[Analgesia after hip fracture repair in elderly patients: the effect of a continuous femoral nerve block: a prospective and randomised study]. / Analgésie postopératoire par cathéter fémoral après fracture du col du fémur chez la personne âgée: étude prospective randomisée.

INTRODUCTION: The usefulness of peripheral femoral nerve block for pain management after hip fracture has been established. This prospective and randomised study compared the analgesia effect of a continuous femoral nerve block (CF) versus two conventional analgesia procedures after hip fracture. PATIENTS AND METHODS: Patients. (n=62) scheduled for surgery under spinal anaesthesia were prospectively included. After surgery, analgesia (48 hours) was randomised: group FC (femoral catheter, anterior paravascular approach, initial bolus followed by continuous infusion of ropivacaine 0.2%), group P (iv 2 g propacetamol/6 hours), group M (sc morphine, 0.05 mg/kg per 4 hour). Intravenous morphine titration was performed, followed by subcutaneous (sc) morphine every 4 hours according to the VAS score. The primary end-point was the morphine requirements. Secondary end-points were VAS score, side effects, and mortality. RESULTS: Demographic data and surgical procedures were similar between groups. After morphine titration, the VAS pain score did not differ between groups. All patients in-group M received additional morphine. Morphine mean consumption was increased in CF group: 26 mg (5-42) versus P: 8 mg (3-12) (p=0.0001) or M: 19 mg (8-33) (p<0.006) while constipation was decreased in P group vs CF. Percentage of patients requiring no morphine was similar between P (n=6; 28%) and CF (n=6; 28%) and greater than M (n=0; 0%). Hospital discharge, cardiovascular or pulmonary complications and mortality after 6 months showed no statistical difference. CONCLUSION: Continuous femoral nerve block provided limited pain relief after hip fracture did not reduced side effects and induced an expensive cost.

Insertion time of the pulmonary artery catheter in critically ill patients.

OBJECTIVES: Measurement of the time elapsed from the decision to use a pulmonary artery catheter to the onset of the adapted treatment. DESIGN: Prospective study. SETTING: Critical care unit of a university hospital. PATIENTS: A total of 104 critically ill patients. INTERVENTIONS: The time elapsed from the decision to use a pulmonary artery catheter to the onset of the adapted treatment. Five time intervals (availability, preparation, catheterization, data collection, and therapeutic intervals) were individualized according to the times of decision of pulmonary artery catheter insertion, operator's hand washing, venipuncture, postoperative dressing, data collection, and the effective onset of subsequent therapy. MEASUREMENTS AND MAIN RESULTS: Among 120 used pulmonary artery catheters, seven could not be inserted. The time to use the pulmonary artery catheter was never shorter than 45 mins (median value = 120 mins). For availability, preparation, catheterization, data collection, and therapeutic intervals, the median values were 30, 20, 20, 20, and 10 mins, respectively. The availability and data collection intervals were shortened during the night period and the fourth quarter of the study, respectively. CONCLUSIONS: The pulmonary artery catheter use is time consuming. However, the availability and data collection intervals could be shortened.

[Benefit-risk and monitoring modalities of different techniques and methods of postoperative analgesia]. / Bénéfices-risques et modalités de surveillance des différentes techniques et méthodes d'analgésie postopératoire.

This review aimed to determine the benefits-risks ratio of postoperative analgesia. The various agents usually used for intravenous postoperative analgesia (paracetamol, NSAID's, opioids), and the techniques for postoperative analgesia (PCA, epidural, perinervous block) are analysed. The rules proposed for the monitoring of postoperative analgesia are considered.

Training is required to improve the reliability of esophageal Doppler to measure cardiac output in critically ill patients.

