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chronic suppurative otitis media

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ANAESTHESIA—LOCAL<br />

P.Charters<br />

Mode of Action<br />

Local anaesthetic (LA) agents produce a reversible block in the transmission of impulses along nerve fibres.<br />

They vary in terms of potency, toxicity, water solubility, ability to penetrate mucous membranes and<br />

duration of action. When applied to different sites their efficacy is influenced by these properties and the<br />

local blood supply can have implications for both duration of action and liability to toxic effects. Removal<br />

from the site of action tends to be by the circulation, diffusion, metabolism or dilution which reduce local<br />

tissue concentration of the LA to restore nerve function. Local anaesthetics are weak bases and the degree<br />

of ionization depends on the individual drug’s pKa and the surrounding pH. At a low pH, more of the drug<br />

remains in the ionized form, preventing it from diffusing across the axonal membrane and therefore<br />

reducing efficacy.<br />

There are two broad classes of LA:<br />

Classification<br />

• esters (e.g. benzocaine, cocaine and procaine);<br />

• amides (e.g. lignocaine, prilocaine, bupivacaine, ropivacaine and levobupivacaine).<br />

Complications<br />

Complications associated with the use of local anaesthesia may not be common but can be life threatening<br />

and for this reason their use should be restricted to areas where resuscitation facilities are to hand.<br />

1. Toxicity. This depends on the dose of the agent and speed of uptake into the circulation. Where the<br />

circulation is poor or when vasoconstrictors (e.g. adrenaline) are administered with the LA, larger doses can<br />

be tolerated. For ENT surgery, toxicity most commonly results from inadvertent direct intravascular<br />

injection or rapid absorption via mucous membranes and toxicity from any concomitant vasoconstrictor is<br />

likely. The blood supply may be increased in infected tissue where the choice of local anaesthesia must be<br />

questioned. Manifestations of toxicity usually start during drug administration or very shortly afterwards.<br />

They include:<br />

• CNS: lightheadedness, perioral paraesthesia, slurred speech, tinnitus, facial twitching, convulsions and<br />

coma.

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