrine 3–6 mg IV if bradycardic; adrenaline 10–100 micrograms IV for severe hypotension/bradycardia or peri-arrest.
If arrest: adrenaline 1 mg IV per ALS; continue CPR and treat reversible cause.

Describe how you would prevent high/total spinal when topping up an epidural for Caesarean section.

Aim to avoid intrathecal/intravascular injection and avoid rapid large boluses.

Assess catheter function/history: quality of labour analgesia, recent boluses, any unilateral/patchy block; check catheter markings and securement.
Aspirate catheter before dosing (recognise false negatives).
Fractionate the top-up: incremental doses with close monitoring between aliquots; avoid rapid large-volume injection.
Consider a test dose strategy per local policy; be mindful that pregnancy blunts tachycardic response and spinal opioids/analgesia can confound interpretation.
Continuous monitoring with frequent NIBP cycles; have vasopressors drawn up and LUD in place.

What is subdural block and how does it present compared with intrathecal block?

Subdural injection is uncommon but important; it can cause unexpectedly high block with atypical features.

Anatomy: potential space between dura and arachnoid; spread can be extensive and unpredictable.
Presentation: delayed onset (often 10–20+ min), patchy sensory block, disproportionate cephalad spread, variable motor block; may cause hypotension and respiratory compromise.
Compared with intrathecal: intrathecal onset is typically rapid and dense with predictable progression; subdural tends to be slower and more patchy/unpredictable.

A patient becomes hypotensive after spinal anaesthesia. When should you suspect high spinal rather than ‘simple’ spinal hypotension?

Look for progression beyond expected dermatomes and associated respiratory/upper limb symptoms.

Rapidly rising sensory level towards T1–T4 or above; numbness/weakness in hands/arms.
Marked bradycardia (cardiac accelerator fibre involvement) and refractory hypotension.
Dyspnoea, difficulty speaking, agitation, or decreasing consciousness.

What are the key human factors and system issues in high/total spinal events, and how would you reduce recurrence?

Many cases involve communication failures, dosing errors, and inadequate monitoring/escalation.

Contributors: rushed top-ups, inadequate supervision, poor labelling/line confusion, failure to fractionate, failure to recognise early signs, delayed call for help.
Mitigations: standardised top-up protocols, neuraxial-only connectors, clear labelling, checklists, simulation training, readily available vasopressors, robust escalation pathways.
Post-incident: structured debrief, incident reporting, duty of candour, governance review and dissemination of learning.

Describe the causes, clinical features and management of a high spinal block.

Structure your answer: causes/risk factors → features → immediate management → prevention.

Causes/risk factors: excessive intrathecal dose; unrecognised intrathecal epidural catheter; subdural injection; pregnancy/obesity/short stature; head-down tilt; rapid epidural top-up; hypovolaemia.
Clinical features: nausea, dizziness; hypotension; bradycardia; dyspnoea; high sensory level; upper limb paraesthesia/weakness; reduced consciousness; apnoea/asystole in total spinal.
Management: call for help; ABC; high-flow O2; assist ventilation; LUD in pregnancy; IV fluids; vasopressors (phenylephrine/ephedrine; adrenaline if severe); atropine for bradycardia; intubate/ventilate if needed; ALS if arrest.
Prevention: correct dosing; avoid excessive tilt; fractionated epidural top-ups with aspiration and close monitoring; preparedness with vasopressors and frequent BP checks; clear labelling and governance measures.

You are asked to give a spinal anaesthetic for an emergency Caesarean section. What steps will you take to minimise hypotension and how will you treat it?

In FRCA answers, include non-pharmacological, fluid, and vasopressor strategies, plus obstetric specifics.

Minimise: left uterine displacement; avoid aortocaval compression; consider prophylactic vasopressor infusion (commonly phenylephrine) per local protocol; crystalloid co-load; appropriate intrathecal dose; prompt positioning; frequent NIBP monitoring.
Treat: rapid vasopressor boluses/infusion titrated to BP; phenylephrine if HR adequate; ephedrine if bradycardic; atropine for significant bradycardia; fluids; escalate to adrenaline and airway support if high/total spinal suspected.

Outline the differential diagnosis and immediate management of sudden cardiovascular collapse in a patient receiving neuraxial anaesthesia.

Examiners want a broad differential but a practical, time-critical plan.

Differential: high/total spinal; LAST; anaphylaxis; haemorrhage; pulmonary embolus/amniotic fluid embolism; myocardial ischaemia/arrhythmia; aortocaval compression (obstetrics); tension pneumothorax (if regional + sedation/line insertion).
Immediate management: call for help; ABC with 100% O2; support ventilation; treat hypotension with fluids and vasopressors; manage bradycardia; stop potential triggers (stop LA injection); prepare lipid if LAST suspected; give adrenaline early if anaphylaxis/peri-arrest; ALS if arrest; LUD in pregnancy.