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EDRA > 8.4 Local Anaesthetic Toxicity > Flashcards

8.4 Local Anaesthetic Toxicity Flashcards

1
Q

Local anaesthetic toxicity includes the following

A

1
Allergic response –
immediate (anaphylaxis)
or delayed (urticaria)

2
Myotoxicity –
muscle damage consequent
to intramuscular injection

3
Neurotrauma –
direct nerve injury or
transient neurological syndromes

4
Systemic toxicity –
most severe (life-threatening); manifests as
central nervous system symptoms and cardiovascular system collapse.

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2
Q

Response to vasoconstrictor

A

Response to vasoconstrictors

(manifested as headache, apprehension,
tachycardia and hypertension)

constitutes another differential diagnosis of
local anaesthetic (LA) toxicity
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3
Q

Adhesive arachnoiditis

A

Adhesive arachnoiditis is due to
contamination of LA solution
with skin-prep solutions (betadine or
chlorhexidine) and is not due to LA toxicity.

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4
Q

Systemic toxicity onset

A

Systemic toxicity can manifest

either immediately
(within minutes),

because of too rapid
an intravascular injection,

or be delayed (after 5–15 minutes),

because of toxic plasma concentrations
of LA achieved over a period of time.

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5
Q

Is toxicity additive

A

toxicity is additive; mixtures may be more toxic than individual drugs.

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6
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

amide v ester

A

Amides > esters

rapidly metabolised by esterases: lower toxicity

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7
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

lipophilicty

A

Hydrophobic (lipohilic) >

hydrophilic (less lipophilic) agents

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8
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

side chain

A 
More potent (bigger side chains) 
> less potent (smaller side chains
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9
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

vdil v constrictor

A

Vasodilators > vasoconstrictors

ropivacaine

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10
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

binding

A

Protein binding:

only free fraction causes toxicity

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11
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

S v R

A

Stereospecificity:

levorotatory or S/(–) stereoisomers
less toxic than dextrorotatory or R/(+)

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12
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

drugs order

A

Bupivacaine > l-bupicavaine > ropivacaine > lignocaine

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13
Q

Determinants of systemic toxicity

Specific agents: physicochemical properties

least and most toxic esters and amides

A

Least toxic

Ester
2-Chlorprocaine

Amide
Prilocaine

Most toxic

Ester
Tetracaine

Amide
Dibucaine
> bupivacaine

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14
Q

Specific agents: Dose

[peak plasma]

A

Dose
Higher dose > lower dose

High peak plasma concentration
(greater than toxic levels)

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15
Q

Peak plasma conc and weight

A

Peak plasma concentration is not a function of body weight in adults, and
basing LA doses on body weight in adults has no scientific foundation
(except in paediatrics)

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16
Q

Factors increasing systemic toxicity

Site of injection

A

Factors increasing systemic toxicity
Site of injection
(influences rate of absorption):

intravascular >
 intrapleural > 
intercostal > 
caudal > 
epidural >
brachial plexus > 
femorosciatic > 
sub-cutaneous >
intra-articular >
spinal
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17
Q

Factors increasing systemic toxicity

Physiological parameters

A

Physiological parameters:

acidosis (decreases plasma protein binding),

hypercarbia,
hypoxia and

hyperkalaemia (increased proportion of Na+ channels in inactivated state)

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18
Q

Factors increasing systemic toxicity

obs
geris
paeds

A

Specific populations:

obstetrics (progesterone-induced sensitivity to LA)

geriatric: low dose requirements
paediatrics: lower weight and performance of blocks under sedation

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19
Q

Protective factors

additives

breathing

meds

A

Protective factors

Vasoconstrictors:

may decrease rate of
systemic absorption and may help
reducing total dose

Hyperventilation
(reduces respiratory acidosis and
raises seizure threshold)

Benzodiazepine premedication 
(raises seizure threshold)
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20
Q

LAs cause toxicity by blocking the following

Which channels

Cardiac

A

Voltage-gated Na+ channels:

most important.

LA blocks these
channels in open
or inactivated state,
rather than in closed state.

This is a phasic or use-dependent block.

In cardiac muscle fibres,
Ca+ influx during ‘plateau’
phase favours LA binding as the Na+
channels are in the inactivated state.

