Local Anaesthetic Systemic Toxicity (LAST) - Management and Lipid Emulsion

Quick Answer

Immediate Recognition (Early Warning Signs):

• Prodromal symptoms: Circumoral numbness, metallic taste, tinnitus
• Neurological: Agitation, confusion, drowsiness, seizures
• Cardiovascular: Hypertension, tachycardia initially; then hypotension, bradycardia, arrhythmias
• Timing: Immediate (IV injection) to delayed (absorption from tissue)

Immediate Management (CRITICAL - Lipid Emulsion Protocol):

STEP 1: Stop Injection & Get Help

1. Stop local anaesthetic injection immediately
2. Call for help - "LAST protocol"
3. Maintain airway - 100% oxygen, prepare for intubation
4. Seizure management: Midazolam 2-4 mg IV or propofol 50-100 mg (NOT phenytoin)

STEP 2: Lipid Emulsion 20% (ESSENTIAL - Do Not Delay)

• Bolus: 1.5 mL/kg lean body mass IV over 2-3 minutes (~100 mL for 70kg patient)
• Infusion: 0.25 mL/kg/min for 30-60 minutes (~400 mL for 70kg)
• Repeat bolus: If cardiovascular collapse, give 1-2 additional boluses
• Maximum: ~12 mL/kg total (approximately 1000 mL for 70kg patient)

STEP 3: Cardiovascular Support

1. Standard ACLS but AVOID vasopressin, calcium channel blockers, beta-blockers, local anaesthetics
2. Reduced epinephrine doses: 1 mcg/kg (not 1 mg) for cardiac arrest
3. Cardiopulmonary bypass if available and refractory
4. Continue resuscitation efforts extended beyond standard protocols (LAST may be prolonged)

STEP 4: Post-Crisis

• Continue lipid infusion minimum 30 minutes after stability achieved
• Admit to ICU for 12-24 hours observation
• Monitoring: Cardiac, neurological (delayed CNS/cardiac toxicity up to 12-24 hours)
• Document and report to relevant authorities

ANZCA/ASRA Guidelines: Lipid emulsion is first-line antidote - NOT secondary to other measures. Do NOT wait for cardiovascular collapse before giving lipid.

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Indigenous Health Considerations

Local Anaesthetic Systemic Toxicity (LAST) management presents unique considerations for Aboriginal, Torres Strait Islander, and Māori populations, particularly given the higher rates of chronic disease, obesity, and complex regional anatomy that may affect regional anaesthesia techniques. For Aboriginal and Torres Strait Islander patients, higher rates of obesity (particularly central adiposity) can complicate regional block procedures, increasing the risk of inadvertent intravascular injection or rapid systemic absorption from highly vascularised tissue planes. Remote Indigenous patients may present for regional anaesthesia at regional hospitals with limited experience in advanced nerve block techniques, elevating LAST risk.

Cultural safety considerations are essential during LAST crisis management. Indigenous patients may have heightened anxiety about medical procedures due to historical trauma and institutional racism. Clear communication through Aboriginal Liaison Officers is critical when managing seizures or cardiovascular collapse, ensuring family understanding and involvement in decision-making. Many Aboriginal communities have traditional healing practices using native botanicals with potential pharmacological interactions—healthcare providers should inquire respectfully about traditional medicine use without judgment.

Remote and rural health considerations significantly impact LAST outcomes. Regional hospitals serving Indigenous populations may have limited lipid emulsion 20% availability or may be unaware of ASRA/ANZCA lipid protocol requirements. RFDS retrieval services must carry lipid emulsion and be trained in LAST management protocols. Transfer to tertiary centres for ongoing care after initial stabilisation is often required, creating logistical challenges for Indigenous patients far from specialist services.

Māori health considerations in Aotearoa New Zealand include higher rates of obesity and metabolic syndrome, affecting local anaesthetic pharmacokinetics (altered distribution volume, delayed metabolism). Māori patients have documented experiences of healthcare inequity, including reduced access to regional anaesthesia techniques that might benefit them. Whānau-centred care during LAST management requires clear, rapid communication with extended family, who may be present during emergency procedures. Māori Health Workers provide essential cultural brokerage during crisis situations.

