Download Local anesthetic systemic toxicity ( LAST)

Local anesthetic systemic toxicity
( LAST)
Dr. S. Parthasarathy
MD, DA, DNB, Dip Diab.MD ,DCA,
Dip software based statistics,
PhD (physiology) FICA
What is it ??
• Allergic reactions
• Tissue toxicity – TNS, lignocaine spinal
• Probably blockade of calcium channels ---• LAST – systemic
Allergy
• True immunologic reactions to LAs are generally rare.
• True allergic reactions to preservative-free amide-type
local anesthetics are so rare.
• True anaphylaxis appears more common with ester LAs
that are metabolized directly to PABA
• Accidental intravenous injections are often misdiagnosed
as allergic reactions.
• Some patients may react to preservatives, such as
methylparaben, included with LAs.
History
• 1880 = cocaine invented and toxicity described
• 1960 = bupivacaine discovered =
• Later levo bupi and ropi invented
• Lipid emulsion for LAST ( 0.1 in 1000)
Mechanisms
• Cardiovascular effects are caused by blockade of
cardiac VASCs and K+ channels. Levobupivacaine and
ropivacaine are thought less likely to interact with
cardiac VASCs.
• Possible calcium channel block
• Mitochondrial dysfunction
• Convulsions may be caused by the blockade of GABA
A receptors in the CNS
• Fast in fast out -- lignocaine
• Fast in slow out --- bupivacaine
• ( dissociation constant – more with bupi )
Order of toxicity
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Intercostal
Caudal
Epidural
Brachial plexus
Sciatic
IVRA
Why difference
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Age – extremes
Additive
Speed
Which drug
Concurrent illness
Concurrent drugs
Site
• Bupi – 2-3 mg / kg
• Ligno – 4-5 mg/kg
• Ligno with adrenaline
7 mg / kg
• But beware of
combinations – additive
toxicity
Toxicity
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Cocaine
Tetracaine
Bupivacaine
L. bupi
Ropi
Mepi
Ligno
Prilo
2– chlorprocaine
worst
least
Moving towards safer molecules ?
Pick up here
Starts from to
• (auditory changes, circum oral numbness,
metallic taste, and agitation),
• central nervous system (CNS) findings
(seizure, coma, respiratory arrest)
• Inhibitory neurons first !!- so seizures
• cardiovascular events (hypertension,
hypotension, tachycardia, bradycardia,
ventricular arrhythmias, cardiac arrest)
• Injection of lignocaine in the brain induced
arrhythmias
• Cause – for cardiac effects – CNS depression
hypotension and rhythm disturbances .
• Hypercarbia , acidosis enhance CNS toxicity
Differential diagnosis
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Vasovagal
High spinal
Total spinal
Concomitant disease High epinephrine dosage
Management
Prevention is the essence
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USG
Check dose of local and epinephrine
Effective dose in increments – catheters ??
Aspirate frequently
Negative aspiration not foolproof
because probe will compress the vein
Discard bloody locals
Monitor CVS and IV access
Hepatic or
Talk with the patient
renal disease
Stop injecting
(CC:CNS ratio 2 : 7.1
for the two LA)
lignocaine
Convulsion
Lethality
22 mg/kg
76mg/kg
Bupivacaine 5mg/kg
20mg/kg
Are they clinically relevant ??
• the reduced toxic potential of the two pure leftisomers supports their use in those clinical
situations in which the risk of systemic toxicity
related to either overdosing or unwanted
intravascular injection is high, such as during
epidural or peripheral nerve blocks.
Treatment
• Convulsions
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Thiopentone 1-3 mg/kg
Diazepam - 0.15 mg/kg
Midazolam – 0.1 mg / kg
Less doses – because thio itself is myocardial
depressant .propofol may cause more
hypotension
• Benzodiazepines also decrease arrhythmias
Arrhythmias
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Better to use calcium channel blockers
Valproate ( fits and rhythm disturbances )
Phenytoin
Bretylium
• NO XYLOCAINE
Resuscitation
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Airway- breathing- circulation
Oxygen - 100 %
Ventilation
Special
Vasopressin ?
CPB ?
GIK
Amiodarone
if preliminary resuscitation fails ----
Lipid emulsion
• Bolus of intralipid – 20 % - 1.5 ml/kg – 1
minute
• Infusion – 0.25 ml /kg/minute
• Chest compressions – lipid should circulate
• Can increase to 0.5 ml/kg/min
• Maximum of 8 ml/kg - 12 ml /kg – guidelines
vary
Mechanism
• Direct
• Sink theory – sticks to lipid soluble LA and get
rid of the drug out of the tissue
• Indirect
• Overrides mitochondrial translocase from the
LA
• Predominant CNS changes – anticonvulsants
• Predominant CVS changes – Go for intra lipid
early
Prilocaine
• More than 600 mg
• Associated with – o toluidine and
methemoglobinemia
• IV methylene blue is the treatment
Summary
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Intercostal , IVRA
Toxic doses
Which local anesthetic
Symptoms and DD
Prevention
Treatment
Lipid emulsion or anticonvulsants -
Thank you all