LOCAL ANAESTHETICS

By;
Dr Dennis K Barnes, BSc,MBChB,DiPAnaesth.,MWACS,MGCPS Specialist Anaesthesiologist KATH

22-Jun-11

Definition of a local anaesthetic

A local anaesthetic can be defined as a drug which reversibly prevents transmission of the nerve impulse in the region to which it is applied, without affecting consciousness.

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The structural classification of local anaesthetics



Local anaesthetics generally have a lipid-soluble lipidhydrophobic AROMATIC group and a charged, hydrophilic AMINE group. The bond between these two groups determines the class of the drug, and may be; 1) Amide E.g include lidocaine, bupivacaine and lidocaine, prilocaine. prilocaine. 2)Ester E.g include cocaine and amethocaine. amethocaine.

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Msm of action
 

 

L.A act by preventing axon depolarization They stabilize the NM membrane and prevent the migration of ions across it Small fibres are blocked before large fibres Order of blockade is; Pain,temperature and lastly motor

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caudal

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Pharmacokinetics of local anaesthetics



Absorption and distribution Local anaesthetic drugs are administered to the areas around the nerves to be blocked which include skin, subcutaneous tissues, intrathecal and epidural spaces. how much ABSORBED, will depend on the vascularity of the area to which the drug has been applied and intrinsic effects of the drug or its additives on vessel diameter.

Some local anaesthetics have vasodilatory effects at low concentrations, increasing their systemic absorption. This is countered in some preparations which include a vasoconstrictor such as adrenaline or felypressin. felypressin. Cocaine, in contrast, has a vasoconstrictive effect.

22-Jun-11

Metabolism and excretion

 

Ester and amide anaesthetics differ in their metabolism. Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal. Amides are metabolised hepatically by amidases. This is amidases. a slower process, hence their half-life is longer and they halfcan accumulate if given in repeated doses or by infusion. Prilocaine is also metabolised extra-hepatically. extra-hepatically.

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Clinical uses of local anaesthetics



Preparations Local anaesthetics are available as solutions for injection, sprays, creams and gels. Most local anaesthetic preparations contain a preservative agent such as 0.1% sodium metabisulphite, with or metabisulphite, without a fungicide.

The drug may also be combined (by the manufacturer or in some cases the clinician) with other local anaesthetics (e.g. EMLA cream eutectic mixture of local anaesthetics) or additives designed to enhance their effects. These include adrenaline 1/200,000, bicarbonate (eg 0.15ml of (eg 8.4% solution added to 10ml 0.5% bupivacaine) or glucose (usually bupivacaine) 80mg/ml).

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spinal

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How might adrenaline, bicarbonate and glucose variously affect the action of local anaesthetics?

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L.A Xtics
  

Potency is directly related to lipid solubility DOA is related to protein binding Speed of Onset depends on degree of ionisation,pH and pKa A higher pKa is associated with slow onset in normal pH settings

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L.A TOXICITY
Toxic side effects of local anaesthetic drugs occur when excessive blood levels occur. This is usually due to:  Accidental rapid intravenous injection.  Rapid absorption, such as from a very vascular site ie mucous membranes. Intercostal nerve blocks will give a higher blood level than subcutaneous infiltration, whereas plexus blocks are associated with the slowest rates of absorption and therefore give the lowest blood levels.  Absolute overdose if the dose used is excessive
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UnUn-Bolt !! During injection

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Case History


 

A 20 year old mother who had just delivered a baby started to fit and then developed a cardiac arrest whilst a midwife was injecting lignocaine prior to suturing her episiotomy infiltration. What is the cause? What do u do?

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Mx


Prompt resuscitation with airway, intubation and ventilation, chest compressions, intravenous fluid and adrenaline saved her life. When the ampoule of lignocaine was checked it was found that the midwife had used 10mls of 10% lignocaine for infiltration (1000mg), more than 5 times the maximum permitted dose for

22-Jun-11

CNS signs & symptoms

Early or mild toxicity: light-headedness, lightdizziness, tinnitus, circumoral numbness, abnormal taste, confusion and drowsiness. Patients often will not volunteer information about these symptoms unless asked. Throughout the injection talk to the patient asking them how they feel. Any suggestion of confusion should alert you to the possibility of toxicity and you should stop any further injection.
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Severe toxicity: tonic-clonic convulsion toxicity: tonicleading to progressive loss of consciousness, coma, respiratory depression, and respiratory arrest. Depending on the drug and the speed of the rise in blood level the patient may go from awake to convulsing within a very short time.

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CVS signs & symptoms



Early or mild toxicity: tachycardia and rise toxicity: in BP. This will usually only occur if there is adrenaline in the local anaesthetic. If no adrenaline is added then bradycardia with hypotension will occur.

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Severe toxicity: Usually about 4 - 7 times the convulsant dose needs to be injected before cardiovascular collapse occurs. Collapse is due to the depressant effect of the local anaesthetic acting directly on the myocardium. Bupivacaine is considered to be more cardiotoxic than lignocaine. Severe and intractable arrhythmias can occur with accidental iv injection. The acute toxicity of local anaesthetics is due to the speed of rise of blood concentration. Therefore a rapid concentration. injection of a small volume may cause toxicity

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Essential Precautions


ALWAYS secure intravenous access before injection of any dose that may cause toxic effects. Always have adequate resuscitation equipment and drugs available before starting to inject.

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Treatment of Toxicity


If a patient you are attending shows any signs or symptoms of toxicity during injection of local anaesthetic stop the injection and assess the patient. Treatment is based on the A B C D of Basic Life Support Call for help while treating the patient

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A.Ensure A.Ensure an adequate airway, give airway, oxygen in high concentration if available. B.Ensure B.Ensure that the patient is breathing adequately. Ventilate the patient with a SIB if there is inadequate spontaneous respiration. Intubation may be required if the patient is unconscious and unable to maintain an airway.
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C.Treat circulatory failure with C.Treat intravenous fluids and vasopressors such as ephedrine (10mg boluses) if hypotension occurs. Adrenaline may be used cautiously intravenously in boluses of 0.5 - 1ml of 1:10,000 (1mg in 10ml) if ephedrine is either not available or not effective in correcting the hypotension. Treat arrhythmias.Start chest compressions if cardiac arrest occurs.

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D.Drugs to stop fitting such as Diazepam 0.20.2-0.4mg/kg intravenously slowly over 5 minutes repeated after 10 minutes if required, or 2.5mg - 10 mg rectally. Propofol,midazolam,Thiopentone intravenously may also be used in theatre.Observe the patient closely after any reaction.

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To do?
     

Toxic doses of various L.A agents PKa Onset of action Relative Potency Relative lipid solubility LIDOCAINE as prototype

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CHEERS.

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