[Infraclavicular block].
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Brachial Plexus↗
Biomedical subjects
X Paqueron
Publications and source records attributed to X Paqueron.
[Axillary block].
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Anesthesia, Conduction↗
What pain scales do nurses use in the postanaesthesia care unit?
BACKGROUND AND OBJECTIVE: The visual analogue scale (VAS) is considered as the gold standard method for postoperative pain assessment. Nevertheless, in some clinical situations, this method may not be reliable. We performed an observational study to assess the use of the VAS and other pain scales by nurses in the postanaesthesia care unit. METHODS: We studied the reasons for not using the VAS and asked if it may be less appropriate in certain age groups. RESULTS: Among 600 patients included in the study (16% = 70 yr), nurses used the VAS in 53%, the numerical rating scale in 30%, the verbal rating scale in 12% and the behavioural scale in 5%. In 43% of the assessments, nursed did not use the VAS; the most frequently cited reason was related to their preference for other methods. In 54% of the assessments, the reason for not using the VAS was related to the patients, mainly when they were in too much pain to use it (22%). When the patient was in too much pain, the numerical rating scale was chosen in 54% and the behavioural scale in 27%. There was no difference between young patients and elderly patients. CONCLUSIONS: Although the VAS is the standard method to assess pain, the nurses preferred using the numerical rating scale, both spontaneously or when VAS assessment was not possible.
Adolescent↗
The phenomenology of body image distortions induced by regional anaesthesia.
Patients with peripheral nerve or spinal cord lesions frequently report perceptual distortions related to position, shape, texture or temperature of the affected areas. This study aimed to describe the phenomenology of such body image alterations during the course of upper limb, lower limb or spinal anaesthetic blocks in patients (n = 36) undergoing orthopaedic surgery. Multimodal sensory testing and assessment of motor function were performed at regular intervals, and the relationship between the reported body image distortions and the progression of sensory and motor impairment was analysed. We found that perceptual changes concerning the shape and size of the deafferented limb occurred in the great majority of patients. In all of them, illusions of swelling, elongation or shortening of the limb coincided with the impairment of warm, cold and/or pinprick sensations, suggesting that thin myelinated Adelta- and/or unmyelinated C-fibres may provide a source of tonic modulation to the limb's cortical representation. Such perceptual alterations of shape and size of body parts differed clearly from postural illusions in terms of frequency, time course and influence of vision. In addition to perceptual changes in the deafferented area, almost half of the patients felt their unanaesthetized lips and/or mouth swelling during the course of upper limb block, suggesting the unmasking of dynamic interactions between somatotopically adjacent cortical representations. Conflicting sensations could co-exist in the patient's body image, such as the illusion of swelling of a limb, which, at the same time, was felt to be missing. The sense of ownership of the deafferented limb was impaired in some cases. These observations show that the perception of body shape and the awareness of its postural variations are built from different plastic models. They also underline the contribution of peripheral afferent activity to the maintenance of a unified body image.
Adolescent↗
Is morphine-induced sedation synonymous with analgesia during intravenous morphine titration?
BACKGROUND: Postoperative morphine titration frequently induces sedation. The assumption is made that patients sleep when their pain is relieved. Some patients complain of persistent pain when they awake. We studied the time-course of sedation and analgesia to understand the determinants of patients' sleep during morphine titration. METHODS: Seventy-three patients requiring morphine titration in a post-anaesthetic care unit after major surgery, were studied. Fifty-two patients slept (Sleep group) and 21 did not (Awake group). When a patient slept during titration, morphine was discontinued. Visual analogue pain scale (VAS), Ramsay score (RS), and the bispectral index (BIS) were recorded at the beginning of titration (STonset), at sleep onset (STsleep), then 5, 10, 20, and 30 min afterwards (ST4). RESULTS: In the Sleep group, mean (SD) RS increased from 1.7 (0.4) to 2.4 (0.6) (P<0.05 vs STonset) and BIS decreased from 95 (5.0) to 89.8 (10.2) between STonset and STsleep (P<0.05), RS remained stable thereafter. Conversely, RS and BIS remained unaltered in the Awake group. The reduction in VAS was comparable between groups (from 78 (17) to 39 (21), and from 64 (16) to 30.4 (11), respectively). Even though mean (SD) VAS was 39 (21) at ST4 in the Sleep group, 13 patients (25%) maintained a VAS above 50 mm. CONCLUSION: We observed dissociated effects of morphine on the time-course of sedation and analgesia with sedation occurring first, followed by analgesia. Therefore, morphine-induced sedation should not be considered as an indicator of an appropriate correct level of analgesia during i.v. morphine titration.
Adult↗
Activation of cardiac endothelium as a compensatory component in endotoxin-induced cardiomyopathy: role of endothelin, prostaglandins, and nitric oxide.
