Xavier Paqueron

The lateral approach to the sciatic nerve at the popliteal fossa: one or two injections?

UNLABELLED It has not been proven whether one or multiple nerve stimulations and injections provide a higher rate of complete sensory block in both major sciatic nerve sensory distributions below the knee when a popliteal sciatic nerve block is performed using the lateral approach. This prospective, randomized, single-blinded study compared the success rate of the sciatic nerve block using this approach when one or both major components of this nerve (i.e., tibial nerve and common peroneal nerves) are stimulated in 50 patients undergoing foot or ankle surgery. In Group 1 STIM, 24 patients received a single injection of 20 mL of a mixture of 2% lidocaine and 0.5% bupivacaine with 1:200,000 epinephrine after foot inversion had been elicited. In Group 2 STIM (n = 26), 10 mL of the same solution was injected after stimulation of each sciatic nerve component. For patients with complete sensory motor block, there was no difference in onset between groups. However, Group 2 STIM showed a greater success rate compared with the Group 1 STIM (2 STIM: 88% vs 1 STIM :54%; P = 0.007). When two stimulations were used, the onset time of anesthesia in the cutaneous distribution of the common peroneal nerves was shorter than in the tibial nerve (17.5 vs 30 min; P < 0.0001). We conclude that a two-stimulation technique provides a better success rate than a single-injection technique when a popliteal sciatic nerve block is performed using the lateral approach with 20 mL of local anesthetic. IMPLICATIONS A better success rate is achieved with a double stimulation technique than with a single injection for the sciatic nerve block via the lateral approach at the popliteal fossa when 20 mL of local anesthetics is used.

The clinical efficacy and pharmacokinetics of intraperitoneal ropivacaine for laparoscopic cholecystectomy.

Postoperative pain after laparoscopic surgery is less than after laparotomy, and patients may benefit from an intraperitoneal injection of local anesthetic. Thirty-seven ASA physical status I or II patients received in double-blinded fashion 20 mL of 0.9% saline solution (placebo), ropivacaine 0.25% (Rop 0.25%), or ropivacaine 0.75% (Rop 0.75%) immediately after trocar placement and at the end of surgery. We measured pain and morphine consumption until 20 h after surgery. Plasma ropivacaine concentrations were measured. The three groups were comparable for shoulder pain, parietal pain, and incidence of side effects. Visceral pain at rest, during cough, and on movement and total consumption of morphine were significantly smaller in Groups Rop 0.25% and Rop 0.75% when compared with Placebo. Although no adverse effect occurred in any patient, the largest dose led to large plasma concentrations of ropivacaine (2.93 ± 2.46 &mgr;g/mL and 3.76 ± 3.01 &mgr;g/mL after the first and second injection, respectively). We conclude that intraperitoneal administration of ropivacaine before and after surgery significantly decreases postoperative pain. Because the smaller dosage (2 × 50 mg) provided similar analgesia and was associated with significantly smaller plasma concentrations than the larger dosage (2 × 150 mg), this smaller dosage seems more appropriate.

Brachial plexus nerve block exhibits prolonged duration in the elderly.

Background Upper limb trauma occurs frequently in elderly patients for whom peripheral nerve blocks are often preferred for anesthesia. The characteristics of such regional blocks have, however, never been described in an elderly population. Therefore, the authors assessed prospectively the onset and duration of upper extremity peripheral nerve block (the mid-humeral block) in elderly and young patients undergoing emergency upper extremity surgery. Methods Consecutive patients aged > 70 yr or < 70 yr received a mid-humeral block with a small volume of ropivacaine, 0.75%. Five milliliters was injected onto each of the musculocutaneous, radial, ulnar, and median nerves. Time to complete sensory and motor block and durations of complete sensory and motor block were assessed. Results are shown as median and its 95% confidence interval. Results Median ages were 77 yr (95% CI, 72–81 yr) and 39 yr (95% CI, 27–46 yr) in the two groups. Both groups had similar times to complete sensory blockade. The elderly group had longer durations of complete sensory (390 min [range, 280–435 min]vs. 150 min [range, 105–160 min];P < 0.05) and motor (357 min [range, 270–475 min]vs. 150 min [range, 90–210 min];P < 0.05) blockade. Duration of complete sensory block was significantly correlated with age (&rgr; = 0.56;P < 0.05). Conclusions Age is a major determinant of duration of complete motor and sensory blockade with peripheral nerve block, perhaps reflecting increased sensitivity to conduction failure from local anesthetic agents in peripheral nerves in the elderly population.

