Tox - Viva - LA Toxicity Flashcards

1
Q

Maximum doses of LA

A

Lignocaine - 3mg/kg
Lig with Adren 7mg/kg

Bupiv - 2mg/kg
L-bupiv 2mg/kg

Prilocaine - 6mg/kg

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2
Q

List in order with most vascular and therefore most lethal routes of LA admin

A

Intravenous

Intercostal

Caudal

Lumbar epidural

Brachial

Subcut

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3
Q

Risk factors for LA toxicity

A

Choice and dose of LA

Site and vascular Itu

Continuous infusion

Block factors - speed of injection, no use of ultrasound, no test dose
(Adrenaline, controversy).

Problems not detected in sedated patients

Patient - Age, weight, liver/renal/cardiac failure, pregnancy

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4
Q

Mechanism of LA (normal)

A

LA crosses cell membrane unionised

Binds to fast Na channel when ionised, inactive, prevent depolarisation

Reversible prevention of transmission of neuronal AP

Consider also the membrane expansion theory

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5
Q

Signs of LA toxicity

A

Cardio - collapse, hypotension, arrhythmia, asystole

ECG - sinus Brady, prolonged QRS, AV block,

Neuro - two stage
Excitable - peri oral tingling, tinnitus, tremor, seizures
Depressive - low GCS, coma apnoea

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6
Q

Pathophysiology of LAST

A

LA antagonises oxidative phos at mitochondria

Heart and brain need aerobic metabolism so vulnerable

OR non-neuronal sodium inhibition - cerebral cortex inhibiting inhibitory pathways, therefore more excitable then depressions

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7
Q

Management LA Toxicity

A

STOP GIVING IT
This is an emergency call for help
If arrested, CPR as per ALS

ABCDE, secure airway, 100% O2, iv access

Give Intralipid - AAGBI
Bolus 1.5ml/kg over 1 minute
Infuse 15ml/kg/hr

2 further boluses every 5 minutes, and increase to 30mls/kg]

Seizure - benzo, thio, propofol

Crit care

Report to National patient safety agency

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8
Q

Max dose of intra lipid

A

12ml/kg in first hour

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9
Q

What is intralipid

A

Lipid emulsion, soya oil, egg phosphatic and glycerol

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10
Q

Mechanism of intralipid

A

Not really known

Lipid sink - new lipid compartment in iv space, during off LA

Enhanced fatty acid metabolism - heart uses fatty acids as substrate, bupiv inhibits fatty acid oxidation, therefore intralipid is source of fatty acid

Competitive binding - fatty acid in intralipid directly inhibit LA binding

PK - intralipid reduces the CSHT of bupiv

Cytoprotection, activates Akt (Protein kinase B)

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