BACKGROUND: In view of growing evidence of an important endothelial paracrine regulation of cardiac function, the present study investigated the role of cardiac endothelium-derived endothelin-1 (ET-1), prostaglandins, and nitric oxide (NO) during endotoxin-induced cardiomyopathy in rabbits. METHODS AND RESULTS: Immunohistochemical studies showed a marked transient coinduction of the inducible isoforms of NO synthase (NOS-2) and cyclooxygenase (COX-2) in endocardial endothelium and coronary arteriolar endothelium of hearts 12 hours after intravenous administration of lipopolysaccharide (LPS+12h); staining for both isoforms was much weaker 24 hours later (LPS+36h). Nitrotyrosine localization was similar to that of NOS-2, suggesting a NOS-2-related endothelial formation of peroxynitrite in septic hearts. Contractile performance of papillary muscles was depressed in both LPS-treated groups. In the LPS+12h group, however, isometric twitches were significantly prolonged (482+/-14 versus 420+/-14 ms in the saline-treated group, P<0.005). This twitch prolongation was completely reversed by simultaneous administration of BQ-123 and indomethacin to block endogenous ET-1 and prostaglandins, respectively. In addition, in the LPS+12h group, myocardial inotropic responsiveness to exogenous ET-1 was enhanced (P<0.01). CONCLUSIONS: Cardiac endothelial activation and myocardial sensitization to endothelium-derived mediators may be part of an adaptive response in the early (12 hours) stages of septic cardiomyopathy.
Animals↗
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.
Acetylcholine↗
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 alpha2-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 alpha2-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 microg clonidine. The spinal cord was removed, and spinal cord acetylcholine content, cholinergic neuron number and distribution, and alpha2-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 anti-allodynic effect of clonidine. AF64-A did not reduce alpha2-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 alpha2-adrenergic receptors colocalized on spinal cholinergic interneurons.
Acetylcholine↗
[Conjunctivitis associated with the inadequate use of Bodedex while decontaminating a facial mask].
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Conjunctivitis↗
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 microg 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.
Adult↗
Norepinephrine release from spinal synaptosomes: auto-alpha2 -adrenergic receptor modulation.
BACKGROUND: Clonidine produces analgesia after spinal injection by activating alpha2-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 alpha2a-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 microm. The effect of clonidine was inhibited by the alpha2-adrenergic antagonists, yohimbine and idazoxan, but not by alpha1-adrenergic, muscarinic, or opioid antagonists. Intrathecal pretreatment with antisense ODN to alpha2A-adrenergic receptors reduced alpha2A-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 alpha2-adrenergic receptors in the spinal cord, probably of the alpha2Asubtype. They further suggest that clonidine-induced stimulation of spinal NE release must occur from indirect actions, presumably due to activation of a spinal circuit.
Adrenergic alpha-Agonists↗
Effects of propofol, propofol-nitrous oxide and midazolam on cortical somatosensory evoked potentials during sufentanil anaesthesia for major spinal surgery.
Recording of cortical somatosensory evoked potentials (CSEP) enables monitoring of spinal cord function. We studied the effects of propofol, propofol-nitrous oxide or midazolam during sufentanil anaesthesia on CSEP monitoring during major spinal surgery. Thirty patients with normal preoperative CSEP were allocated randomly to one of the following anaesthesia regimens: propofol (2.5 mg kg-1 followed by 10-6 mg kg-1 h-1) with or without nitrous oxide, or midazolam (0.3 mg kg-1 followed by 0.15 mg kg-1 h-1) combined with sufentanil 0.5 microgram kg-1 h-1 in the propofol and midazolam groups, or 0.25 microgram kg-1 h-1 in the propofol-nitrous oxide group. CSEP were elicited by alternate right and left tibial posterior nerve stimulation and recorded before and after induction (15 min, 1, 2 and 3 h), and during skin closure. CSEP latencies were not significantly modified in the three groups. CSEP amplitude decreased significantly in the propofol-nitrous oxide group (from mean 2.0 (SEM 0.3) to 0.6 (0.1) microV; P < 0.05) but not in the propofol (from 1.8 (0.6) to 2.2 (0.3) microV) or midazolam (1.7 (0.5) to 1.6 (0.5) microV) groups. The time to the first postoperative voluntary motor response (recovery) delay was significantly greater in the midazolam group (115 (19) min) compared with the propofol and propofol-nitrous oxide groups (43 (8) and 41 (3) min, respectively). Consequently, the use of propofol without nitrous oxide can be recommended during spinal surgery when CSEP monitoring is required.
Adult↗
No enhancement of sensory and motor blockade by neostigmine added to mepivacaine axillary plexus block.