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21
Q

How does the binding of LA To cardiac fibres affect rhythm

A

Consequently, Vmax
(max upstroke velocity of the action potential)

is reduced,

causing QRS widening,
and action potential duration
(APD) is prolonged,

causing QT prolongation
(leading to ventricular arrhythmias).

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22
Q

How does physiologica state affect cardiac arrhytmia

A

Hypoxia, acidosis and hyperkalaemia increase the proportion of Na+ channels in the inactivated state,
favouring LA binding and hence toxicity

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23
Q

Type of sodium channel blockade by local anaesthetic

A

Blockade Local anaesthetic Toxicity

Fast in, fast out
Lignocaine Less toxic

Slow in, slow out
Bupivacaine – lower doses Intermediate

Fast in, slow out
Bupivacaine – high doses More toxic

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24
Q

Voltage-sensitive K+ channels:

A

Voltage-sensitive K+ channels:

APD increased; QT prolongation
leading to ventricular arrhythmias

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25
Voltage-sensitive Ca+ channels:
Voltage-sensitive Ca+ channels: inhibition of myocyte Ca+ release and utilisation
26
Other sites of LA toxicity
Other channels: HERG, NMDA, nicotinic acetlycholie receptors, β- adrenergic, KATP channels and so forth. Mitochondrial dysfunction: uncouple oxidative phosphorylation.
27
How does LAST present generally
In general, central nervous system (CNS) signs are first to manifest, followed by cardiovascular system (CVS) signs.
28
CNS toxicity early
``` CNS toxicity Early excitement phase: perioral numbness, tinnitus tremors myoclonic jerks convulsions ```
29
CNS toxicity late
Late depression phase: hypoventilation respiratory acidosis and hypoxia coma
30
CVS toxicity
CVS toxicity Early excitement from CNS stimulation: tachycardia hypertension ``` Late CVS depression (from direct LA toxicity): arrhythmias pump failure arrest ```
31
ECG changes
ECG: QRS widening and QT prolongation; ventricular arrhythmias
32
CNS Ratio
CVS : CNS ratio describes ratio of dose required to cause CV toxicity to that required to cause CNS toxicity. It is 2:1 for bupivacaine and 7 : 1 for lignocaine. This implies that bupivacaine is more cardiotoxic than lignocaine
33
The order of toxicity (and cardiotoxicity) is:
The order of toxicity (and cardiotoxicity) is: Bupivacaine > l-bupicavaine > ropivacaine > lignocaine. There are clinical reports of simultaneous CNS and CVS toxicity with bupivacaine
34
TABLE 8.12 Recommended doses of common local anaesthetics (LAs)
Procaine 7 8.5 (w epi) Metabolised rapidly by esterases
35
2-Chlorprocaine
11 14 w epi
36
Lignocaine Without epinephrine With epinephrine Toxic plasma levels
4 7 w epi 5
37
Mepivacaine Without epinephrine With epinephrine Toxic plasma levels
4 7 w epi / not reco 5
38
Bupivacaine
2 2 w epi not reco 3
39
Levo-bupivacaine
2 2 not reco 4
40
Ropivacaine
3 3 not reco 5
41
Max dose influenced by
shows the generally accepted guideline. However, maximum recommended doses by the manufacturer should be abided by. Dosages are said to be site- and block-specific rather than dependent upon weight of the patient.
42
Dose-dependent systemic effects of lignocaine
Analgesia 1–5 Tinnitus, perioral numbness 5-10 Seizures 10-15 Coma and respiratory arrest 15-25 Cardiovascular depression >25
43
Measures to reduce LA likelihood of toxicity are:
1 using smallest possible doses for the given block 2 using less cardiotoxic agents 3 use of vasoconstrictors to reduce systemic absorption 4 fractionation of total dose 5 aspiration before injection and using test doses
44
Monitoring
Adequate patient monitoring may help to recognise LA toxicity at an earlier stage, but it may not reduce its likelihood.
45
Rx of LA toxicity abc
Treatment of LA toxicity: always start with ABC (resuscitation). Airway: Clear the airway and suction (if needed). Breathing: Oxygenation and adequate ventilation to avoid hypoxia and respiratory acidosis (both potentiate LA toxicity). Intubation and controlled ventilation if needed. Circulation: Maintain BP: leg elevation, fluids, inotropes or vasoconstricto
46
Drugs: Seizures
Drugs: Seizures: diazepam, midazolam, thiopentone or propofol
47
Muscle relaxant:
Muscle relaxant: succinylcholine
48
Arrhythmias
