Local Anaesthetics Flashcards
Give your approach to postoperative weakness and hypoventilation
HHH - Declare situation | Get help
ABCDE - Resuscitate
- ? More FiO2 | ? Re-intubate IPPV | ? leave ETT in
Central causes
- Opioid | Volatile | Benzo | low/high CO2
Reverse potentiators of prolonged paralysis
- Electrolytes (Ca/K down | Mg up or given)
- Acidosis
- Hyperthermia (NDMR) | hypothermia (SUX)
- Drug interaction (Mg/aminoglycosides)
- Disease: Pre-existing renal dx / Myasthaenia gravis
Peripheral nerve stimulator
- TOF
- Post-tetanic facilitation
–> IF SUSPECT PERSISTENT NON DEPOLARIZING BLOCK - 1 further dose of reversal may be given. DO NOT EXCEED Neostigmine 5mg as more than this will cause weakness itself.
CONTINUE SUPPORTIVE MANAGEMENT
Give your approach to local anaesthetic toxicity
NB to mention is prevention
HHH - Declare | Help
ABCDE FGHIJKLMNOPQ
Specific measures for LA systemic toxicity
Goals
1. Limit LA exposure
2. Prolong normal resuscitation
3. Intralipid
4. Acidosis prevention (Hyperventilation | NaHCO3)
Specific measures
- Seizures (MIDAZ/DIAZ 0.1 mg/kg | THIO 2 mg/kg)
- Hyperventilate (Seizures/hypoxia/hypoxia/hypercarbia –> Acidosis–> traps ionized LA in cells)
- Intralipid 20% (Repeated boluses 1.5 ml/kg x 3 plus infusion 0.25 ml/kg/hr) Increase infusion to 0.5 ml/kg/hr if BP falling.
- Consider cardiopulmonary bypass
What is intralipid, what is its suggested mechanism of action and what is its uses?
20% Lipid emulsion
- Soya oil
- Egg phosphatide
- Glycerol
Uses:
- Lipid sink for highly lipid soluble drug toxicity
- lipid substance in TPN
- Solvent for propofol
Mechanism suggested
- “Circulating lipid sink” - draws bupivacaine out of the plasma and binding it so no more free fraction exists to bind the receptors.
Simplify the dosing of intralipid. Confirm maximum dosage.
For 70 kg
20 ml/hr —-> 40 ml/hr infusion (titrate to BP)
100 ml bolus | | 3 mins | 100 ml bolus | | 3mins | 100 ml bolus
CPR to distribute
Continue infusion until haemodynamic stability restored
Max dose 10ml/kg = 700 mls
Summarize the goals in the treatment of local anaesthetic toxicity
Get the drug out of the cells alkalinize and bound to the intralipid
- Limit LA exposure
- Prolong CPR (consider cardiopulmonary bypass)
- Intralipid
- Prevent acidosis (hyperventilation | NaHCO3)
How can LA systemic toxicity be prevented? What is the mnemonic for this
mnemonic: MASSIVE
- Maximum doses (L 4.5 / 7) (B 2.5 / 3) (LB 2.5 / 3) (R 2.5 /2.5)
- ASPIRATE
- SLOW INJECTION with communication
- SITE (Consider vascularity)
- INCREMENTAL TEST DOSING
- VASOCONSTRICTORS
- ENSURE HOMEOSTASIS (Acidosis/hypoxia/hypercapnoea increase LA toxicity)
Which group of local anaesthetics are more likely to cause anaphylaxis?
Esters
- metabolised by plasma cholinesterase
- metabolite: p-aminobenzoic acid = PABA
- PABA associated with hypersensitivity and anaphylaxis
Explain how the addition of vasoconstrictors enhance the efficacy of local anaesthetics
- Prolong duration of action
Decrease the rate of systemic absorption of LA (through VC and decreased washout) –> enhances the amount of drug available for neuronal uptake.
- more effective with lignocaine than bupivacaine
- more effective with SC route than epidural - Enhance quality of analgaesia
- Limit toxic side effects
- Decrease surgical bleeding
List 5 situations when vasoconstrictors are contraindicated with LA
- Sites that lack collateral supply: digits, penis, eyes
- IV local anaesthesia (Bier’s)
- High CVS risk
- Utero-placental insufficiency
- Drug interactions: TCAs and MAOIs –> HPT/dysrhythmia
What two effects does alkalinisation of LA have and how is this done for lignocaine and bupivacaine
- Faster onset (more unionized)
- Less burning on injxn
Lignocaine: 1 ml NaHCO3 8.5% added to 10ml ligno
Bupivacaine: 0.1 ml NaHCO3 8.5% added to 10 ml bup.
(bupivacaine precipitates if too alkaline)
How does the addition of glucose to the LA affect its effect
LA are hypobaric compared to CSF meaning the tend to rise when added to CSA
Addition of glucose makes the LA solution hyperbaric which allows the anaesthetist to manipulate the distribution of the LA with knowledge of spinal curvatures and strategic positioning of the patient.
Which drugs can be added to LA during neuraxial anaesthesia? What is their effect with regard to LA efficacy
PRESERVATIVE FREE:
- Opioids (RSA!)
- Ketamine
- Clonidine
- Midazolam
- Neostigmine
- Adrenalin
Addition of opioids to the neuraxial anaesthetic injection have a synergistic effect with the local anaesthetic enhancing both the quality and duration of the analgaesia.
Compare the clinical uses of lignocaine and bupivacaine
Lignocaine
- Topical
- Biers block
Lignocaine and bupivacaine
- Infiltration
- Peripheral
- Epidural
- Spinal
Why can’t bupivacaine be used for Bier’s block?
Contra-indicated in Bier’s block due to high risk of severe cardiotoxicity if given IV.
Describe the steps and drugs for doing a Bier’s block
- Emergency equipment & monitoring available
- IV line
- Elevate arm for 3 minutes then inflate proximal cuff to 250 mmHg
- Lidocaine 3mg/kg 0.5% (mini-Bier’s 1.5 mg/kg) - slow
- Blotchy erythema = working
- Paraesthesia/warmth in 3 - 5 mins from fingertips to proximal
- Single cuff deflation ok after minimum 30 minutes
- Sensation returns when cuff is deflated - to baseline function in 5 - 10 mins