The increase in early analgesia without increased lidocaine content may be explained by a pharmacodynamic action of epinephrine that transiently enhances lidocaine's potency, but also by a pharmacokinetic effect that alters the distribution of the same net content of lidocaine within the nerve.
DURING peripheral nerve block with lidocaine, vasomotor effects often result in diverse changes in local blood flow. Little reduction in nerve blood flow occurs when 0.
Furthermore, the initial blood flow change may itself be reversed over time as the effective LA concentration naturally decreases as a result of the local redistribution into the different tissues and removal by the circulation. Anesthesiologists often add epinephrine to lidocaine during peripheral nerve block procedures.
First, it reduces the LA plasma concentration and thus minimizes the possibility of systemic toxicity, 8 and second, it improves the quality and prolongs the duration of peripheral nerve block. It appears that epinephrine binds to those adrenergic receptors located on the extrinsic plexus of vessels in the epineural space.
An increase in the duration of LA block by epinephrine is accompanied by a potentiation of effect at submaximal LA doses. However, such potentiation may also occur by pharmacodynamic actions of epinephrine on nerve membranes. To discriminate between these two mechanisms, we correlated measures of intraneural lidocaine with assays of analgesia.
To do this, we performed percutaneous sciatic nerve blocks in rats with 0. We chose this relatively low concentration of lidocaine, which alone does not produce complete impairment of nociception, to resolve differences in the intensity as well as the duration of block and so that any vasoactive effects of lidocaine would be small and not obscure those of epinephrine.
For similar reasons, we chose , epinephrine, twice the usual concentration coinjected with LA, to produce a greater vasoconstriction and to overcome any vasodilator actions of lidocaine.
Just before nerves were dissected, the intensity of sensory block was assessed by the withdrawal response to a strong forceps pinch to the fifth metatarsal. The general objective was to compare and correlate intraneural lidocaine content with the intensity of block and to determine if epinephrine modified that relation. All behavioral testing and surgical procedures were approved by the Harvard Medical Area Committee on Animals. Two solutions of [ 14 C] radiolabeled lidocaine, both at 0.
Ten milliliters of 0. Epinephrine HCl solution , prepared by dissolving epinephrine HCl crystal Sigma Chemical in sterile water, was further diluted in the lidocaine solutions to a final epinephrine concentration of , The pH of all lidocaine solutions was adjusted to pH 7.
These solutions were made slightly alkaline pH 7. Lidocaine is stable for several hours at pH 7. Since the objective of this investigation was to correlate the degree of analgesia with intraneural lidocaine content using solutions of lidocaine alone and lidocaine containing epinephrine LE , it is important to mention the results of a previous study performed in our laboratory.
The injection of epinephrine alone at a concentration of , in the rat sciatic nerve produced no impairment of nocifensive function for 60 min. Two solutions of 0. The injection technique used in this study was the same used previously to produce motor and sensory block of the sciatic nerve in the rat.
Full recovery of behavior occurred within 90— s after removal of sevoflurane anesthesia in rats receiving no LA. Before the nerves were excised for analysis of neural content, the lateral toe of the hind limb on the injected side was pinched strongly until bone resistance was felt with serrated forceps —12; Fine Science Tools, Foster City, CA.
This was done to directly correlate the intensity of nerve block with intraneural lidocaine content in individual animals used for the uptake studies. In separate experiments conducted to account for any general anesthetic effects on the subsequent analgesia, we periodically monitored the course of functional deficits in rats from which no nerves were removed. These animals, handled and familiarized according to our standard procedures, 20 were never anesthetized by sevoflurane.
To assess the intensity of nerve block, we used a modification of the neurologic evaluation described by Thalhammer et al. Previous reports showed that motor block of the sciatic nerve could not account for withdrawal response deficits, proving that true nociceptive loss was being tested.
In addition, the percent of animals in each group that were fully blocked score of 0 was assessed, and differences between this parameter in epinephrine-containing and epinephrine-free groups were compared for identical times after injection. After injection of a radiolabeled lidocaine solution, the sciatic nerve was excised at one of eight time points: 2, 4, 7, 10, 15, 30, 60, and min. Animals were killed by deep inhalation anesthesia with a cotton ball saturated with sevoflurane.