Arrhythmias: amiodarone (best choice out of anti-arrhythmics), epinephrine (higher doses may be needed)
49
Specific therapy:
Specific therapy: Intralipid.
50
anti-arrhythmics to be avoided in setting of LA-induced arrhythmias are
anti-arrhythmics to be avoided in setting of LA-induced arrhythmias are sodium valproate, phenytoin, Ca+ channel blockers, lignocaine and bretylium.
51
Regarding Intralipid rescue therapy what % available what's recommended
Intralipid is available as a 10%, 20% and 30% lipid emulsion. However, the recommended concentration to be used (lipid rescue) is 20%. Propofol is not an appropriate substitute.`
52
cpr and intralipid
CPR should be continued while giving Intralipid in cardiac arrest (lipids must circulate).
53
Proposed MOA intralipid indirect
Indirect: acts as a sink for the lipid-soluble LA, drawing it back into circulation (from tissues)
54
Proposed MOA intralipid Direct
Direct: the inhibition of mitochondrial carnitine-acylcarnitine translocase by LA is overridden by high plasma triglycerides (this enzyme is essential for the tricarboxylic acid cycle in mitochondria, i.e. oxidative phosphorylation).
55
Intralipid Dose bolus infusion
Dose used: initially 1.5 mL/kg bolus over 1 minute followed by infusion of 0.25 mL/kg/minute.
56
Intralipid can further doses be given?
If CVS stability is not restored or adequate circulation deteriorates, give an additional two boluses at an interval of 5 minutes and continue infusion at the same or double rate (0.5 mL/kg/minute). The maximum cumulative dose should not exceed 12 mL/kg 840 mL in a 70-kg man
57
Which is metabolised to PABA
Ester LAs are metabolised to PABA compounds, which make them more allergenic than amides PABA compounds may be present in cosmetic products, causing patients to react
58
True allergy to LA?
True allergy to preservative-free amide LA is rare, and patients may react to paraben derivatives used as preservative.
59
Cauda equina with 2 chlorprocaine
Reports of ‘cauda equina syndrome’ with unintentional intrathecal administration of high doses of 2- chlorprocaine intended for epidural use were attributed to sodium metabisulphite added to the solution. The present preparations for intrathecal use are free of such preservatives.
60
Cauda equina syndrome (CES) with regional
Cauda equina syndrome (CES) has been reported after unintentional intrathecal injection of high doses of LA (mainly lignocaine) intended for the epidural space. In other reports, the administration of LA through continuous spinal microcatheters (smaller than 27 G) produced a restricted sacral block, and repeated doses were required to achieve adequate surgical anaesthesia.
61
CES attributed to adding what worsens
The neurotoxicity was attributed to the maldistribution of LA within the CSF, and subsequently the use of microcatheters was withdrawn. The addition of vasoconstrictors is another risk factor
62
CES presents
The syndrome presents as multiple-root involvement, varying degrees of bowel and bladder dysfunction, perineal sensory loss and lower-limb motor weakness.
63
CES ix and Rx
The differentials may include epidural haematoma or epidural abscess, with urgent MRI to ascertain the cause. There is no effective treatment, and the patient may need considerable supportive care
64
Transient neurologic symptoms are a group of neurologic symptoms experienced by patients after spinal anaesthesia, characterised by:
1 mostly aching/pain in one or both buttocks 2 often with dysaethesia radiating into anterior or posterior thighs 3 with lower-back pain in some patients 4 symptoms beginning within 24 hours after the resolution of spinal anaesthetic 5 symptoms resolving in 6 hours to 4 days 6 no neurological finding upon physical examination.
65
TNS name
The name ‘transient neurologic symptoms’ itself is controversial, as it implies a neurologic aetiology that is not yet proven.
66
TNS RF
Proposed risk factors include use of intrathecal lignocaine, lithotomy position, outpatient surgery and obstetric patient population, but not baricity and dose of LA used.
67
TNS RF
Treatment constitutes use of NSAIDs, muscle relaxants, leg elevation, heat pads, trigger-point injections and reassurance.
68
Abnormal Neuro exam
An abnormal neurological exam should prompt an evaluation for epidural haematoma, abscess or CES

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