Over the recent period, the use of induced hypothermia has gained an increasing interest for critically ill patients, in particular in brain-injured patients. The term "targeted temperature management" (TTM) has now emerged as the most appropriate when referring to interventions used to reach and maintain a specific level temperature for each individual. TTM may be used to prevent fever, to maintain normothermia, or to lower core temperature. This treatment is widely used in intensive care units, mostly as a primary neuroprotective method. Indications are, however, associated with variable levels of evidence based on inhomogeneous or even contradictory literature. Our aim was to conduct a systematic analysis of the published data in order to provide guidelines. We present herein recommendations for the use of TTM in adult and paediatric critically ill patients developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) method. These guidelines were conducted by a group of experts from the French Intensive Core Society [Societe de reanimation de longue francaise (SRLF)] and the French Society of Anaesthesia and Intensive Care Medicine [Societe francaise d'anesthesie et de reanimation (SFAR)] with the participation of the French Emergency Medicine Association [Societe francaise de medecine d'urgence (SFMU)], the French Group for Paediatric Intensive Core and Emergencies [Groupe francophone de reanimation et urgences pediatriques (GFRUP)], the French Notional Association of Neuro-Anesthesiology and Critical Care [Association notionale de neuro-anesthesie reanimation francaise (ANARLF)], and the French Neurovascular Society [Societe francaise neurovasculaire (SFNV)]. Fifteen experts and two coordinators agreed to consider questions concerning TTM and its practical implementation in five clinical situations: cardiac arrest, traumatic brain injury, stroke, other brain injuries, and shock. This resulted in 30 recommendations: 3 recommendations were strong (grade 1), 13 were weak (grade 2), and 14 were experts' opinions, after two rounds of rating and various amendments, which are exposed in the present article.

La physiopathologie du syndrome douloureux complexe (SDRC) semble de plus en plus être orientée vers un dysfonctionnement vasculaire et surtout neuronal dont la modulation centrale semble être prépondérante sur la modulation périphérique. Les critères diagnostiques ont été récemment actualisés. Les revues de la littérature et autres métaanalyses recommandent la physiothérapie intensive et toutes les procédures antalgiques médicamenteuses ou non qui pourront favoriser cette remise en charge. Ainsi, les anesthésies locorégionales intraveineuses (ALRIV) ne sont plus recommandées, alors que les anesthésies locorégionales (ALR) prolongées semblent prendre de plus en plus de place dans cette stratégie thérapeutique.

Background: Because poor echogenicity of the needle remains a safety issue, we decided to analyze the learning process of the hydrolocalization technique (Hloc) performed to continuously identify needle‐tip anatomical position during many ultrasound‐guided regional anesthesia procedures.Methods: Ten senior anesthesiologists naïve to the Hloc agreed to participate in the study. They were requested to perform 40 out‐of‐plane (OOP) approach ultrasound‐guided axillary blocks (AB) each using the Hloc. The Hloc, which is a needle‐tip localization principle, was performed by means of repetitive injections of a small amount of a local anesthetic solution (0.5–1 ml) under an ultrasound beam. Details of the learning process and skill acquisition of the Hloc were derived from the following parameters: the duration of block placement, a measure of the perceived difficulty of needle‐tip visualization, a measure of block placement difficulty, and the amount of local anesthetics solution required for the technique.Results: Four hundred ABs were performed. The success rate of an ultrasound‐guided AB was 98%. The Hloc was successful in all patients. Skill acquisition over time of the Hloc was associated with a significant reduction of both the duration and the perceived difficulty of ABs placement. Apprenticeship data revealed that 20 blocks were required to successfully place AB within 5 min in most cases using the Hloc.Conclusion: The Hloc performed during the OOP approach of ultrasound‐guided regional anesthesia is a simple technique with a relatively short learning process feasible for efficient placement of ABs.

