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At least 19 recordsLinked to original sources
PubMed2026

Morbidity and mortality from local anesthetics: localized and systemic toxicity.

PURPOSE OF THE REVIEW: Local anesthetics remain vital to modern medicine, yet their narrow therapeutic window continues to result in complications. This review synthesizes recent literature to define the current landscape of local anesthetic-associated adverse events. RECENT FINDINGS: Perioperative mortality attributable to local anesthetics persists despite sustained safety initiatives and professional society recommendations. Pharmacovigilance and case data identify lidocaine (oropharyngeal, topical, and via local infiltration) as the predominant contributor to adverse outcomes, including death. Local anesthetic systemic toxicity remains an issue, with a recent shift in epidemiology: an increasing proportion of toxic events originates from surgeon- and proceduralist-administered analgesia. Anesthesiologist-controlled methods also cause toxicity via catheter-based delivery and nerve blocks in highly vascular regions. Localized toxicity in the form of high neuraxial contributes to morbidity, with recent reviews reinforcing known risk factors; whereas localized neurotoxicity appears less troublesome when managed appropriately. SUMMARY: The cumulative evidence identifies shifts in the patterns of systemic and localized toxicities. Bupivacaine-based peripheral nerve blocks no longer represent the principal cause of complications because of the advent of ultrasound guidance and lipid emulsion therapy. In contrast, high neuraxial techniques persist as a cause of morbidity, accompanied by intravenous/oropharyngeal lidocaine, proceduralist-administered local infiltration analgesia, and catheter-based delivery.

Humans↗
PubMed1980

Skeletal muscle oxygen pressure fields in rats. A study of the normal state and the effects of local anesthetics, local trauma and hemorrhage.

The MDO (Mehrdraht Dortmund Oberfläche) oxygen electrode was used for studies of oxygen pressure fields in rat skeletal muscle. With this multiwire oxygen electrode, the three-dimensional oxygen pressure field was measured and presented as a two-dimensional frequency distribution, i.e., a histogram. Statistical analysis of the histograms was carried out with the two-sample Kolmogorov-Smirnov test. This eliminated the influence of mean values, since these do not always represent the actual biological situation. The oxygen pressure fields in skeletal muscle of anesthetized normal rats breathing air spontaneously were investigated. When the oxygen pressure in the inspired gas was changed (50% and 95%), changes were seen in muscle oxygen pressure curves. The normal oxygen pressure field histograms were compared with those obtained after local anesthesia, after local trauma to the muscle and after hemorrhage. After local anesthesia the histograms were unchanged. Significant changes in the distribution types of the histograms were found after trauma in all rats studied. After hemorrhage significant changes, similar to those seen after trauma, were found in 15 of the 23 rats studied. Local blood flow was also measured with the 133xenon-clearance method in the hemorrhage experiments. No correlation was found between the changes in the mean oxygen tension values and the changes in 133xenon-clearance.

Animals↗
PubMed1997

[Clinical study of patients with positive reactions in patch tests with local anesthetics].

Local anesthetics have been contained in various OTC drugs and the number of cases of allergic contact dermatitis due to local anesthetics has increased recently. Thirty-five hundreds and fourteen cases suspected of suffering from drug eruption or contact dermatitis were the subjects of this study during the 8 years from January, 1988 to December, 1995. One hundred and thirty-eight cases, suspected of having allergic contact dermatitis were patch tested with topical medicaments including local anesthetics and 70 (50.7%) of them showed positive. In 49 of the 60 cases who reacted positively to anesthetics extensive patch tests with the individual ingredients of the products were carried out. The local anesthetics causing positive reactions were as follows (in order of frequency): dibucaine hydrochloride (35 cases: 71.4%), ethyl aminobenzoate (12 cases: 24.5%), lidocaine hydrochloride (2 cases: 4.1%), and procaine hydrochloride (1 case: 2.0%). The number of patients displaying allergies to local anesthetics has increased, especially cases caused by dibucaine hydrochloride. And the total positive reaction rate to dibucaine hydrochloride in the patch tests was 3.7%, which was as high that to the well-known strong sensitizer PPDA (3.9%) and neomycin (2.9%). Forty-three cases sensitive to local anesthetics were also studied for cross-sensitivity.

Anesthetics, Local↗
PubMed2000

Direct inhibition of microtubule-based kinesin motility by local anesthetics.