Sedation with sufentanil and midazolam decreases pain in patients undergoing upper limb surgery under multiple nerve block.

Multiple nerve blocks may be painful and a source of discomfort. We assessed the efficacy of sufentanil 5 &mgr;g combined with midazolam 1 mg in decreasing pain in outpatients after a midhumeral multiple nerve stimulation technique. Visual analog scores for pain were significantly lower in those patients who received sedation before the block, both at the time of block performance (14 ± 1 vs 27 ± 2 mm, P < 0.0001) and at discharge (11 ± 1 vs 24 ± 2 mm, P < 0.0001). We conclude that the association of sufentanil and midazolam produced minimal sedation while significantly reducing pain experienced by patients undergoing multiple nerve stimulation. Implications In a prospective trial of 168 patients, the use of sedation significantly reduced pain during a multiple-nerve stimulation block. The combination of sufentanil and midazolam produced either minimal or no sedation and allowed the performance of the block in awake and cooperative patients. Light sedation may improve patient acceptance of this technique

Plasticity in Action of Intrathecal Clonidine to Mechanical but Not Thermal Nociception after Peripheral Nerve Injury

Background Intrathecal clonidine reduces tactile allodynia in animal models of neuropathic pain, and this effect is blocked by atropine. However, the role of tonic spinal cholinergic activity and its interaction with &agr;2-adrenergic systems in normal and neuropathic conditions and to different sensory methods has not been systematically examined. The authors examined cholinergic receptor involvement in thermal and mechanical sensitivity in normal and neuropathic animals and its interaction with intrathecal clonidine. Methods Normal rats and rats that received L5/L6 spinal nerve ligation were tested with acute radiant heat, paw pressure, and punctate mechanical stimulation before and after the intrathecal administration of saline, the muscarinic receptor antagonist, atropine, or a toxin to destroy cholinergic neurons, and then after intrathecal clonidine. Results Atropine, the cholinergic neuronal toxin, and saline did not alter baseline withdrawal thresholds. In nerve-injured rats, neither saline nor atropine altered antinociception from clonidine to a thermal stimulus, but atropine reduced the effect of clonidine to von Frey filament withdrawal threshold (34 ± 5.6 vs. 14 ± 5.8 g [mean ± SEM], saline vs. atropine;P < 0.05) and to withdrawal threshold to paw pressure after clonidine (174 ± 18 g vs. 137 ± 16 g, saline vs. atropine;P < 0.05). Conclusions These data suggest that after nerve injury, mechanical but not thermal antinociception from intrathecal clonidine relies on a muscarinic interaction, because only mechanical antinociception was antagonized by atropine. These results do not favor a regulation of nociceptive transmission by a tonic release of acetylcholine in nerve-injured rats.

Time sequence of sensory changes after upper extremity block: Swelling sensation is an early and accurate predictor of success

