Lidocaine For Analgesia Research Articles

Lidocaine for prevention of propofol injection-induced pain: A prospective, randomized, double-blind, controlled study of the effect of duration of venous occlusion with a tourniquet in adults

Background: Many patients experience pain on injection of propofol. The use of lidocaine to prevent propofol injection pain is common. The analgesic effect of pre-injected lidocaine has been found to increase when a tourniquet is used. Objective: The aim of this study was to compare the effectiveness of various venous occlusion times with lidocaine analgesia to prevent pain during propofol injection. Methods: In this prospective, randomized, double-blind, controlled study, women aged 18 to 45 years, classifed as American Society of Anesthesiologists physical sta- tus I or II, who were scheduled to undergo elective surgery under general anesthesia induced with propofol, were randomly assigned to 1 of 5 groups: group 1, 2% lidocaine 20 mg in saline in a total volume of 10 mL and no venous occlusion; group 2, 2% lidocaine 20 mg in saline in a total volume of 10 mL plus venous occlusion for 15 seconds; group 3, 2% lidocaine plus venous occlusion for 30 seconds; group 4, 2% lidocaine plus venous occlusion for 60 seconds; and group 5, saline 10 mL and no venous occlusion. When the first 25% of the calculated propofol dose was administered, patients were asked about propofol-induced pain using a verbal pain scale (0 = no pain; 1 = mild pain; 2 = moderate pain; and 3 = severe pain). All patients and the anesthesiologist who evaluated pain severity were blinded to the study preparation being used. Results: The study comprised 100 women who were randomly divided into 5 groups of 20 patients each. Significantly more patients in group 5 (18 [90%] patients; P < 0.05) reported pain compared with the other treatment groups. In groups 2, 3, and 4, in which venous occlusion was applied, pain was reported during propofol injection in 6 (30%), 7 (35%), and 2 (10%) patients, respectively. The incidence of reported pain was significantly greater in group 1 (lidocaine without venous occlusion) than in group 4 ( P < 0.05); however, the incidence of pain was similar in group 1 compared with groups 2 and 3. Conclusions: The present study found that pretreatment with lidocaine 20 mg with or without venous occlusion significantly reduced the incidence and the severity of pain during the injection of propofol when compared with the group with no venous occlusion administered saline. In addition, pretreatment with lidocaine 20 mg plus venous occlusion for 60 seconds significantly reduced the incidence of propofol-induced pain compared with lidocaine without venous occlusion.

277 Reorganization of DRG neurons following chronic sciatic nerve constriction injury: Correlation with topical morphine and lidocaine analgesia

277 Reorganization of DRG neurons following chronic sciatic nerve constriction injury: Correlation with topical morphine and lidocaine analgesia

Reorganization of dorsal root ganglion neurons following chronic sciatic nerve constriction injury: Correlation with morphine and lidocaine analgesia

Chronic constriction injury of the sciatic nerve is an animal model for neuropathic pain. In this model, the analgesic potency of systemic morphine was significantly diminished in nerve-injured mice (ED 50 19.4 mg/kg) compared with sham-operated mice (ED 50 3.3 mg/kg) using a unilateral hot plate withdrawal test, with a similar reduction in sensitivity of intrathecal morphine. The sciatic nerve injury resulted in a reorganization of the dorsal root ganglion (DRG) neurons. Immunohistochemically, the chronic constriction injury triggered a withdrawal of C-fibers from the ipsilateral dorsal horn of the spinal cord. Although A-β terminals centrally sprouted into Lamina II of the dorsal horn of the spinal cord, the peripheral A-β fibers in the skin retracted from the epidermis to deeper layers of the dermis. To explore the functional significance of these dermal changes, we examined the topical morphine and lidocaine analgesia following chronic sciatic nerve constriction. Both morphine and lidocaine retained topical activity following chronic sciatic nerve injury, but their analgesic dose–response curves were shifted to the right when compared to sham-operated mice. Thus, the chronic nerve constriction injury model is associated with pathological changes in distribution of the central and peripheral axons of the dorsal root ganglion neurons that correspond to a decreased pharmacological sensitivity to topical analgesic agents.