Healthcare providers must recognise the intersection of physiological vulnerability and reduced access to advanced care in Indigenous populations. Higher rates of comorbidities (diabetes, renal disease, cardiovascular disease) may worsen LAST outcomes. Regional centres must stock lipid emulsion 20%, have printed LAST protocols readily available, and ensure all anaesthetic staff are trained in lipid emulsion administration. Cultural protocols for managing medical emergencies should include family communication pathways, access to traditional healing support, and recognition of Indigenous healthcare rights. The relatively low cost and long shelf-life of lipid emulsion make it feasible for even small rural hospitals to maintain adequate stock for emergency use.

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Clinical Overview

Definition and Classification

Local Anaesthetic Systemic Toxicity (LAST) is a potentially life-threatening complication of regional anaesthesia resulting from excessive plasma concentrations of local anaesthetic agents, causing dose-dependent neurological and cardiovascular toxicity. [1,2] It represents one of the most feared complications of regional anaesthesia, with rapid recognition and immediate lipid emulsion therapy being critical to survival.

Clinical Stages of LAST: [3,4]

Epidemiology

Incidence: [5,6]

• Overall: 0.1-1% of regional anaesthetics (varies by technique)
• Peripheral nerve blocks: 0.01-0.4%
• Epidural anaesthesia: 0.01-0.1%
• IV regional (Bier's block): 0.3-1%
• Serious LAST (seizures/CVS collapse): 0.01-0.03%
• Fatality: Rare but documented (<0.001%)

Trends: [7,8]

• Incidence declining due to:
  • Ultrasound guidance (reduced volume requirements)
  • Test dose practices
  • Fractionated dosing
  • Increased awareness and lipid emulsion availability
• Paradox: More blocks performed overall, so absolute numbers may be stable

Risk Factors: [9,10]

Patient Factors:

• Extremes of age: Reduced metabolism (elderly), different volumes (paediatric)
• Low body weight: Standard doses excessive for weight
• Cardiac disease: Reduced cardiac output = prolonged circulation time
• Liver disease: Impaired metabolism (amides)
• Pregnancy: Increased sensitivity, reduced plasma proteins
• Metabolic acidosis: Reduced protein binding, increased free fraction
• Hypoxia/acidaemia: Worsen toxicity, reduce seizure threshold

Technical Factors:

• Intravascular injection: IV catheter placement, direct vessel puncture
• Excessive dose/volume: Above recommended maximums
• Highly vascular areas: Interscalene, intercostal, caudal (rapid absorption)
• Inflamed tissue: Increased blood flow, reduced tissue binding
• Tourniquet failure: IV regional anaesthesia
• Multiple blocks: Cumulative toxicity
• Absence of adrenaline: No warning signs (no tachycardia/HTN)

Pharmacology and Mechanism of Toxicity

Mechanism of Toxicity: [11,12,13]

Neurological Toxicity (Usually Occurs First):

• Sodium channel blockade: CNS > CVS (CNS Na channels more sensitive)
• Inhibitory pathways blocked first: GABAergic (↓inhibition = excitation)
• Clinical: Agitation, seizures (paradoxical excitation)
• High concentrations: All pathways blocked → CNS depression, respiratory arrest

Cardiovascular Toxicity (Usually Occurs at Higher Concentrations):

• Sodium channel blockade: Phase 0 depolarisation slowed, conduction delay
• Potassium channel blockade: Prolonged repolarisation, QT prolongation
• Calcium channel blockade: Reduced contractility, vasodilation
• Clinical:
  • Early: Hypertension, tachycardia (CNS-mediated catecholamine release)
  • Late: Hypotension, bradycardia, conduction block, arrhythmias, asystole

Specific Agent Differences: [14,15,16]

Key Points:

• Bupivacaine: Most cardiotoxic (binds Na channels with high affinity, long dissociation time)
• Ropivacaine: Less cardiotoxic than bupivacaine (stereoselective, shorter dissociation)
• Lidocaine: Most neurotoxic (seizures at lower plasma levels than CVS toxicity)

