Local Anaesthetics - Lignocaine, Bupivacaine

Adrenaline

1% = 1gm in 100 ml (1: 100) or

1000 mg in 100 ml (1:100)

0.1% = 0.1 gm in 100 ml (1:1000) or

1gm in 1000 ml (1:1000) or

1000 mg in 1000 ml or

1mg in 1 ml (1:1000) that is the amount of adrenaline in 1 ml ampule is 1 mg (when it is written as 1:1000 strength)

Taking another example

if the strength is 1:10,000 or

0.01 gm in 100 ml or

1gm in 10,000 ml (1:10,000)

Taking another example

if the strength of adrenaline is 1:2,00,000 then it means

1gm in 2,00,000 ml or

1000 mg in 2,00,000 ml or

1mg in 200 ml or

0.05 mg in 1 ml or

50 μgm in 1ml

How to make 1:1,00,000 solution of Adrenaline from 1 ampule of 1:1,000 (1mg in 1ml)

mix 1ml of 1:1,000 adrenaline solution in 9 ml of saline = dilution achieved is 10ml solution of strength of 1:10,000

now mix 1ml of above solution (1:10,000) and mix with 9 ml of saline = total of 10 ml solution of dilution 1:1,00,000

Background

The toxic mechanism is via local anaesthetic agent binding reversibly to sodium channels. There may be other effects, including blockade of potassium and calcium channels, interaction with cholinergic or N-methyl-D-aspartate (NMDA) receptors and interference with cellular metabolic processes.

Most local anaesthetics are eliminated by hepatic metabolism. Most agents have elimination half-lives of 2 hours, but bupivacaine has a longer elimination half-life (5 hours or longer).

Examination

Early clinical features include:

Tinnitus
Difficulty with visual focus
Dizziness or lightheadedness
Anxiety, agitation, confusion, disorientation, drowsiness
Perioral and/or tongue numbness
Metallic taste
More severe toxicity manifests by:
CNS: seizures, coma
Cardiovascular: bradycardia, hypotension, atrial and ventricular dysrhythmias, conduction blocks, cardiovascular collapse, asystole
Respiratory: respiratory depression, apnoea.
Methaemoglobinaemia: blue mucous membranes progressing to CNS and cardiovascular manifestations of cellular hypoxia and then death.

Cardiac arrest may be the first clinical manifestation following massive intravenous overdose.

Investigations

Urea, Creatinine and Electrolytes, arterial blood gases (ABG), methaemoglobin concentration,

Serial ECGs looking for evidence of sodium channel blockade (prolonged PR and QRS intervals, large terminal R wave in aVR)

Management

Resuscitation

Standard procedures and supportive care
If there is evidence of cardiotoxicity, immediate intubation and ventilation is necessary to prevent hypoxaemia, hypercarbia and acidosis
Treat ventricular dysrhythmias with sodium bicarbonate (1 – 2mmol/kg up to 100mmol) IV every 1-2 minutes until perfusing rhythm;
amiodarone;
AVOID calcium channel blockers, beta blockers, local anaesthetics (Xylocard)
Treat seizures with benzodiazepines
Treat hypotension with intravenous normal saline 20mL/kg followed by inotropes if required;
AVOID vasopressin
Intravenous lipid emulsion

Recovery from local-anaesthetic induced cardiac arrest may take > 1hr

Antidotes

Sodium bicarbonate for ventricular dysrhythmias secondary to sodium channel blockade (see above).
Methylene blue for methaemoglobinaemia: 1 - 2 mg/kg IV over 5 minutes.
Intravenous lipid emulsion (intralipid 20%) in severe cardiovascular toxicity or cardiac arrest.

Administration of lipid emulsion therapy with 20% lipid emulsion

Bolus 1.5 mL/kg IV over 1 minute
Continuous infusion 0.25 mL/kg/minute

Wait 5 Minutes, then

Give a maximum of 2 repeat boluses for persistent cardiovascular collapse or deterioration (at least 5 minutes between boluses), AND
Double infusion to 0.5 mL/kg/minute
Continue infusion until stable and adequate circulation or maximum dose of lipid emulsion has been given (maximum cumulative dose is 12ml/kg)

Surgical Diseases