Effects of epidural lidocaine analgesia on labor and delivery: A randomized, prospective, controlled trial

BackgroundWhether epidural analgesia for labor prolongs the active-first and second labor stages and increases the risk of vacuum-assisted delivery is a controversial topic. Our study was conducted to answer the question: does lumbar epidural analgesia with lidocaine affect the progress of labor in our obstetric population?Method395 healthy, nulliparous women, at term, presented in spontaneous labor with a singleton vertex presentation. These patients were randomized to receive analgesia either, epidural with bolus doses of 1% lidocaine or intravenous, with meperidine 25 to 50 mg when their cervix was dilated to 4 centimeters. The duration of the active-first and second stages of labor and the neonatal apgar scores were recorded, in each patient. The total number of vacuum-assisted and cesarean deliveries were also measured.Results197 women were randomized to the epidural group. 198 women were randomized to the single-dose intravenous meperidine group. There was no statistical difference in rates of vacuum-assisted delivery rate. Cesarean deliveries, as a consequence of fetal bradycardia or dystocia, did not differ significantly between the groups. Differences in the duration of the active-first and the second stages of labor were not statistically significant. The number of newborns with 1-min and 5-min Apgar scores less than 7, did not differ significantly between both analgesia groups.ConclusionEpidural analgesia with 1% lidocaine does not prolong the active-first and second stages of labor and does not increase vacuum-assisted or cesarean delivery rate.

Evidence in orthopaedics: comparison of intra-articular lidocaine vs. intravenous analgesia and sedation for reduction of acute shoulder dislocation

Acute shoulder dislocation is the most common joint dislocation managed in emergency department. It has been commonly treated with closed reduction and the use of intravenous analgesia and sedation (IVAS). Recently, intra-articular lidocaine (IAL) has been advocated as an alternative to sedation, since intravenous access and patient monitoring are not required. A careful literature analysis was performed to establish which anesthetic method is best indicated to reach a reduction that is easily performed, effective, relatively painless and safe, and to allow for expeditious discharge of the patient. To find the best evidence on the topic, we searched in the Cochrane Library, Health Technology Assessment (HTA) database, TRIP, Medline, CINAHL, and EMBASE. In the four prospective randomized clinical trials found, no statistically significant difference was detected between IAL and IVAS for reduction of acute anterior shoulder dislocations with regard to pain score, difficulty of reduction, and success rate. Although we cannot definitively state which is the best anesthetic method, we conclude that intra-articular injection of lidocaine is an excellent alternative for those patients for whom IVAS is not indicated.

Clonidine prolongation of lidocaine analgesia after sciatic nerve block in rats Is mediated via the hyperpolarization-activated cation current, not by alpha-adrenoreceptors.

Although clonidine is commonly combined with local anesthetics to extend duration of peripheral nerve block, the mechanism by which clonidine potentiates local anesthetic action in vivo is unclear. Male Sprague-Dawley rats received percutaneous injections of 1% lidocaine with/without clonidine or epinephrine into the sciatic notch and duration of sensory blockade was quantified by inhibition of pinprick foot withdrawal. The antagonists prazosin or yohimbine were injected before lidocaine with clonidine or epinephrine to determine the role of alpha-adrenergic receptors. The role of the hyperpolarization-activated cation current (Ih) was evaluated by injecting the current blocker ZD 7288 as well as the current enhancers forskolin and 8-Br-cAMP before lidocaine alone or with 15 micrograms/ml clonidine. Mean duration of sensory block for lidocaine alone was 69 +/- 2 min. Sensory block duration increased monotonically with increasing doses of added clonidine or epinephrine. Preinjection of prazosin but not yohimbine prevented the increase in block duration seen with epinephrine. Neither alpha-adrenergic antagonist attenuated the extended duration of block with clonidine. ZD 7288 extended sensory blockade equivalent to the prolongation observed with clonidine. There was no additive effect when ZD 7288 and clonidine were combined, and a decreased duration of nerve block when either forskolin or 8-Br-cAMP preceded injection of lidocaine with clonidine. The findings indicate that prolongation of duration of in vivo lidocaine nerve blockade by clonidine is not mediated by an alpha-adrenergic mechanism but likely involves the Ih current.