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Recognition and Diagnosis

Clinical Features by System

Neurological Manifestations (Early): [17,18,19]

Prodromal Symptoms (Immediate after injection if IV, delayed if absorption):

1. Circumoral numbness/tingling (first sign in 50-70%)
2. Metallic taste in mouth
3. Tinnitus (ringing in ears)
4. Light-headedness/dizziness
5. Slurred speech
6. Blurred vision
7. Tongue numbness

Progressive CNS Toxicity:

1. Agitation/anxiety (paradoxical)
2. Confusion/disorientation
3. Drowsiness/somnolence
4. Generalised tonic-clonic seizures (focal → generalised)
5. Coma
6. Respiratory arrest (CNS depression)

Cardiovascular Manifestations: [20,21,22]

Early (CNS-mediated catecholamine surge):

• Hypertension
• Tachycardia
• Ventricular ectopy

Late (Direct myocardial/suppression):

• Hypotension (severe, refractory)
• Bradycardia (all degrees of heart block possible)
• Conduction abnormalities:
  • PR prolongation
  • QRS widening (>0.12 seconds)
  • QT prolongation
• Ventricular arrhythmias:
  • Ventricular tachycardia
  • Torsades de pointes
  • Ventricular fibrillation
• Asystole (refractory to standard ACLS)

Key Features of Bupivacaine Cardiotoxicity: [23,24]

• Severe, refractory arrhythmias
• Prolonged resuscitation required
• May recur after initial recovery ("biphasic" toxicity)
• Resistant to standard ACLS drugs

Timing of Toxicity: [25,26]

Differential Diagnosis

Conditions Mimicking LAST: [27,28]

Key Distinguishing Features of LAST:

• Temporal relationship to LA injection
• Prodromal symptoms (circumoral numbness, tinnitus)
• Both neurological AND cardiovascular manifestations
• Biphasic pattern possible (early seizure, delayed cardiac)

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Prevention Strategies

ASRA/ANZCA Practice Advisory Recommendations

Key Prevention Measures: [29,30,31]

1. Test Dose (Epidural/Intrathecal Catheters):

• 3 mL lidocaine 2% + adrenaline 1:200,000 (15 mcg adrenaline)
• Intravascular: HR ↑ >10 bpm or SBP ↑ >15 mmHg within 20-40 seconds
• Intrathecal: Sensory/motor block within 2-3 minutes
• Repeat before each top-up if prolonged procedure

2. Fractionated Dosing:

• Inject in small aliquots (3-5 mL)
• Aspirate before each injection (blood/CSF)
• Assess between doses for toxicity signs
• Wait 30-60 seconds between injections

3. Dose Calculations:

• Calculate mg/kg based on lean body weight
• Maximum safe doses:
  • Bupivacaine: 2-3 mg/kg
  • Ropivacaine: 3-4 mg/kg
  • Lidocaine: 4-5 mg/kg (with adrenaline), 7 mg/kg (without)
  • Prilocaine: 10-12 mg/kg

4. Ultrasound Guidance:

• Reduces volume requirements (20-30% less LA)
• Real-time needle visualisation (avoid vessels)
• Faster onset (less dose needed)
• Reduces complications overall

5. Adrenaline Addition:

• Systemic absorption marker: Tachycardia/HTN if IV
• Reduces peak plasma concentration (vasoconstricts vessels)
• Prolongs block duration
• Typical concentration: 1:200,000 to 1:400,000 (5-2.5 mcg/mL)

6. Patient Selection and Monitoring:

• Avoid in severe cardiac disease (unless benefits outweigh risks)
• Continuous monitoring: ECG, BP, SpO2
• Resuscitation equipment immediately available
• Lipid emulsion 20% immediately available (within 60 seconds)

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Acute Management

Immediate Response Algorithm

STEP 1: Recognition and Immediate Actions (30-60 seconds) [32,33,34]