To the Editor:—We read with great interest the article by Urmey and Stanton. 1It would appear, however, that the validity of the results must be viewed with some caution and the authors’ conclusions, in particular, call for several comments.First, use of fresh batteries for a nerve stimulator is not sufficient to prove its adequacy. A peripheral nerve stimulator in use for several months might not perform as well as a new one. 2For use of this importance, the stimulator output should have been tested with a calibrated oscilloscope. A stimulator that underestimates current output can mislead the operator. Moreover, a stimulator with clearly marked polarity would have been preferable. If polarity is inversed inadvertently, more current is needed.Nerves are not fixed in the surrounding tissue. Despite the needle presumably being near the nerve and immobilized when paresthesia are reported, imperceptible patient movement or breathing can dislodge the needle. There is no doubt that for patient comfort and security, as well as ethical reasons, the solution was injected after applying the stimulator only long enough to achieve paresthesia and not while maintaining paresthesia. To date, how close a needle must be to a sensory fascicle to produce mechanical paresthesia has not been established. 3Is the needle situated inside the nerve in contact with the sensory fascicle of the reported paresthesia, just touching the nerve, or somewhere in the vicinity of the nerve? Shoulder paresthesia can be provoked by deep palpation of the interscalene groove in thin patients.Why varied responses are observed after mechanical or electrical stimulation of the same root or trunk can be explained by fine details of anatomy. With the interscalene technique, the plexus is located at the level of the trunk and/or anterior branch of the spinal nerve. As a result, the response elicited is clearly metameric. The upper trunk and C5-C6 contain sensory fascicles that distribute to the upper lateral brachial cutaneous nerve (axillary nerve; C5), the lower lateral brachial cutaneous nerve (radial nerve; C5-C6), the lateral antebrachial cutaneous nerve (musculocutaneous nerve; C6), and the palmar cutaneous branch of the median nerve (C6). Consequently, paresthesia extending from the shoulder to the hand is not surprising with the interscalene approach. Similarly, with a nerve stimulator, the contractions commonly mediated by the cephalad roots (C5-C6) or upper trunk are those of the supraspinatus, infraspinatus (C4-C6), deltoid (C4-C6), biceps brachii (C5-C6), brachioradialis (C5-C6), extensor carpi radialis longus (C6-C7), pronator teres (C6-C7), and flexor carpi radialis (C6-C8) muscles. A distal paresthesia or motor response does not necessarily imply that the needle has been inserted too deeply, contrary to what had been suggested elsewhere. 4Lastly, satisfactory results require taking care not to regard as positive the shoulder responses that are due to stimulation of a collateral branch either directly or with the shaft of an uninsulated needle.In addition, electrophysiologic aspects of nerve stimulation and its clinical application are important to consider. Nerves coursing from the plexus are mixed, consisting of different nerve fascicles, including groups of axons that determine a common and specific motor or sensory innervation. With the minimum current able to produce a stimulus, large A α motor fibers are stimulated, while small A δ and C fibers are not. In such cases, a motor response is obtained without pain or patient discomfort. The shoulder is innervated by 30% of the fibers of the brachial plexus, 28.4% for motor innervation, and only 1.6% for sensory innervation. 5The assumption by Urmey and Stanton that each paresthesia constituted evidence of contact with a sensory fascicle alone was probably unfounded. Sensory and motor fascicles do not appear to be very distant from each other in the brachial plexus. Eliciting a motor response rather than a sensory response should occur frequently.However, when pure sensory fibers were stimulated, confirmation of the needle tip being in contact with the nerve is obtained by eliciting paresthesia with each pulsation. 2For successful peripheral nerve blockade, electrical paresthesia at 0.4–0.6 mA (100–200 μs) have been used as endpoint without evidence of mechanical paresthesia or nerve damage. 6,7If contact persisted with a sensory component of the nerve root, how was it possible for none of the patients to report electrical paresthesia to the two observers in spite of the maximum attained current of 1.0 mA, when they clearly indicated having the corresponding mechanical paresthesia several seconds earlier? As a very high stimulus is needed once the tip is some distance away from the nerve according to Coulomb's law, the only credible explanation is that, in 70% of the patients studied, the needle was sufficiently remote from the nerve after the initial paresthesia.On the contrary, a very low current was sufficient to produce the response in the other 30% of cases. An uninsulated needle would have required more current to stimulate the nerve. Achievement of a response with such minimal intensity indicates that the needle remained in very close contact or was touching the nerve. 8Urmey and Stanton are to be congratulated because they provided good evidence that the needle has to be quite close to the nerve when paresthesia is elicited. A motor response at 0.1–0.2 mA for 200 μs was obtained in several patients after the paresthesia disappeared. When responses are observed for currents this low, injection should be avoided, notably in unconscious subjects. 9When performing nerve stimulation with an insulated needle, the proper endpoint is the minimal stimulating current. The needle is then released and if the response persists, the needle-nerve relationship should remain unchanged at low current (0.2–0.5 mA for 100 μs). The operator should verify that the motor response disappears by applying decreased current once again before injection. The response should be abolished instantaneously with a painless and easily injected 1 ml-test dose.Paresthesia occurs and serves as a warning with all techniques including use of nerve stimulators. Paresthesia is usually difficult to elicit with a short-bevelled, insulated needle. 3The observed 30% increase in ability to obtain nerve stimulation with a long-bevelled needle is most likely due to a tendency of short-bevelled needles to press or push the nerve away. 10Long-bevelled needles are sharper, may penetrate the nerve easier, and potentially increase the risk of postoperative dysesthesia. In contrast, despite frequent unintentional paresthesia during block placement, the withdrawal and redirection of stimulating short-bevelled needles is not associated with an increased incidence of neurologic complication, even when using a multiple injection technique. 11Urmey and Stanton would probably have consistently observed a motor response before mechanical or electrical paresthesia had they chosen to begin with an adequate procedure of nerve stimulation at a recommended higher current.Currently, no compelling evidence exists to endorse a single technique or needle as superior with respect to success rate or incidence of complications. There are no prospective randomized controlled studies that compare the relative risks of regional anesthesia performed on anesthetized or conscious patients. Nevertheless isolated case reports, 12and medicolegal reports provide a background of suspicion, which is difficult to refute with a lack of data either for or against the practice. The incidence of dramatic complications appears to be higher following interscalene approaches to the brachial plexus. 12In the absence of firm data to the contrary, the weight of clinical practice suggests that the majority of peripheral nerve blocks, with the possible exception of the interscalene approach to the brachial plexus, can be performed under sedation. The anesthesiologist should carefully consider whether the benefits of regional anesthesia performed on an anesthetized patient are greater than the risk of a catastrophic outcome. It is important that authors not draw conclusions erroneously based on slight imperfections in a study design, especially conclusions leading to recommendations or contraindications with significant medicolegal connotations.