OBJECTIVES: Assessment of and effect of training on reliability of esophageal Doppler (ED) versus thermodilution (TD) for cardiac output (CO) measurement. DESIGN: Prospective study. SETTING: Intensive care unit of a university hospital. PATIENTS: 64 consecutive critically ill patients requiring a pulmonary artery catheter, sedation, and mechanical ventilation. INTERVENTIONS: Esophageal Doppler CO measurements were performed by the same operator, whereas TD CO measurements were carried out by other independent operators. A training period involving the first 12 patients made the operator self-confident. In the remaining patients, the reliability of ED was assessed (evaluation period), using correlation coefficients and the Bland and Altman diagram. Between training and evaluation periods, correlation coefficients, biases, and limits of agreement were compared. MEASUREMENTS AND RESULTS: During training and evaluation periods, 107 and 320 CO measurements were performed in 11 out of 12 patients and in 49 out of 52 patients, respectively. Continuous CO monitoring was achieved in 6 out of 11 patients and in 38 out of 49 patients during training and evaluation periods, respectively. Between the two periods, correlation coefficients increased from 0.53 to 0.89 (p < 0.001), bias decreased from 1.2 to 0.1 l x min(-1) (p < 0.001), and limits of agreement decreased from 3.2 to 2.2 l x min(-1) (p < 0.001). CONCLUSION: A period of training involving no more than 12 patients is probably required to ensure reliability of CO measurement by ED.

The addition of opioids to local anaesthetics in brachial plexus block: the comparative effects of morphine, buprenorphine and sufentanil.

We compared the duration of analgesia produced by a mixture of lignocaine and bupivacaine, either alone or combined with morphine (75 micrograms.kg-1), buprenorphine (3 micrograms.kg-1) or sufentanil (0.2 microgram.kg-1) in 80 patients after brachial plexus block for orthopaedic surgery of the upper limb. The characteristics of analgesia were evaluated hourly using a visual analogue scale. The analgesia was considered satisfactory for scores of 30 or less. The median duration (range) of satisfactory analgesia was: 11.5 (8-15) h without an opioid, 21 (9-27) h with morphine, 20 (14-34) h with buprenorphine and 24.5 (11-38) h with sufentanil. We conclude that the addition of an opioid to a local anaesthetic mixture lengthens the duration of analgesia.

Effects of ketamine on ventricular conduction, refractoriness, and wavelength: potential antiarrhythmic effects: a high-resolution epicardial mapping in rabbit hearts.

BACKGROUND: The aims of the study were to verify the effects of ketamine on ventricular conduction velocity and on the ventricular effective refractory period, to determine its effects on anisotropy and on homogeneity of refractoriness, and to use wavelength to determine whether ketamine has antiarrhythmic or arrhythmogenic properties. METHODS: A high-resolution epicardial mapping system was used to study the effects of 50, 100, 150, and 200 microM racemic ketamine in 15 isolated, Langendorff-perfused rabbit hearts. Five hearts were kept intact to study the effects of ketamine on spontaneous sinus cycle length (RR) interval and its putative arrhythmogenic effects. In 10 other hearts, a thin epicardial layer was obtained by an endocardial cryoprocedure (frozen hearts) to study ventricular conduction velocity, ventricular effective refractory periods (five sites), and ventricular wavelength. RESULTS: Ketamine induced a concentration-dependent lengthening of the RR interval. Ketamine slowed longitudinal and transverse ventricular conduction velocity with no anisotropic change, and it prolonged the ventricular effective refractory period with no significant increase in dispersion. Ventricular longitudinal and transverse wavelengths tend to increase, but this was not statistically significant. Finally, no arrhythmia could be induced regardless of the ketamine concentration. CONCLUSION: Ketamine slowed ventricular conduction and prolonged refractoriness without changing anisotropy or increasing dispersion of refractoriness. Although these effects should result in significant antiarrhythmic effects of ketamine, this should not be construed to suggest a protective effect in ischemic or other abnormal myocardium.

Electrophysiologic and proarrhythmogenic effects of therapeutic and toxic doses of imipramine: a study with high resolution ventricular epicardial mapping in rabbit hearts.