Local anesthetics are known to inhibit neuronal fast anterograde axoplasmic transport (FAAT) in a reversible and dose-dependent manner, but the precise mechanism has not been determined. FAAT is powered by kinesin superfamily proteins, which transport membranous organelles, vesicles, or protein complexes along microtubules. We investigated the direct effect of local anesthetics on kinesin, using both in vitro motility and single-molecule motility assays. In the modified in vitro motility assay, local anesthetics immediately and reversibly stopped the kinesin-based microtubule movement in an all-or-none fashion without lowering kinesin ATPase activity. QX-314, a permanently charged derivative of lidocaine, exerted an effect similar to that of lidocaine, suggesting that the effect of anesthetics is due to the charged form of the anesthetics. In the single-molecule motility assay, the local anesthetic tetracaine inhibited the motility of individual kinesin molecules in a dose-dependent manner. The concentrations of the anesthetics that inhibited the motility of kinesin correlated well with those blocking FAAT. We conclude that the charged form of local anesthetics directly and reversibly inhibits kinesin motility in a dose-dependent manner, and it is the major cause of the inhibition of FAAT by local anesthetics.

Adenosine Triphosphatases↗
PubMed2026

Adductor Canal Block and Local Anesthetic Versus Local Anesthetic Alone in ACL Reconstruction: A Double-Blind Randomized Controlled Trial.

BACKGROUND: Effective postoperative analgesia is crucial for early recovery after anterior cruciate ligament reconstruction (ACLR). Local infiltration analgesia (LIA) and adductor canal block (ACB) are common regional techniques, but their combined efficacy remains unclear. PURPOSE: To compare the effectiveness of LIA alone versus LIA combined with ACB in patients undergoing ACLR, with primary outcomes including postoperative opioid consumption and quadriceps function. STUDY DESIGN: Randomized controlled trial; Level of evidence, 1. METHODS: A double-blind randomized controlled trial enrolled 100 patients undergoing ACLR under general anesthesia. Patients were randomized into 2 groups: LIA + sham (saline injection) (n = 50) and LIA + ACB (n = 50). The primary outcome was postoperative opioid consumption in the first 24 hours. Secondary outcomes included visual analog scale (VAS) pain score, quadriceps function assessed by straight leg raise (SLR) at 3 hours, Quality of Recovery-15 (QoR-15) score, and Knee Injury and Osteoarthritis Outcome Score (KOOS) at 1 week. Statistical analysis was performed using t tests and chi-square tests with a P value <.05 considered significant. RESULTS: There was no significant difference in 24-hour opioid consumption between the LIA + ACB and LIA-only groups (P = .109). Similarly, VAS pain scores at 24 hours postoperatively showed no significant differences between the groups (P = .0804). Early functional recovery, assessed by SLR performance at 3 hours, was equivalent between groups (P = .6711). Additionally, QoR-15 scores on postoperative day 1 and KOOS values at 1 week demonstrated no significant differences (P = .6486 and P = .9054, respectively). Intraoperative opioid consumption was not different between the groups (P = .127). CONCLUSION: These findings indicate that the addition of ACB to LIA does not yield postoperative analgesic in ACLR. Consequently, LIA alone suffices for routine ACLR, potentially enabling clinicians to optimize perioperative workflows without incurring the additional time, financial burden, and resources associated with routine ACB administration. TRIAL REGISTRATION: ClinicalTrials.gov; NCT04721119.

Humans↗
PubMed1992

[Local anesthetics. CVII. Local anesthetic effects of phenylcarbamates--the effect of connecting chain modification].

The preceding study of the effect of the branching of the connecting chain by the metoxymethyl-, ethoxymethyl- and propoxymethyl group on the alpha carbon on local anaesthetic activity was a stimulus for the preparation of 16 drugs of the group of 1-ethoxyethoxymethyl-2-(1-pyrrolidinyl-), 2-piperidino- and 2-(1-perhydroazepinyl) ethyl esters of o-, m- and p-alkoxyphenylcarbamic acids. The discontinuation of the substituent on the alpha carbon of the connecting chain by another oxygen atom (introduction of an ethoxyethoxymethyl group) has a positive effect on surface and infiltration anaesthesia. Of the prepared agents, 2-piperidino- and 2-(1-perhydroazepinyl-) derivatives with a hexyl or heptyloxy group in the o-position of the benzene ring were most effective; they exceeded the standards cocaine and procaine more than one hundred times. p-Derivatives were least effective; in some cases their indices of effectiveness did not achieve the effectiveness of the standards in both surface and infiltration anaesthesia under study. Acute toxicity of all drugs lies within the range of the toxicities of the standards.

Anesthetics, Local↗
PubMed1976

Molecular mechanisms of nerve block by local anesthetics.