Background:Sensory assessment to estimate spread and effectiveness of a peripheral nerve block is difficult because no clinical test is specific for small sensory fibers. Occurrence of a swelling illusion (SI) during a peripheral nerve block corresponds to the impairment of small sensory fibers. The authors investigated the usefulness of SI in predicting successful peripheral nerve block by assessing the temporospatial correlation between progression of sensory impairment in cutaneous distributions anesthetized and localization of SI during peripheral nerve block installation. Methods:Interscalene, infracoracoid, or sciatic nerve blocks were performed using a nerve stimulator and 1.5% mepivacaine in 53 patients, with a total of 201 nerves to be anesthetized. Pinprick, cold, warm, touch, and proprioception were assessed every 3 min, while patients were asked to describe their perception of size and shape of their anesthetized limb and localization of these illusions. Data are presented as mean ± SD and percentage (95% confidence interval). Results:Failure occurred in 12 cutaneous distributions out of a total of 201 theoretically blocked nerves. SI appeared earlier than warmth impairment (4.3 ± 2.7 vs. 6.2 ± 2.0 min; P < 0.05), always corresponding to successfully anesthetized cutaneous distributions, with the exception of 1 patient, who developed SI in 2 cutaneous distributions while sensory testing indicated failure in 1 distribution. SI successfully predicted the blockade of a cutaneous distribution with a sensitivity of 1.00 (0.98–1.00), a specificity of 0.92 (0.65–0.99), and an accuracy of 0.99 (0.97–1.00). Conclusions:Swelling illusion may provide an early assessment of the success of a peripheral nerve block in unsedated patients.

An obligatory role for spinal cholinergic neurons in the antiallodynic effects of clonidine after peripheral nerve injury.

Background Indirect evidence supports a role of spinal cholinergic neurons in tonically reducing response to noxious mechanical stimulation and in effecting analgesia from &agr;2-adrenergic agonists. This study directly assessed the role of cholinergic neurons in regulating the level of mechanical allodynia and in participating in the antiallodynic effect of the clinically used &agr;2-adrenergic agonist, clonidine, in an animal model of neuropathic pain. Methods Allodynia was produced in rats by ligation of the left L5 and L6 spinal nerves. Rats received a single intrathecal injection of saline or one of three different doses of the cholinergic neurotoxin, ethylcholine mustard aziridinium ion (AF64-A; 2, 5, and 15 nmol). Seven days later, allodynia was assessed before and after intrathecal injection of 15 &mgr;g clonidine. The spinal cord was removed, and spinal cord acetylcholine content, cholinergic neuron number and distribution, and &agr;2-adrenergic receptor expression were determined. Results AF64-A administration reduced both the number of cholinergic cells and the acetylcholine content of the lumbar dorsal spinal cord by 20–50% but did not affect level of mechanical allodynia. AF64-A did, however, completely block the antiallodynic effect of clonidine. AF64-A did not reduce &agr;2-adrenergic ligand binding in dorsal lumbar cord. Conclusions These data suggest that spinal cholinergic tone does not affect the level of mechanical allodynia after peripheral nerve injury. There is a quantitative reliance on spinal cholinergic neurons in the allodynia relieving properties of intrathecal clonidine, and this reliance does not depend on &agr;2-adrenergic receptors colocalized on spinal cholinergic interneurons.

Influence of sensory and proprioceptive impairment on the development of phantom limb syndrome during regional anesthesia.

BackgroundThe relation between impairment of sensorimotor function and occurrence of phantom limb syndrome (PLS) during regional anesthesia has not been described. This study assessed the temporal relation between PLS and the progression of sensorimotor impairment during placement of a brachial plexus nerve block. MethodsFifty-two patients had their arm randomly placed either alongside their body (group A) or in 90° abduction (group B) immediately after brachial plexus nerve block placement. Responses to pin prick, cold, heat, touch, proprioception, and voluntary movement were assessed every 5 min for 60 min. Meanwhile, patients described their perceptions of the size, shape, and position of their anesthetized limb. ResultsPhantom limb syndrome occurred 19 ± 9 min after nerve block placement. Proprioception was impaired and abolished after 22 ± 9 and 43 ± 17 min, respectively (P < 0.05 vs. PLS onset). When PLS occurred, responses to pin prick, cold, heat, and proprioception were abolished in 96, 94, 87, and 4% of patients, respectively. Patients were more likely to feel their anesthetized limb in adduction and in abduction in groups A and B (P < 0.05 vs. group A), respectively. After PLS had become motionless, two stereotyped positions were identified: arm adduction, elbow flexion, hand over the abdomen (68% of group A patients) and arm abduction, elbow flexion, hand held close to the homolateral ear (48% of group B patients). ConclusionsThis study provides a better understanding of the determinants of PLS by showing that the final position of PLS is related both to the abolition of proprioception and the initial position of the anesthetized limb.