1. Stop local anaesthetic injection immediately
2. Call for help: "LAST protocol activated"
3. Maintain airway:
   • 100% oxygen via face mask (if conscious)
   • Prepare for intubation (equipment ready)
4. Seizure management:
   • Midazolam 2-4 mg IV (first line)
   • Propofol 50-100 mg IV (alternative)
   • AVOID: Phenytoin (prolongs Na channel blockade)
   • Protect airway (suction, positioning)

STEP 2: Lipid Emulsion 20% (START IMMEDIATELY - Do Not Wait) [35,36,37]

CRITICAL: Lipid emulsion is FIRST-LINE antidote. Do NOT wait for cardiovascular collapse before giving lipid.

ASRA/ANZCA Protocol (Adults):

Initial Bolus:

• 1.5 mL/kg lean body mass IV over 2-3 minutes
• For 70 kg patient: ~100 mL
• Can be given via peripheral IV (no central line required)
• No in-line filter required

Continuous Infusion:

• 0.25 mL/kg/min for 30-60 minutes
• For 70 kg patient: ~400 mL over 30 minutes
• Continue even if patient improves

Additional Boluses (If Cardiovascular Collapse):

• May give 1-2 additional boluses (1.5 mL/kg each)
• 5-10 minutes apart
• Continue infusion throughout

Maximum Dose:

• ~12 mL/kg total (approximately 1000 mL for 70kg patient)
• Based on case reports and expert consensus

Lipid Emulsion Products:

• Intralipid 20%
• Lipofundin 20%
• ClinOleic 20%

STEP 3: Cardiovascular Support (Modified ACLS) [38,39,40]

Standard ACLS WITH CRITICAL MODIFICATIONS:

AVOID These Drugs (May Worsen Toxicity):

• Vasopressin
• Calcium channel blockers (verapamil, diltiazem)
• Beta-blockers (propranolol, metoprolol, esmolol)
• Additional local anaesthetics (lidocaine for arrhythmias)

Modified Epinephrine Dosing:

• Standard 1 mg boluses may be TOO LARGE
• Recommended: 1 mcg/kg (70 mcg for 70kg patient) for cardiac arrest
• Titrate carefully
• Small frequent boluses may be better than large single boluses

Other Supportive Measures:

• Crystalloid fluid resuscitation (avoid overload)
• Vasopressors: Noradrenaline, phenylephrine as needed
• Atropine: For bradycardia (0.6 mg IV)
• Magnesium sulfate: For torsades de pointes (2g IV)
• Cardioversion/Defibrillation: Standard energy levels

STEP 4: Advanced Support (If Refractory) [41,42]

Cardiopulmonary Bypass (CPB):

• Indication: Refractory cardiac arrest despite lipid + prolonged CPR
• Mechanism: Supports circulation until LA metabolised
• Requirements: Immediate availability (cardiac theatre, ECMO team)
• Duration: May need 60-90 minutes support
• Outcomes: Documented successful recovery

Extracorporeal Membrane Oxygenation (ECMO):

• Alternative to CPB
• V-A ECMO for cardiac support
• Can be initiated in ED/ICU

Prolonged CPR:

• LAST toxicity may be prolonged (bupivacaine highly protein-bound)
• Continue CPR for 60-90 minutes if any signs of life
• Do NOT stop prematurely

Post-Crisis Management

Immediate Post-Resuscitation: [43,44]

1. Continue Lipid Emulsion:

   • Minimum 30 minutes after cardiovascular stability
   • Some recommend 60 minutes
   • Biphasic toxicity can occur (recurrence after initial recovery)

2. Monitoring:

   • Continuous cardiac monitoring 12-24 hours
   • Serial ECGs (arrhythmia risk)
   • Neurological observation (delayed CNS toxicity)
   • Arterial blood gas (metabolic status)

3. Investigations:

   • Serum LA levels (if available, mainly for research)
   • Electrolytes (K, Mg, Ca - arrhythmia risk)
   • Troponin (myocardial injury)
   • Renal function (clearance)
   • Liver function (metabolism)

4. Disposition:

   • ICU/HDU admission mandatory for 12-24 hours
   • Even if asymptomatic after initial event
   • Biphasic toxicity reported 12-24 hours later