Local anesthetics block nerve conduction by preventing the increase in membrane permeability to sodium ions that normally leads to a nerve impulse. Among anesthetics containing tertiary amine groups, the cationic, protonated form appears to be more active than the neutral form. However, the neutral forms, as well as uncharged molecules like benzocaine and the aliphatic alcohols, also depress sodium permeability. Studies of single myelinated nerves and squid axons show no direct interaction between calcium ions and local anesthetics, thus disproving theories based on competition between these two agents. Likewise, hypotheses attributing local anesthesia to changes in electrical potentials at the membrane-water interface are disproven by the demonstrated potencies of electrically uncharged anesthetics. Hypotheses that propose that local anesthetics act by expanding the nerve membrane and causing a change in protein conformation that blocks sodium permeability are vague in conception and difficult to test experimentally. Evidence from voltage-clamp studies of single nerve fibers indicates that anesthetic molecules interact with the sodium channels directly, from the inner side of the nerve membrane. Anesthetics bind within sodium channels which have opened during membrane depolarization, preventing the normal sodium ion flux. Anesthetic molecules can dissociate from open channels, but not from channels that remain closed when the nerve is kept at rest. The "gating" properties that regulate the opening and closing of sodium channels are reversibly modified during anesthesia. Specifically, the inactivation function responds more slowly and requires more negative membrane potential changes to reach the same values as in unanesthetized nerves. A second, slow inactivation is observed following external application of tertiary amine anesthetics. The selective binding of anesthetics to open sodium channels provides a simple explanation for Wedenski inhibition, in which the block increases with the frequency of nerve impulses. When impulses occur at higher frequencies more sodium channels are open over a period of time comparable to the time necessary for the anesthetic binding reaction, thus more channels are blocked. In addition the changes of the inactivation function result in a longer refractory period and, thus, a decrease of impulse height at higher frequencies. Charged anesthetic molecules may bind in the pore of the sodium channel. Their binding can be modulated by the electrical field in the membrane. The channel has a higher affinity for larger anesthetic molecules, but this may result from their greater hydrophobicity as well as from their size. The binding site favors molecules that contain more polar linkages between the amine group and the aromatic residue. Binding of amine anesthetics is weakly stereospecific and, surprisingly, shows no absolute requirement for the terminal alkyl ammonium moiety present in most local anesthetics...

Action Potentials↗
PubMed1995

Ropivacaine: an introduction to a new local anesthetic.

Local anesthetic drugs interrupt nerve transmission by inhibiting the passage of sodium ions (Na+) across neuronal membranes. Signal propagation and transmission along central and peripheral nerve pathways are impeded after the injection of these drugs near or on neuronal tissue. This article briefly reviews the basic pharmacology and toxicology of local anesthetic agents as well as recent studies of regional anesthesia performed with ropivacaine, a versatile new amide local anesthetic with a duration of action similar to bupivacaine, but with less systemic toxicity.

Amides↗
PubMed1994

Local anesthetics.

Local anesthetics have been especially important in establishing pain control as a fundamental accomplishment in clinical dentistry. When used conscientiously, local anesthetics are effective and safe. It is helpful for clinical dentists to understand the workings of these adjuncts. The more we understand them, the better we will be able to use them.

Anesthesia, Dental↗
PubMed1977

Neural blockade by local anesthetics.

Local anesthetics block nerve impulse propagation by occluding transmembrane sodium channels, so preventing depolarization. First, the uncharged lipid-soluble anesthetic base pentrates the membrane; then the positively charged cation binds to anionic components of the sodium channel's internal axoplasmic mouth. Though primarily a carrier, the base contributes to blockade by causing the membrane to swell, so pinching the sodium channels. Dissolved in water, local anesthetic salt crystals dissociate into anesthetic cation and base-proportional to the drug's fixed pKa and the tissue's variable pH. The cation-base concentration ration is critical to optimal neural blockade. If there is too little base, few anesthetic molecules will penetrate to the neural target; if too little cation, few sodium channels will be plugged.

Anesthetics, Local↗
PubMed1981

Multiple sites of inhibition of mitochondrial electron transport by local anesthetics.

Local anesthetics and alcohols were found to inhibit mitochondrial electron transport at several points along the chain. THe anesthetics employed were the tertiary amines procaine, tetracaine, dibucaine, and chlorpromazine, and the alcohols were n-butamol, n-pentanol, n-hexanol, and benzyl alcohol. Uncoupled sonic submitochondrial particles from beef heart and rat liver were studied. We report the following: (1) All of the anesthetics were found to inhibit each of the segments of the electron transport chain assayed; these included cytochrome c oxidase, durohydroquinone oxidase, succinate oxidase, NADH oxidase, succinate dehydrogenase, succinate-cytochrome c oxidoreductase, and NADH-cytochrome c oxidoreductase. (2) NADH oxidase and NADH-cytochrome c oxidoreductase required the lowest concentration of anesthetic for inhibition, and cytochrome c oxidase required the highest concentrations. (3) We conclude that there are several points along the chain at which inhibition occurs, the most sensitive being in the region of Complex I (NADH dehydrogenase). (4) Beef heart submitochondrial particles are less sensitive to inhibition than are rat liver particles. (5) Low concentrations of several of the anesthetics gave enhancement of electron transport activity, whereas higher concentrations of the same agents caused inhibition. (6) The concentrations of anesthetics (alcohol and tertiary amine) which gave 50% inhibition of NADH oxidase were lower than the reported concentrations required for blockage of frog sciatic nerve.