Will ion-channel blockers be useful for management of nonneuropathic pain?

For neuropathic pain, there is evidence that the analgesic effect of intravenous sodium-channel blockers is robust and dose dependent. Oral agents are less impressive, but efficacious nonetheless, especially at higher doses. Despite the evidence from animal studies for a role of sodium channels in inflammatory hyperalgesia, the clinical evidence of analgesic effect of oral and intravenous sodium channel blockers in both acute and chronic nonneuropathic pain is equivocal. The results to date from human experimental pain models suggest a lack of effect of systemic lidocaine on acute nociceptive pain and that the effect on cutaneous hyperalgesia is modest, at best. Furthermore, the literature suggests that the systemic lidocaine analgesia is both dose and diagnosis dependent.

Patient-controlled lidocaine analgesia for acromioplasty surgery

Twenty-four consecutive patients undergoing shoulder acromioplasty were given postoperative analgesia with a new method in which a patient-controlled continuous infusion of lidocaine infiltrated the subacromial space. Seventeen of the acromioplasties were done with arthroscopy, whereas 7 were performed with an open procedure. A 2% solution of lidocaine without epinephrine was used for both a continuous dose of 2 cc/h and patient-controlled interval doses of 1 cc administered at 15-minute intervals. The catheter was left in place for 72 hours. We prospectively studied complications, the patient's subjective pain level, the amount of supplementary pain medication used, and serum levels of lidocaine. In addition, we evaluated a control group of 24 patients undergoing acromioplasty by the same surgeon without the use of this method of pain control. No wound complications occurred. No adverse reactions to lidocaine or overdose of lidocaine occurred. Blood levels of lidocaine averaged 0.3 microgram/mL in the 12 patients studied. Subjective pain levels and the amount of supplementary pain medication used were both lower in the group receiving patient-controlled lidocaine analgesia at statistically significant levels (P = .168 measuring subjective pain level, and P = .0212 measuring supplementary pain medication use). Patient-controlled lidocaine analgesia in the subacromial space appears to be a safe method for achieving high levels of pain control in patients undergoing an acromioplasty.

Patient-controlled lidocaine analgesia for acromioplasty surgery

Twenty-four consecutive patients undergoing shoulder acromioplasty were given postoperative analgesia with a new method in which a patient-controlled continuous infusion of lidocaine infiltrated the subacromial space. Seventeen of the acromioplasties were done with orthroscopy, whereas 7 were performed with an open procedure. A 2% solution of lidocaine without epinephrine was used for both a continuous dose of 2 cc/h and patient-controlled interval doses of 1 cc administered at 15-minute intervals. The catheter was left in place for 72 hours. We prospectively studied complications, the patient's subjective pain level, the amount of supplementary pain medication used, and serum levels of lidocaine. In addition, we evaluated a control group of 24 patients undergoing ocromioplasty by the same surgeon without the use of this method of pain control. No wound complications occurred. No adverse reactions to lidocaine or overdose of lidocaine occurred. Blood levels of lidocaine averaged 0.3 μg/ml in the 12 patients studied. Subjective pain levels and the amount of supplementary pain medication used were both lower in the group receiving patient-controlled lidocaine analgesia at statistically significant levels (P = .168 measuring subjective pain level, and P = .0212 measuring supplementary pain medication use). Patient-controlled lidocaine analgesia in the subacromial space appears to be a safe method for achieving high levels of pain control in patients undergoing an acromioplosty.