Electrophysiologic and proarrhythmogenic effects of imipramine were studied by use of 21 Langendorff-perfused rabbit hearts and high-resolution mapping to analyze epicardial activation of the left ventricle. In 16 hearts, a thin layer of epicardium was obtained by an endocardial cryotechnique (frozen hearts). Five hearts were kept intact (nonfrozen imipramine-treated group). Preparation stability was verified in six frozen hearts. In 10 frozen and in 5 nonfrozen hearts, 0.01, 0.1, 1.0, 2.0 and 5.0 micrograms/ml imipramine were administered. In nonfrozen imipramine-treated hearts, imipramine induced bradycardia at 5.0 micrograms/ml (291.8 +/- 40.5 vs. 495.2 +/- 54.4 msec, P = .02), one A-V block at 5.0 micrograms/ml and two monomorphic ventricular tachycardias (MVT) at 2.0 and 5.0 micrograms/ml. In 4/10 frozen hearts, three MVT were induced at 1.0 microgram/ml imipramine and one MVT at 2.0 micrograms/ml imipramine. All MVT were based on reentry around a line of functional conduction blocks. Imipramine (2.0 micrograms/ml) slowed longitudinal and transversal ventricular conduction velocities at a pacing cycle length of 1000 msec from 71.7 +/- 6.1 to 63.0 +/- 7.7 cm/sec (P = .008) and from 32.9 +/- 2.6 to 27.7 +/- 2.8 cm/sec (P = .009), respectively, and prolonged ventricular effective refractory period from 141.9 +/- 9.3 to 279.1 +/- 112.6 msec (P = .03). Imipramine induced dose- and use-dependent slowing of ventricular conduction velocity facilitating functional conduction blocks and reentrant MVT.

Comparative electrophysiologic and hemodynamic effects of several amide local anesthetic drugs in anesthetized dogs.

Large and equipotent doses of several local anesthetics were administered in a cardiac electrophysiologic model on closed-chest dogs. Five groups of pentobarbital-anesthetized dogs were each given intravenously 16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocaine, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of atrioventricular node conduction (AH), and marked hemodynamic depression, represented by a decrease in mean aortic pressure (MAoP), in the peak of first derivative of left ventricular pressure (LVdP/dt(max)) and by an increase in left ventricular end-diastolic pressure (LVEDP). Atrial pacing at pacing cycle length (PCL) of 298 ms did not enhance the alteration of variables of ventricular conduction (His ventricle [HV] interval and QRS duration). Mepivacaine induced slight alteration of electrophysiologic variables. Atrial pacing at PCL of 312 ms did not enhance the alteration of HV and QRS duration. Mepivacaine induced transient hemodynamic depression. Etidocaine (4 mg/kg) induced electrophysiologic and hemodynamic alterations similar to mepivacaine but artrial pacing at PCL of 330 ms enhanced HV lengthening and QRS widening (P < 0.05). Etidocaine (8 mg/kg) induced marked impairment of PR, HV, QRS, and QT, and dramatic hemodynamic depression represented by a decrease in MAoP from 123.5 +/- 16.2 at baseline to 36.5 +/- 8.3 mm Hg at 1 min (P < 0.001) and of LVdP/dtmax) from 1446 +/- 379 to 333 +/- 93 mm Hg/s (P < 0.001). Bupivacaine induced dramatic impairment of electrophysiologic variables. Bupivacaine also decreased LVDP/dtmax (from 1333 +/- 347 to 617 +/- 299,P < 0.001) and increased LVEDP. We conclude that mepivacaine induced moderate cardiotoxicity. In contrast, lidocaine induced dramatic hemodynamic depression while etidocaine and bupivacaine markedly impaired both electrophysiologic and hemodynamic variables. This double impairment could explain the great difficulty in resuscitating patients who have had cardiotoxic accidents induced by etidocaine or bupivacaine.

[Severe preeclampsia. Analysis of a case with fatal outcome]. / Pré-éclampsie sévère. Analyse d'un cas d'évolution fatale.