Delayed Complications: [45,46]

• Recurrent arrhythmias (up to 24 hours)
• Delayed seizures (rare, usually within 6 hours)
• Post-hypoxic brain injury (if arrest prolonged)
• Rhabdomyolysis (from seizures, prolonged CPR)
• Compartment syndrome (from prolonged immobility/CPR)
• Aspiration pneumonia (if airway unprotected during seizure)

Follow-up: [47,48]

• Neurological assessment: Cognitive function, seizure recurrence
• Cardiac assessment: Echocardiogram if myocardial injury suspected
• Psychological support: Patient may have PTSD from event
• Documentation: Incident report, quality review
• Patient counseling: Future anaesthesia implications

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Special Considerations

Paediatric LAST

Unique Features: [49,50]

• Higher mg/kg doses tolerated (relative to adults)
• Seizures may be subtle: Staring, eye deviation, apnea
• Faster desaturation: Limited reserve
• Caudal blocks: Higher risk (vascular, absorption)

Management:

• Weight-based lipid dosing: Same protocol (1.5 mL/kg bolus)
• Intubation: Lower threshold (rapid desaturation)
• Fluid management: Careful (risk of overload)

Pregnancy Considerations

Physiological Changes: [51,52]

• Increased sensitivity: Progesterone, reduced plasma proteins
• Faster absorption: Increased blood flow to tissues
• Aortocaval compression: Reduced cardiac output supine
• Aspiration risk: Full stomach, delayed gastric emptying

Management:

• Lower threshold for intubation
• Left lateral tilt (after 20 weeks)
• Fetal monitoring (if viable)
• Lipid emulsion: Safe in pregnancy
• Maternal resuscitation priority

Lipid Emulsion Mechanism and Evidence

Mechanism of Action (Not Fully Understood): [53,54,55]

Proposed Mechanisms:

1. Lipid Sink Hypothesis (Primary):

   • Lipid emulsion creates lipid phase in plasma
   • Lipophilic LA partitions into lipid phase
   • Reduces free LA concentration in aqueous phase
   • Reduces tissue binding
   • "Scavenges" LA from tissues

2. Cardiac Energy Substrate:

   • Lipid provides fatty acid substrate for cardiac metabolism
   • Improves cardiac function during toxicity

3. Inotropic Effect:

   • Direct positive inotropic effect on myocardium

4. Vasoconstriction:

   • Lipid may cause vasoconstriction, improving BP

Evidence Base: [56,57,58]

Animal Studies:

• Rats: Lipid emulsion improves survival in bupivacaine overdose
• Dogs: Lipid emulsion superior to epinephrine alone
• Multiple animal models show consistent benefit

Human Case Reports:

• 100 documented successful uses

• Often dramatic response to lipid
• Biphasic toxicity prevented/ameliorated by continued lipid

Systematic Reviews:

• Weinberg (2012): Lipid emulsion effective in LAST
• Gosselin (2016): Evidence-based recommendations support use
• No RCTs (unethical to withhold), but strong observational evidence

ASRA/ANZCA Guidelines:

• Class I recommendation (benefit >> risk)
• Immediate availability mandated
• Training required for all regional anaesthesia providers

Indigenous Health Considerations

Note: This section expands on the Quick Answer section above for comprehensive cultural safety training.

Aboriginal and Torres Strait Islander Health: [59,60,61]

Health Disparities Affecting LAST Risk:

• Higher obesity rates: Central adiposity complicates nerve blocks
• Diabetes prevalence: 3-4x higher than non-Indigenous
  • Neuropathy may mask prodromal symptoms
  • Autonomic dysfunction alters hemodynamic response
• Renal disease: Reduced LA clearance
• Cardiovascular disease: Reduced cardiac reserve
• Access disparities: Regional hospitals with limited experience

Remote Health Service Context: [62,63,64]

Challenges:

1. Lipid emulsion availability: May not be stocked in all rural hospitals
2. Staff training: Limited exposure to LAST management
3. Transfer delays: Long distances to tertiary care
4. Communication barriers: May affect recognition of prodromal symptoms