Norepinephrine release from spinal synaptosomes: Auto-α2-adrenergic receptor modulation

Background Clonidine produces analgesia after spinal injection by activating &agr;2-adrenergic receptors. Recently, clonidine has been demonstrated to increase spinal release of norepinephrine (NE) in vivo, in contrast to that anticipated by classic presynaptic autoinhibition. The purpose of the current study was to determine if clonidine could inhibit release of NE in a preparation of spinal cord tissue lacking synaptic circuits. Methods Crude synaptosomes were prepared from male Sprague-Dawley rat spinal cord, loaded with [3H]NE, and stimulated by potassium chloride to release [3H]NE. Samples were incubated with clonidine in the absence or presence of various inhibitors. To study the effect of &agr;2a-adrenergic receptor subtypes, some animals were pretreated with an oligodeoxynucleotide (ODN) composed of a sense or antisense sequence to a portion of this receptor. Results Potassium chloride produced a concentration-dependent increase in [3H]NE release, and this release was inhibited by clonidine with a concentration producing 50% maximal inhibition (IC50) of 1.3 &mgr;m. The effect of clonidine was inhibited by the &agr;2-adrenergic antagonists, yohimbine and idazoxan, but not by &agr;1-adrenergic, muscarinic, or opioid antagonists. Intrathecal pretreatment with antisense ODN to &agr;2A-adrenergic receptors reduced &agr;2A-adrenergic receptor protein expression compared with sense ODN control and also reduced clonidine-induced inhibition of [3H]NE release. Conclusions These data demonstrate the existence of classic autoinhibitory &agr;2-adrenergic receptors in the spinal cord, probably of the &agr;2A subtype. They further suggest that clonidine-induced stimulation of spinal NE release must occur from indirect actions, presumably due to activation of a spinal circuit.

P75-EXPRESSING ELEMENTS ARE NECESSARY FOR ANTI-ALLODYNIC EFFECTS OF SPINAL CLONIDINE AND NEOSTIGMINE

Cells expressing nerve growth factor are implicated in development of hypersensitivity following nerve injury and cholinergic neurons are implicated in reduction of such hypersensitivity by alpha2-adrenergic agonists. Intrathecal injection of the cell toxin, saporin, linked to an antibody to the low-affinity nerve growth factor, p75 (192-IgG saporin), an agent which destroys cholinergic neurons in the brain, was used in the current study to further elucidate these mechanisms. Mechanical hypersensitivity was established in rats by ligation of the L5 and L6 spinal nerves. Animals were pretreated with intrathecal saline or 192-IgG saporin, and one week later received intrathecal clonidine or neostigmine. Spinal cords were removed for acetylcholine and norepinephrine analysis and for cholinergic and p75 immunohistochemistry. Treatment with 192-IgG saporin had no effect on mechanical hypersensitivity following spinal nerve ligation, but blocked the anti-hypersensitivity effects of intrathecal clonidine and neostigmine. Destruction of p75-expressing fibers in the superficial dorsal horn by 192-IgG saporin was not accompanied by changes in acetylcholine or norepinephrine content or by reduction in cholinergic neuronal number in the spinal cord dorsal horn. Unlike in the brain, 192-IgG saporin does not destroy cholinergic neurons in the spinal cord dorsal horn and cannot be used as a tool for this purpose. P75-expressing elements are not necessary for the maintenance of mechanical hyperalgesia in this model of neuropathic pain, but their destruction disrupts the targets or circuitry activated by alpha2-adrenergic and cholinergic agents to reduce hypersensitivity.