We report a case of preeclampsia presenting initially as a moderate hypertension, and complicated over a ten-day period by eclampsia, retinal hemorrhage, cerebral and hepatic subcapsular hematomas, HELLP syndrome, disseminated intravascular coagulation and renal failure. Fatal outcome was related to cerebral death and rupture of the liver hematoma. The case analysis points out inaccurate initial management: probable misdiagnosis of epigastric pain related to subcapsular hematoma, ineffective antihypertensive therapy, aspiration of the gastric content after benzodiazepine treatment of eclampsia, transfer of the patient without stabilisation of her clinical status.

Cardiac output measurement in critically ill patients: comparison of continuous and conventional thermodilution techniques.

The purpose of the study was to compare cardiac output (CO) measurement by continuous (CTD) with that by conventional thermodilution (TD) in critically ill patients. In 19 of 20 critically ill patients requiring a pulmonary artery catheterism, 105 paired CO measurements were performed by both CTD and TD. Regression analysis showed that: CTD CO = 1.18 TD CO - 0.47. Correlation coefficient was 0.96. Bias and limit of agreement were -0.8 and 2.4 L.min-1, respectively. When a Bland and Altman diagram was constructed according to cardiac index ranges, biases were -0.2 and -0.3 and -0.8 L.min-1.m-2 and limits of agreement were 0.3, 0.7 and 1.6 L.min-1.m-2 for low (< 2.5 L.min-1.m-2), normal (between 2.5 and 4.5 L.min-1.m-2) and high (> 4.5 L.min-1.m-2) cardiac indexes, respectively. It is concluded that CTD, compared with TD, is a reliable method of measuring CO, especially when cardiac index is < or = 4.5 L.min-1.m-2.

[Does neuroplasticity have a role on postoperative pain?]. / La neuroplasticité intervient-elle dans les phénomènes douloureux postopératoires?

The neurophysiologic concept of neuroplasticity represents one of the current basis of the pathophysiology of painful post-injury phenomenons (postoperative, post-traumatic...). Deriving directly from these experimental data, the idea of preemptive analgesia has gradually developed in the last five years, the central question being to know if an analgesic intervention preceding surgical intervention is more efficient, as efficient, or less efficient than the same intervention following surgery. The authors bring current data of the literature in favor of the role of neuroplasticity in the genesis and the persistence of painful states in the course of postoperative outcome. A review of the various clinical studies and controversies published is proposed, in the attempt to make the point on current therapeutic implications of the concept of preemptive analgesia.

[Optimal use of peripheral nerve blocks]. / Optimisation des blocs périphériques.

The advantages of regional over general anaesthesia have led to an increased use of peripheral nerve blocks. Among the few risks of regional anaesthesia are those of overdosage, systemic and neural toxicity. Techniques have been proposed to improve the success of peripheral nerve blocks and to avoid nerve damage or systemic toxicity. Nerve stimulator, anatomic landmarks, needles and anaesthetic solutions are discussed.

Receptor mechanisms for clonidine reversal of bupivacaine-induced impairment of ventricular conduction in pentobarbital-anesthetized dogs.

