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Discontinued Warning IconPlease Note: This Brand Name drug is no longer available in the US.
(Generic versions may still be available.)


Mechanism of Action

Etidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.

Onset and Duration of Action

In vivo animal studies have shown that etidocaine has a rapid onset (3-5 minutes) and a prolonged duration of action (5-10 hours). Based on comparative clinical studies of lidocaine and etidocaine, the anesthetic properties of etidocaine in man may be characterized as follows: Initial onset of sensory analgesia and motor blockade is rapid (usually 3-5 minutes) and similar to that produced by lidocaine. Duration of sensory analgesia is 1.5 to 2 times longer than that of lidocaine by the peridural route. The difference in analgesic duration between etidocaine and lidocaine may be even greater following peripheral nerve blockade than following central neural block. Duration of analgesia in excess of 9 hours is not infrequent when etidocaine is used for peripheral nerve blocks such as brachial plexus blockade. Etidocaine produces a profound degree of motor blockade and abdominal muscle relaxation when used for peridural analgesia.


Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system, and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.

Pharmacokinetics and Metabolism

Information derived from diverse formulations, concentrations and usages reveals that etidocaine is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon such factors as the site of administration and the presence or absence of a vasoconstrictor agent. Except for intravenous administration, the highest blood levels are obtained following intercostal nerve block and the lowest after subcutaneous administration.

The plasma binding of etidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At 0.5-1.0 µg/mL, 95% is bound to plasma protein.

Etidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.

Etidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidney. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. To date, approximately 20 metabolites of etidocaine have been found in the urine. The percent of dose excreted as unchanged drug is less than 10%.

The mean elimination half-life of etidocaine following a bolus intravenous injection is about 2.5 hours. Because of the rapid rate at which etidocaine is metabolized, any condition that affects liver function may alter etidocaine kinetics. Renal dysfunction may not affect etidocaine kinetics but may increase the accumulation of metabolites.

Factors such as acidosis and the concomitant use of CNS stimulants and depressants affect the CNS levels of etidocaine required to produce overt systemic effects. In the rhesus monkey, arterial blood levels of 4.5 mg/mL have been shown to be threshold for convulsive activity.

Last reviewed on RxList: 12/8/2004
This monograph has been modified to include the generic and brand name in many instances.

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