BACKGROUND: Intrathecal neostigmine induces analgesia but also several side effects. Recently, 500 microg neostigmine administered intraarticularly was shown to produce postoperative analgesia without side effects. The authors' goal was to determine whether 500 microg neostigmine added to mepivacaine in axillary plexus block prolongs postoperative analgesia. In addition, they wanted to determine the incidence of side effects in patients undergoing hand surgery. METHODS: Sixty-nine outpatients scheduled for carpal tunnel syndrome repair with axillary plexus block were randomly assigned to one of three groups that received saline solution in the axillary plexus and subcutaneously (group 1), 500 microg neostigmine in the axillary plexus and saline solution subcutaneously (group 2), or saline solution in the axillary plexus and 500 microg neostigmine subcutaneously (group 3). Sensory and motor block in the four hand nerve distributions were assessed every 5 min for 30 min The duration of the sensory and motor blocks were assessed after operation. Side effects were also recorded. RESULTS: Neostigmine had no effect on sensory and motor block in any of the four nerve distributions, nor did it increase the median duration of sensory block (215 min; range, 120-330 min) compared with group 1 (247 min; range, 190-287 min) or group 3 (236 min; range, 160-280 min). Motor block was slightly shorter (P = 0.045) in group 3 (190 min; range, 135-285 min) compared with group 1 (218 min; range, 145257 min) and group 2 (215 min; range, 105-343 min). Gastrointestinal side effects occurred in 30% of patients in both neostigmine groups but not in group 1 (P < 0.05). CONCLUSIONS: This study suggests that 500 microg neostigmine added to mepivacaine in axillary plexus block does not prolong postoperative sensory block, but it does cause a relatively high incidence of side effects. These two findings raise doubts about the use of neostigmine associated with local anesthetics for plexus neural block.
Adult↗
Sequential changes in autonomic regulation of cardiac myocytes after in vivo endotoxin injection in rat.
We report that in vivo injection of endotoxin (EDTX, 6 mg. kg(-)(1)) induces cardiovascular alterations in rats that closely mimic the clinical situation, as assessed by in vivo hemodynamic measurements in anesthetized and conscious, chronically instrumented animals. The patch-clamp technique was used to characterize the L-type calcium current (I(Ca)) and its autonomic regulation in isolated cardiac myocytes. The density of I(Ca) progressively decreased at 12 and 36 h after EDTX injection. However, the dihydropyridine (+/-)Bay K 8644 (100 nM) enhanced I(Ca) to levels similar to those in control and EDTX-treated myocytes. In addition, the net stimulatory effect of a beta-adrenergic agonist (isoproterenol) on I(Ca) was increased 12 h after EDTX injection. This change in the beta-adrenergic effect declined 24 h later. The potentiation in the beta-adrenergic stimulation of I(Ca) was mimicked by L858051 (10 microM), a direct activator of adenylyl cyclase, but not by IBMX (200 microM), a phosphodiesterase inhibitor. Besides, the antiadrenergic effect of acetylcholine on I(Ca) was unchanged 12 h after EDTX injection, but increased 36 h after EDTX injection. These results support the hypothesis that time-dependent changes in the adenylyl cyclase pathway in cardiac myocytes may contribute, via the autonomic regulation of I(Ca), to the severity of myocardial dysfunction during sepsis.
1-Methyl-3-isobutylxanthine↗
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.
Adult↗
[A low dose of nalbuphine reverses respiratory depression but not analgesia induced by intraspinal morphine].
Postoperative pain management after scoliosis surgery is based in our institution on intrathecal morphine administration. This case report describes an immediate and major postoperative respiratory depression that occurred in the recovery room, requiring the maintenance of the endotracheal tube. This respiratory depression was reversed by i.v. administration of a low dose of nalbuphine, which allowed tracheal extubation without suppression of morphine-induced analgesia.
Adolescent↗
[Autotransfusion during caesarean section with blood containing p salbutamol without adverse effects].
We report the case of a patient presenting with a placenta praevia and who donated autologous blood while she had beta 2-agonist tocolysis. As the restitution of blood containing salbutamol at therapeutic concentration may induce uterine atony and cardiovascular symptoms, we monitored maternal clinical signs and plasma concentrations of salbutamol when autologous blood was retransfused after the end of Caesarean section. The maternal plasma beta 2-agonist levels during tocolysis were in agreement with the usual therapeutic concentrations. The beta 2-agonist infusion was discontinued 30 minutes before the subarachnoid blockade and the blood concentration measured at the time of skin incision was below the therapeutic threshold. The retransfusion of autologous blood neither raised the salbutamol concentration above the therapeutic threshold value, nor induced any clinical symptoms. After Caesarean section the retransfusion of autologous blood containing therapeutic concentration of salbutamol seems to be innocuous.
Adult↗
Severe postadenoidectomy bleeding revealing congenital alpha 2 antiplasmin deficiency in a child.
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Adenoidectomy↗