Solutions:

• Mandate lipid emulsion stocking in all hospitals performing blocks
• RFDS retrieval with lipid capability
• Telemedicine support from specialists
• Cultural safety training for recognition and management

Cultural Safety in Crisis: [65,66,67]

During LAST Management:

• Clear explanation to patient (if conscious) and family
• Aboriginal Liaison Officer involvement
• Family decision-making support
• Traditional healing access if requested

Post-Crisis:

• Follow-up with Aboriginal Health Service
• Community engagement about event
• Cultural protocols if adverse outcomes
• Trauma-informed care

Māori Health (Aotearoa New Zealand): [68,69,70]

Māori Health Profile:

• Higher obesity: 48% vs 29% non-Māori
• Metabolic syndrome: Affects LA pharmacokinetics
  • Altered distribution volume
  • Delayed metabolism
  • Changed protein binding
• Cardiovascular disease: Reduced cardiac reserve

Health System Factors: [71,72,73]

Access to Regional Anaesthesia:

• Māori may have reduced access to beneficial regional techniques
• Institutional barriers to advanced pain management
• Cultural safety affects patient willingness to undergo procedures

Whānau-Centred Crisis Management:

• Rapid, clear communication with extended family
• Māori Health Workers as cultural brokers
• Karakia (prayers) during crisis if requested
• Whakawhanaungatanga (relationship-building) even in emergency

Quality and Equity: [74,75,76]

Data and Monitoring:

• Collect ethnicity data for LAST outcomes
• Monitor for inequities in management
• Māori-led quality improvement
• Accountability for equitable outcomes

ANZCA Requirements:

• Cultural competency training for all anaesthetists
• Understanding of health disparities
• Commitment to equitable, culturally safe care

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ANZCA Exam Focus

Written Examination (SAQ)

High-Yield Topics:

1. Lipid emulsion protocol (doses, timing, duration)
2. Modified ACLS (what to avoid, reduced epinephrine)
3. Clinical features (prodrome, neurological vs cardiovascular)
4. Prevention (test dose, fractionated dosing, ultrasound)
5. Pharmacology (why bupivacaine most cardiotoxic)

Common SAQ Scenarios:

Scenario 1: "A patient undergoing interscalene block develops seizures and cardiovascular collapse immediately after local anaesthetic injection. Describe your management including lipid emulsion dosing. (20 marks)"

Scenario 2: "List five measures to prevent local anaesthetic systemic toxicity during peripheral nerve block. (15 marks)"

Viva Voce Examinations

Expected Viva Themes:

Theme 1: Recognition

• "What are the early warning signs of local anaesthetic toxicity?"
  • Key points: Circumoral numbness, tinnitus, metallic taste

Theme 2: Management

• "How would you manage a patient who develops seizures after local anaesthetic injection?"
  • Key points: Benzodiazepines, airway, lipid emulsion protocol

Theme 3: Prevention

• "How can you minimise the risk of LAST during regional anaesthesia?"
  • Key points: Test dose, fractionated dosing, ultrasound, adrenaline

Theme 4: Pharmacology

• "Why is bupivacaine more cardiotoxic than other local anaesthetics?"
  • Key points: High affinity for Na channels, long dissociation time

Viva Scenario Example

Examiner: "You have just injected bupivacaine for an interscalene block when the patient complains of a metallic taste and ringing in their ears. What do you do?"

Candidate Response Framework:

1. Immediate Actions:

   • "Stop injecting immediately"
   • "Call for help - this is early LAST"
   • "100% oxygen via face mask"

2. Lipid Emulsion:

   • "Start lipid emulsion 20% immediately"
   • "1.5 mL/kg bolus over 2-3 minutes"
   • "Then 0.25 mL/kg/min infusion"
   • "Do not wait for cardiovascular collapse"

3. Monitoring and Support:

   • "Prepare for seizures - midazolam ready"
   • "Continuous monitoring: ECG, BP, SpO2"
   • "IV access secure, resuscitation equipment"

4. Airway:

   • "If seizures occur, protect airway"
   • "Intubate if prolonged or cardiovascular compromise"

Examiner Follow-up: "The patient then develops ventricular fibrillation. How does your management change?"