Subanesthetic concentrations of lidocaine selectively inhibit a nociceptive response in the isolated rat spinal cord

Systemically administered local anesthetics are known to provide analgesia in a variety of pain states; however, the site of action and the mechanism by which these effects are produced remain in question. In the present study, the effects of low (subblocking for nerve conduction) concentrations of lidocaine on a spinal cord nociceptive potential were studied. Spinal cords were removed from neonatal rats and maintained in vitro. Lumbar dorsal and ipsilateral ventral roots were attached to suction electrodes for stimulation and recording, respectively. Following a stabilization period (60–120 min) with control measurements, each preparation was exposed to a single concentration of lidocaine (30–60 min) then returned to control perfusate for recovery (60–120 min). Data were digitized and integrals computed for both monosynaptic and slow ventral root potentials (VRP). Low concentrations of lidocaine produced a selective reduction in the magnitude of the slow-VRP. At lidocaine concentrations of 1–10 μg/ml (3.6–36 μM), the slow-VRP was reduced from 79% to 36% of control. Recovery to pre-exposure control levels was slow and sometimes not complete after 60–120 min in drug-free perfusate. The monosynaptic component of the VRP was unaffected by lidocaine at any concentration, suggesting that the depression of the slow-VRP cannot be attributed to simple conduction block. The addition of naloxone 0.1 μM to the perfusate had minimal effect on lidocaine-induced depression. Although resembling the selective effects of morphine, the antinociceptive effects of lidocaine do not appear to be primarily mediated through opiate receptors. Subblocking concentrations of tetrodotoxin, a selective sodium-channel blocker, did not mimic the effects of lidocaine. However, a subblocking concentration of benzonatate, an orally effective local anesthetic, did produce lidocaine-like selective effects on the slow-VRP. This study demonstrated that lidocaine at clinically relevant concentrations can selectively depress a well-characterized nociceptive response in the isolated rat spinal cord. We propose that the site of action for systemic lidocaine analgesia is, at least in part, at the level of the spinal cord.

Intra-Articular Lidocaine Analgesia in the Treatment of Acute Shoulder Dislocations

Intra-Articular Lidocaine Analgesia in the Treatment of Acute Shoulder Dislocations

Fetal Heart Rate Variability After Epidural Fentanyl During Labor

The effects of epidural fentanyl on fetal heart rate (FHR) were examined in 39 parturients, 19 given 75 micrograms epidural fentanyl and 20 given normal saline in 5-mL volumes administered randomly after establishment of adequate epidural lidocaine analgesia. Fetal heart rate was measured 15 min before and 15 min after lidocaine epidural analgesia, and for 60 min at 5-min intervals after administration of epidural fentanyl/placebo. A perinatologist blinded to the injected epidural solution analyzed FHR tracings. Epidural injections of fentanyl and saline, when given during established epidural lidocaine analgesia, were associated with equal reductions in FHR variability and the frequency of FHR accelerations (P less than 0.003). Neonatal outcome was also similar in both groups. The clinical significance, if any, of these moderate reductions in FHR during epidural lidocaine analgesia is unclear.

Lidocaine analgesia in peripheral angiography: a confirmation of effectiveness.

Lidocaine analgesia in peripheral angiography: a confirmation of effectiveness.

Paradoxic response to intraarterial lidocaine analgesia

injections of contrast-lidocaine solution (1 .2 mg lidocaine/1 ml contrast medium) spaced 15 mm apart. A, First injection; at 3.5 sec popliteal artery is opacified. B, Second injection; 8 sec required for popliteal opacification. C, Third injection; 12 sec elapsed before popliteal opacification. Spasm of muscular branches is slight on first angiogram (A), becoming more pronounced on subsequent angiognams (B and C). Paradoxic Response to Intraarterial Lidocaine Analgesia