BACKGROUND AND OBJECTIVES:Tourniquet pain often limits the use of intravenous regional anesthesia (IVRA). Intravenous (IV) lidocaine has been shown to be effective in the management of acute and neuropathic pains. We tested the hypothesis that a priming IV injection of lidocaine might have an analgesic effect on tourniquet pain during IVRA.METHODS:A prospective, randomized, double- blind study was conducted on 40 patients scheduled for carpal tunnel decompression. No sedation was given. Each patient received either 1 mg/kg of IV lidocaine (group L) or 0.1 mL/kg of IV isotonic saline (group control = C) 5 minutes before IVRA. Thereafter, they received 3 mg/kg of plain 0.5 % lidocaine into the isolated and exsanguinated arm. A double-cuffed tourniquet was used. Pain at the tourniquet and the surgical sites was assessed every 5 minutes using a linear visual analog scale (VAS) and a verbal rating scale (VRS) during the surgical procedure and the immediate postoperative period (60 minutes).RESULTS:Demographic data and duration of proximal and distal tourniquet were similar in each group. Significant differences in the pain scales were observed for the distal tourniquet at tourniquet inflation time and 15 minutes after (P =.03 and.005, respectively) in the group L. For the proximal tourniquet, only the VRS was significantly improved (P =.03). No analgesic benefit was observed in the immediate postoperative period.CONCLUSIONS:Priming IV lidocaine when compared with isotonic saline is effective in reducing tourniquet pain in IVRA.

Background and Objectives This prospective, randomized, and multicentered study was undertaken to evaluate the success rate of coracoid infraclavicular nerve block performed with a nerve stimulator when either 1 or 3 motor responses were sought. Methods Eighty patients who presented for elbow, forearm, or wrist surgery were randomly allocated to one of the following groups: in group 1 (single stimulation), 30 mL local anesthetic (LA) was injected after locating only 1 of the median, ulnar, or radial motor responses. In group 2 (multistimulation), 3 responses were located: musculocutaneous, median or ulnar, and radial response, corresponding, respectively, to the lateral, medial, and posterior cords. A total of 10 mL LA was injected on each response. Bupivacaine 0.5% and lidocaine 2% with epinephrine 1:200,000 (1:1 vol) were used as the LA mixture. Sensory and motor blocks were tested by a blinded observer. Results Block duration was slightly increased in the multistimulation group (P = .004). The onset time of sensory and motor block was faster in each nerve distribution, particularly in the radial, musculocutaneous, and antebrachial nerves. The success of anesthesia increased in the multistimulation group. The success rate of the block, without any additional block, sedation, or general anesthesia, increased from 40% in the single stimulation group to 72.5% in the multistimulation group (P < .0001). If the brachial and antebrachial cutaneous nerves were not included in the evaluation, success rate reached 87.5%. Conclusions We conclude that by performing an infraclavicular block with stimulation of all 3 cords of the brachial plexus, the success rate is higher than when only a single stimulation is used.