Alcohols↗
PubMed1985

Local anesthetics.

Local anesthetics are remarkably useful agents that enhance patient comfort and improve patient compliance. Their use, however, requires an understanding of their action, proper dosages, potential risks, and treatment of reactions. We have presented the history, pharmacokinetics, action, risks of using, and ways in which agents are used to treat the most common agents, with notes on the special aspects of each agent. With the increased awareness that these are, indeed, not benign substances, we hope that serious reactions can be avoided by prophylactic measures and proper treatment in the early stages of toxicity.

Anesthesia, Conduction↗
PubMed1993

Inhibition of brain cell excitability by lidocaine, QX314, and tetrodotoxin: a mechanism for analgesia from infused local anesthetics?

Local anesthetic infusions have been used to provide analgesia in a variety of painful conditions. The mechanism for this drug effect remains unknown. To better define the electrical effects of lidocaine concentrations comparable to those obtained during analgesic infusions, lidocaine (0.05-3 mmol.l-1), QX314 (an obligatorily charged, quaternary lidocaine derivative applied within the cells), and tetrodotoxin (10 mmol.l-1) were applied to rat hippocampal pyramidal cells. The three drugs, which inhibit Na+ currents by varying mechanisms, produced tonic increases in (firing) current threshold, and decreases in the amplitude of action potentials measured using an intracellular microelectrode technique. Lidocaine inhibited action potential spikes and increased current threshold in a concentration-dependent fashion. Lidocaine 50 and 100 mumol.l-1 did not inhibit action potentials, but increased firing threshold by nearly 100%. Lidocaine 1-3 mmol.l-1 significantly inhibited action potential amplitude and increased threshold by as much as 800%. Similarly, QX314 and tetrodotoxin produced greater increases in current threshold than in action potential amplitude. QX314 produced phasic (or frequency-dependent) block during trains of stimuli at 1 Hz, even when almost no tonic block was present. Lidocaine produced less phasic block than QX314, and required both greater tonic block and more frequent stimulation to produce the phenomenon. Tetrodotoxin demonstrated no phasic block. Increases in current threshold occurred in lidocaine concentrations associated with analgesia and toxicity; inhibition of action potentials occurred scarcely at all at these concentrations. Thus, tonic increases in current threshold may underlie analgesia and supplementation of general anesthesia by intravenous lidocaine.

Analgesia↗
PubMedDate not supplied

Alkalinization of local anesthetics. Which block, which local anesthetic?

BACKGROUND AND OBJECTIVES: A number of clinical studies have been performed in an attempt to establish the effects of alkalinization on potency of local anesthetics. Conflicting results were obtained probably because different studies used different methods as well as different definitions of the effects. To determine the efficacy of alkalinization using different local anesthetic solutions and different regional blocks, 180 patients were studied in a randomized, double-blind fashion. The local anesthetic solutions studied were bupivacaine, mepivacaine, and lidocaine; the regional blocks studied were epidural block, axillary brachial plexus block, and femoral and sciatic nerve block. MATERIALS AND METHODS: In this study, 180 patients receiving epidural block (n = 60), sciatic and femoral nerve block (n = 60), and brachial plexus block (n = 60) were randomized to receive, in a double-blind fashion, a plain or a pH-adjusted solution of 2% mepivacaine, 2% lidocaine, or 0.5% bupivacaine. Onset of sensory analgesia, onset of maximum effect (peak effect or complete analgesia), duration of the block, onset, duration and density of motor block were evaluated using pinprick (Hollmen scale) and a 10-point decimal scale (Seow scale). RESULTS: concerning epidural block, the alkalinization of the local anesthetic shortened significantly the onset of sensory analgesia in the dermatome corresponding to the lumbar interspace used for epidural puncture (L3-L4) and increased the spread of the epidural block in all the groups. The onset of sensory analgesia at L4 level ranged from 10 minutes for plain bupivacaine to 3 minutes for alkalinized lidocaine, whereas the onset at T10 level ranged from 16 minutes for plain bupivacaine and mepivacaine to 12.3 minutes for alkalinized lidocaine. The effects of alkalinization were more evident with lidocaine and bupivacaine. Concerning femoral and sciatic nerve blocks, a statistically significant shorter onset of sensory analgesia and motor block were observed with mepivacaine. Concerning brachial plexus axillary block, the effects of alkalinization were more evident with lidocaine. CONCLUSIONS: Alkalinization produced the best results with lidocaine and bupivacaine for epidural block, with lidocaine for brachial plexus block, and with mepivacaine for sciatic and femoral nerve blocks.

Adult↗