The sciatic nerve was then dissected in less than 3 min in a modification of the technique described by Popitz et al. The excised portion of the sciatic nerve was frozen in less than 5 s on a flat surface of dry ice and cut into six segments, 5 mm long.
The specific radioactivity was determined by dividing the counts per minute for each injectate by the moles of lidocaine in the solution. The measured radioactivity represented the amount of intraneural lidocaine, expressed as nanomoles of lidocaine per milligram wet weight of nerve. We used a decaying exponential function to describe the clearance of lidocaine from peripheral nerve, both with and without epinephrine.
Because the large coefficient of variation of experimental data would accommodate fits of other mathematical functions, we chose the simplest one on the principle of parsimony. Parameter L f describes the amplitude of the fast-decaying component, k represents a transport rate coefficient for the rapid removal phase washout from nerve , and L s represents the amplitude of the steady state plateau component, which eventually decays to the baseline value; t is the time after the injection.
By fitting this equation to the intraneural lidocaine content data points, we were able to determine how epinephrine affected the three parameters, L f , k, and L s. Standard deviations were only reported as an indication of the spread of observations but were not used in the statistical analysis.
All behavioral data for each condition were collected from one group for each time point taken for neural content just before animals were killed , so no adjustment was necessary for repeated measures. Addition of epinephrine enhanced sciatic nerve blockade by lidocaine. The degree of analgesia obtained with epinephrine was significantly greater than that without epinephrine throughout almost the entire procedure fig.
The percent of animals fully blocked by lidocaine was almost always greater in the LE group, the single exception occurring at 7 min after injection, the time of maximum block for rats without epinephrine fig. Indeed, at 4 min after the LA injection, all the rats receiving LE were completely blocked, whereas none of the rats receiving lidocaine alone were completely blocked.
Complete block by LE occurring in all rats lasted for 1 h, and complete recovery was achieved after 2 h, whereas, in the fewer rats that were completely blocked by lidocaine alone, that block lasted for about 10 min and fully recovered by 30 min fig.
A Time course of analgesia measured by the response to a deep forceps pinch of the fifth metatarsal after injection of 0. B Time course of percent animals completely blocked measured by response to deep pinch of fifth metatarsal after injection of 0. Injection of the LE solution produced generally higher total intraneural drug content compared with the solution without epinephrine fig. For the first 10 min after injection, this difference did not reach significance because of, at least in part, the large variances , but at 15, 30, and 60 min, differences in intraneural lidocaine content were significant.
At 15 min, the intraneural lidocaine content was 3. The ratio of mean lidocaine content for injections of LE to that of lidocaine alone was 1. Therefore, the effect of epinephrine on content grew stronger at longer times after injection, primarily because of the decay in lidocaine content in epinephrine-free nerves over this period.
Time course of total intraneural lidocaine content nanomoles per milligram wet weight of nerve after injection of 0. Parameters of the fit are shown on the figure.
The intraneural content of lidocaine over time can be described by an early, transient washout phase whose rapid disappearance is followed by a constant plateau phase, which eventually decreases to zero over 1—2 h fig. These kinetics can be fit from 4 to 60 min by a fast exponentially decaying function, with rate constant k, superimposed on a constant level, with respective amplitudes L f and L s see Methods.
Fits of this function to the data show that the transient decay rate constant, k, was almost twofold greater with epinephrine than without 0. The amplitude of the fast transient, L f , i. We emphasize the empirical basis for this fitting and the arbitrary assumption of a constant content for the plateau from 4 min onward.
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Read more…. CDA Oasis March 22, Dosage May be used in concentrations of , to , Depending on the local anesthetic with which epinephrine is combined, maximum recommended doses of the local anesthetic component are typically reached BEFORE the maximum recommended dose of the epinephrine component.
This may not be the case for more concentrated solutions which are normally reserved for local hemostasis, such as cartridges containing , epinephrine i. Special Clinical Implications Use with caution In patients taking non-selective beta-adrenergic blocking agents and who require simple restorative procedures, it is preferable to avoid epinephrine.
For complex procedures that require a more prolonged duration of local anesthesia, keep initial vasoconstrictor doses to an absolute minimum 0. Pregnancy and lactation Use during pregnancy when the potential benefit to the mother outweighs the possible risk to the fetus.
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