Analyser le syndrome d'embolie graisseuse (SEG) en se basant notamment sur les récents moyens d'investigation que sont l'échocardiographic transœsophagienne, le lavage bronchoalvéolaire, le cathétérisme cardiaque et l'imagerie cérébrale par résonance magnétique. Ceux-ci permettent en effet une évaluation quantitative et qualitative du SEG. Recherche dans la banque de données Mediine des articles en langue anglaise et française, à l'aide des mots clés ≪ fat ≫ ≪ embolism ≫ employés séparément ou en combinaison. Ont été sélectionnés les articles originaux, les cas cliniques et les lettres à la rédaction. Ces articles ont été analysés selon une approche essentiellement physiopathologique, afin de mieux cerner les mécanismes responsables des embolies de graisse (Eg) et d'un SEG. Le SEG reste surtout une complication liée à la traumatologie. La migration d'Eg, sous l'action d'un phénomène d'hyperpression, est beaucoup plus fréquente que les manifestations cliniques du SEG tant en traumatologie qu'en chirurgie orthopédique. Dans des situations non traumatiques, des Eg peuvent apparaître et entraîner un SEG, par désolubilisation des graisses. Le diagnostic clinique du SEG se fait à partir de la triade, rarement complète, constituée d'une insuffisance respiratoire aiguë, de troubles neurologiques et de pétéchies. Le traitement préventif associe une stabilisation rapide et efficace des foyers de fracture et le maintien d'un état hémodynamique correct. Des gestes orthopédiques, moins producteurs d'Eg que l'enclouage centromédullaire, peuvent être préconisés en cas d'insuffisance respiratoire aiguë d'origine embolique et/ou traumatique. The occurrence of a fat embolism syndrome (FES) can be explained by two hypothetic mechanisms. In the mechanical hypothesis, bone marrow enters into the cardiovascular system during an intramedullary peak pressure. This peak could occur during either long bone fracture and/or intramedullary nailing or cemented or noncemented arthroplasty. According to the biochemical hypothesis, the FES could occur in nontraumatic conditions such as lipid emulsion infusion or sickle cell disease. The C-reactive protein is a possible factor for destabilizing plasma fat (chylomicrons or Intralipid® liposomes). Treatment with heparin has been reported to interfere with lipid metabolism through a ≪ creaming ≫ phenomenon. Plasma fatty acids increase lipid peroxidation, with potential severe oxidative stress of lung. Vascular lung injury is increased by granulocytes and the clotting cascade is activated by neutral fat. After a symptom-free period, the full clinical picture is characterized by pulmonary insufficiency with hypoxaemia, neurological impairment, pyrexia and petechial haemorrhages. The accurate incidence cannot be assessed as many subclinical forms remain unrecognized. Transoesophageal echocardiography with color-flow Doppler allows considerable insight into the sequence of embolic events and patent foramen ovale (PFO). A PFO induces an increase in right-to-left shunt in case of an elevated intrapulmonary pressure. PFO might elicit systemic manifestations of the FES, particularly with neurological impairment. Carotid ultrasonography helps to visualize embolism. Magnetic resonance imaging of cerebral fat emboli is a better diagnostic tool for detecting brain embolism than computerized tomography. Quantification of cells containing fat droplets in bronchoalveolar lavage material could also be helpful. Pulmonary microvascular cytology analysis of capillary blood samples obtained through a pulmonary artery catheter in combination with blood gas changes are of value for earlier stage FES. Prophylactic and therapeutic measures are aimed to counteract the various mechanisms leading to FES. The decrease in time delay of fracture management is probably the most effective prophylactic means. A reaming procedure can be noxious, particularly in a patient with a severe thoracic trauma. The insertion without reaming of a small diameter nail, plating or external fixation have several advantages. Albumin infusion is recommended for restoration of blood volume and binding of fatty acids. Among pharmacologic measures, only corticosteroids have a proven benefit, not only for prophylaxis but also for therapy. Aprotinin and heparin are beneficial in counteracting blood cell aggregation. A prophylactic use of vena cava filters has been advocated. Prevention or early treatment of hypovolaemia and hypoxaemia are essential.

The transmissible spongiform encephalopathies (TSE) represent a group of neurodegenerative diseases with lethal outcome. They include Creutzfeldt-Jakob disease (CJD) and kuru, among others in humans, scrapie in sheep and spongiform encephalopathy in cattle (bovine spongiform encephalopathy: BSE). Some are autosomal dominant disorders like CJD, Gerstmann-Straüssler-Scheinker disease (GSS), with point mutation of the prion protein gene. Most of these diseases are idiopathic rather than sporadic. Iatrogenic CJD could be obtained by central inoculation (neurosurgical instruments or dura mater grafts) or by peripheral inoculation (pituitary hormone therapy). A new variant clinicopathological type of CJD (nvCJD) has been reported. The nvCJD has strain characteristics distinct from other types of CJD, close to those of BSE transmitted (studies with intracerebral inoculation), consistent with BSE being the source of this new disease. All of these spongiform encephalopathies (SE) are characterized by spongiform degeneration of the brain, reactive gliosis in the cortical and subcortical gray matter, neuronal loss and presence of the abnormal isoform of the cellular prion protein (PrPc). In prion disease, PrPc undergoes conformational changes involving a shift from α-helix to β-sheet structure. These neurologic lesions are characterized by major variations from case to case. Neuropathological studies in sporadic CDJ have emphasized phenotypic variations.