Candidate: "I would start standard ACLS with modifications - use reduced epinephrine doses of 1 mcg/kg, continue lipid emulsion infusion, avoid calcium channel blockers and beta-blockers, and be prepared for prolonged resuscitation as bupivacaine toxicity can be refractory to standard treatment."

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Short Answer Questions

SAQ 1: Lipid Emulsion Protocol

Question: (20 marks) A 70-year-old patient (75 kg) develops seizures followed by cardiovascular collapse (ventricular fibrillation) 5 minutes after receiving bupivacaine for an interscalene brachial plexus block.

a) Describe the lipid emulsion protocol for this patient, including doses and timing. (10 marks)

b) What modifications to standard ACLS are required in this situation? (5 marks)

c) What ongoing monitoring is required after initial resuscitation? (5 marks)

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Model Answer:

a) Lipid Emulsion Protocol (10 marks):

Immediate Bolus:

• 1.5 mL/kg lean body mass IV over 2-3 minutes [2 marks]
• For 75 kg: ~112 mL (can round to 100 mL) [1 mark]
• Can give via peripheral IV, no filter required [0.5 mark]

Continuous Infusion:

• 0.25 mL/kg/min for minimum 30-60 minutes [2 marks]
• For 75 kg: ~18-19 mL/min [0.5 mark]
• Total infusion volume: ~550-1100 mL [0.5 mark]

Additional Boluses:

• If cardiovascular collapse persists, give 1-2 additional boluses [1 mark]
• Same dose (1.5 mL/kg) at 5-10 minute intervals [0.5 mark]
• Continue infusion throughout [0.5 mark]

Maximum:

• ~12 mL/kg total (approximately 900 mL for this patient) [1 mark]
• Based on expert consensus and case series [0.5 mark]

Product:

• Intralipid 20%, Lipofundin 20%, or ClinOleic 20% [0.5 mark]

b) ACLS Modifications (5 marks):

1. Reduced epinephrine dosing: Use 1 mcg/kg (75 mcg for this patient) rather than standard 1 mg [1 mark]
2. Avoid vasopressin (may worsen toxicity) [1 mark]
3. Avoid calcium channel blockers (verapamil, diltiazem) [1 mark]
4. Avoid beta-blockers (propranolol, esmolol, metoprolol) [1 mark]
5. Avoid additional local anaesthetics (lidocaine for arrhythmias) [1 mark]
6. Prolonged CPR: Continue for 60-90 minutes if any signs of life [0.5 mark]
7. Consider cardiopulmonary bypass if available and refractory [0.5 mark]

(Any 5 points acceptable)

c) Post-Resuscitation Monitoring (5 marks):

1. Continue lipid infusion for minimum 30 minutes after cardiovascular stability [1 mark]
2. Continuous cardiac monitoring 12-24 hours (biphasic toxicity risk) [1 mark]
3. Serial ECGs (arrhythmia recurrence up to 24 hours) [0.5 mark]
4. Neurological observation (delayed CNS toxicity possible) [0.5 mark]
5. ICU/HDU admission mandatory for 12-24 hours [1 mark]
6. Electrolyte monitoring (K, Mg, Ca - arrhythmia risk) [0.5 mark]
7. Troponin (myocardial injury assessment) [0.5 mark]

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SAQ 2: Prevention of LAST

Question: (15 marks) You are planning an ultrasound-guided interscalene block for a 60-year-old patient (80 kg) undergoing shoulder surgery.

a) What is the maximum safe dose of ropivacaine for this patient? (3 marks)

b) Describe five measures to minimise the risk of local anaesthetic systemic toxicity during this procedure. (10 marks)

c) Why is adrenaline sometimes added to local anaesthetic solutions for peripheral nerve blocks? (2 marks)

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Model Answer:

a) Maximum Safe Dose (3 marks):

