Why is lidocaine given with epinephrine

Few randomized, double-blind trials have assessed the benefits of mixing short- and long-acting anesthetic solutions. Before injection, alcohol wipes should be used to clean the anesthetic vial and the skin. Alcohol wipes have been shown to be as effective as chlorhexidine Peridex or povidone-iodine Betadine on intact skin. The needle should be inserted into the site and the plunger withdrawn slightly to reduce the risk of injection directly into the vascular space.

Finally, the anesthetic should be infused slowly into the tissue, moving slowly from treated to untreated areas to reduce the pain of reinsertion. The pain of injection is caused by insertion of the needle and infiltration of the anesthetic into the skin. Ideally, the smallest gauge needle, usually 25 to 30, should be used to inject all anesthetics.

Adjunctive techniques using topical anesthetics, cryotherapy, or distraction may complement the routine use of lidocaine.

Pinching the skin stimulates local sensory nerves, partially blocking the transmission of other painful stimuli. Injecting slowly and steadily can minimize the pain of the anesthetic itself. If clinically indicated, injecting into the subcutaneous tissues is less painful than infiltrating directly into the dermis to raise a wheal. Physicians should remember that ethyl chloride is flammable and should not be used with electrocautery.

Several experiments have shown that adding sodium bicarbonate to lidocaine significantly decreases any burning sensation during infusion. Raising the pH of the anesthetic solution also appears to reduce the pain of injection without affecting the efficacy of the anesthesia. Buffered anesthetics left on the shelf may not be effective after one week.

Most local anesthetics rarely produce side effects. The most common complications occur during epidural administration or accidental intravascular administration. If large amounts of local anesthetics are absorbed rapidly, central nervous system CNS and cardiovascular toxicity may occur.

The signs and symptoms of CNS toxicity induced by local anesthetic resemble vasovagal responses. Early symptoms, such as a metallic taste, tinnitus, lightheadedness, and confusion, are followed by tremors and shivering. Ultimately, generalized seizures and respiratory arrest may occur. Local anesthetics can also have profound effects on the cardiovascular system. At low doses, local anesthetics cause systemic vasoconstriction and raise blood pressure. At high doses, local anesthetics may cause negative inotropic effects on the heart as well as heart block.

In addition, the high protein binding and lipid solubility of bupivacaine may explain rare reports of ventricular arrhythmias with the use of this agent. Toxic reactions to local anesthetics are best avoided by slow and careful injection to avoid intravascular administration. Low doses well below the toxic range should be used in patients with known peripheral vascular and cardiovascular disease Table 2 3 — 5. Epinephrine can also be used to slow absorption.

However, epinephrine is a two-edged sword because it may cause an exaggerated vasoconstrictor response and arrhythmias in susceptible patients. Warm compresses are useful if any signs of excess vasoconstriction, such as cyanosis or decreased capillary refill, are noted. Halting the injection and administering oxygen will often suffice to treat CNS and cardiovascular toxicity. If systemic toxicity appears to be worsening, immediate referral to an emergency department is indicated.

Although safety has been demonstrated with the use of both local anesthetics and epinephrine in infants and young children, the pharmacokinetics of local anesthetics are distinctly different in children and adults. The half-life of local anesthetics is also prolonged, secondary to a greater volume of distribution and decreased hepatic metabolism. 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.

The early increase in intensity is not matched with an increase in intraneural lidocaine content at these early times, although the prolonged duration of block by epinephrine appears to correspond to an enlarged lidocaine content in nerve at later times, as if a very slowly emptying "effector compartment" received a larger share of the dose.

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. Abstract Background: Adding epinephrine to lidocaine solutions for peripheral nerve block potentiates and prolongs the action, but by incompletely understood mechanisms.

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