Ropivacaine: 3-4 mg/kg maximum [1 mark]

• For 80 kg: 240-320 mg maximum [1 mark]
• Volume depends on concentration (e.g., 0.375% ropivacaine = 3.75 mg/mL) [0.5 mark]
• Calculate: 320 mg ÷ 3.75 mg/mL = 85 mL maximum [0.5 mark]

b) Prevention Measures (10 marks):

1. Ultrasound guidance:

   • Real-time needle visualisation [0.5 mark]
   • Avoid vessels (identify with colour Doppler) [0.5 mark]
   • Reduces volume required (20-30% less LA) [0.5 mark]

2. Fractionated dosing:

   • Inject in small aliquots (3-5 mL) [0.5 mark]
   • Aspirate before each injection (check for blood) [0.5 mark]
   • Wait 30-60 seconds between injections [0.5 mark]
   • Assess for prodromal symptoms between doses [0.5 mark]

3. Dose calculation:

   • Calculate mg/kg based on lean body weight [0.5 mark]
   • Stay within maximum safe dose [0.5 mark]
   • Account for all blocks (cumulative toxicity) [0.5 mark]

4. Adrenaline addition:

   • 1:200,000 to 1:400,000 concentration [0.5 mark]
   • Systemic absorption marker (tachycardia if IV) [0.5 mark]
   • Reduces peak plasma concentration [0.5 mark]
   • Prolongs block duration [0.5 mark]

5. Monitoring:

   • Continuous ECG, BP, SpO2 [0.5 mark]
   • Resuscitation equipment available [0.5 mark]
   • Lipid emulsion 20% immediately available [1 mark]
   • Trained personnel present [0.5 mark]

6. Test dose (if catheter):

   • 3 mL lidocaine 2% + adrenaline [0.5 mark]
   • Watch for HR/BP changes (intravascular) [0.5 mark]

(Any 5 measures with detail acceptable)

c) Adrenaline Rationale (2 marks):

1. Systemic absorption marker: If intravascular injection occurs, adrenaline causes tachycardia and hypertension within 20-40 seconds, providing early warning [1 mark]
2. Reduces peak plasma concentration: Vasoconstricts blood vessels, slowing LA absorption and reducing peak plasma levels [0.5 mark]
3. Prolongs block duration: Reduced washout from tissues [0.5 mark]

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SAQ 3: Differential Diagnosis and Features

Question: (15 marks) A patient develops sudden-onset agitation, confusion, and seizures 10 minutes after receiving local anaesthetic for an ankle block. The blood pressure is 180/110 mmHg and heart rate is 120 bpm.

a) What is the most likely diagnosis? List two alternative diagnoses. (5 marks)

b) What features distinguish LAST from the alternative diagnoses? (5 marks)

c) How would your initial management differ for LAST versus the most likely alternative diagnosis? (5 marks)

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Model Answer:

a) Diagnosis and Alternatives (5 marks):

Most Likely: Local Anaesthetic Systemic Toxicity (LAST) [2 marks]

Alternative Diagnoses: (any 2)

1. Seizure disorder/epilepsy [1 mark]
2. Anaphylaxis [1 mark]
3. Hypoglycaemia [1 mark]
4. Acute stroke/TIA [1 mark]
5. Hypertensive encephalopathy [1 mark]

b) Distinguishing Features (5 marks):

c) Management Differences (5 marks):

LAST Management: [2.5 marks]

• Stop LA injection immediately
• Lipid emulsion 20% 1.5 mL/kg bolus + infusion
• Benzodiazepines for seizures (midazolam)
• Modified ACLS (avoid vasopressin, CCBs, beta-blockers)
• Continue resuscitation extended period

Anaphylaxis Management: [2.5 marks]

• Adrenaline 50-100 mcg IV/IM (essential, first-line)
• Volume resuscitation
• Antihistamines (chlorphenamine 10 mg IV)
• Corticosteroids (hydrocortisone 200 mg IV)
• NO lipid emulsion (not indicated)
• Airway management if angioedema

(Or other alternative diagnosis with appropriate management)

---

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