Possible mechanisms of the ability of clonidine to correct bupivacaine-induced ventricular electrophysiologic impairment were evaluated in an electrophysiologic model on closed-chest dogs. Nine groups (n = 6) of pentobarbital-anesthetized dogs were given atropine, 0.2 mg/kg intravenously (i.v.), and bupivacaine, 4 mg/kg i.v., over a 10-s period. Group 1 was then given only saline solution. Group 2 was given clonidine, 0.01 mg/kg i.v., over a 1-min period. Group 3 was given clonidine followed by i.v. administration of yohimbine, 1 mg/kg, an alpha 2-antagonist. Group 4 was given carbachol, 1 mg/kg i.v., a long-lasting cholinergic agonist, over a 1-min period. Group 5 was given electrical stimulation of the left vagus nerve. Group 6 was given physostigmine, 0.1 mg/kg i.v., known to inhibit cholinesterase degradation, 5 min before bupivacaine administration, and Group 7 received a combination of physostigmine pretreatment and electrical vagal stimulation. Group 8 was given physostigmine, 0.1 mg/kg i.v., and pancuronium bromide, 1 mg/kg i.v., known to inhibit nicotinic receptors, 5 min before bupivacaine administration. Then electrical stimulation of the left vagus nerve was performed. Group 9 was given nicotine, 0.1 mg/kg i.v., 1 min after bupivacaine injection over 1 min. Bupivacaine induced bradycardia, markedly increased the His-Purkinje conduction time (HV interval) and QRS duration. Bupivacaine decreased the peak of first derivative of left ventricle pressure (LVdP/dtmax) and increased left ventricular end-diastolic pressure (LVEDP). Clonidine improved QRS duration and HV interval. Yohimbine did not modify the effects of clonidine. QRS duration and HV interval were significantly improved in Groups 4-7. In Group 8, pancuronium pretreatment inhibited the beneficial effects of the combination of physostigmine pretreatment and electrical vagal stimulation. In contrast, in Group 9, like clonidine, nicotine improved QRS duration and HV interval. Three other groups of anesthetized dogs (n = 6) were then studied. All dogs were given hexamethonium, 10 mg/kg i.v. Then, Group 10 was given only saline solution; Group 11 was given bupivacaine, 4 mg/kg, and Group 12 was given bupivacaine and nicotine as in Group 9. In Group 11, bupivacaine induced its usual alterations. In contrast, nicotine did not modify the cardiotoxic profile of bupivacaine after hexamethonium pretreatment. We conclude that the beneficial effect of clonidine on the variables of ventricular conduction altered by bupivacaine 1) is not mediated by central alpha 2-activation, 2) is mediated by the activation of parasympathetic pathways, and 3) is indirect and not mediated by acetylcholine release but is mediated by the activation of parasympathetic ganglionic nicotinic receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanisms of the putative cardioprotective effect of hexamethonium in anesthetized dogs given a large dose of bupivacaine.

BACKGROUND: Some reports suggest that activation of the autonomic nervous system by bupivacaine could participate in its cardiotoxicity. This is based in part on the fact that hexamethonium suppresses cardiac disturbances in anesthetized rabbits given small intracerebroventricular doses of bupivacaine. The aims of the current study were to determine, in anesthetized dogs, (1) whether the activation of the autonomic nervous system is deleterious after a large intravenous dose of bupivacaine and (2) whether the parasympathetic or sympathetic system is implicated in the bupivacaine-induced deleterious activation of the autonomic nervous system. METHODS: We used an electrophysiologic model in closed-chest dogs anesthetized with sodium pentobarbital. In group 1 (n = 6), dogs were given 4 mg/kg intravenous bupivacaine over 10 s. In group 2 (n = 6), dogs were given the same dose of bupivacaine 5 min after having received 0.2 mg/kg intravenous atropine sulfate. In group 3 (n = 9), dogs were pretreated with 10 mg/kg intravenous hexamethonium and then given bupivacaine 4 mg/kg. In addition, in group 3, the right atrium was paced at a basic cycle length of 400 ms to obtain a heart rate similar to that of group 1. RESULTS: Bupivacaine in group 1 induced significant bradycardia; lengthening of PR, atria-His, His-ventricle, and QTc intervals; and QRS widening. The first derivative of left ventricular pressure was significantly decreased, whereas left ventricular end-diastolic pressure was increased. Atropine pretreatment did not modify cardiac disturbances induced by bupivacaine. Hexamethonium pretreatment induced significantly less QRS widening and QTc lengthening than was seen in group 1 but worsened the bupivacaine effects on bradycardia, atria-His and PR intervals, mean aortic pressure, and first derivative of left ventricular pressure. Moreover, atrial pacing in group 3 induced alterations of QRS similar to those in group 1. CONCLUSIONS: Considering that marked slowing of ventricular conduction velocity (i.e., QRS widening) is known to facilitate reentrant ventricular arrhythmias, we conclude that (1) the activation of the autonomic nervous system by bupivacaine is not as deleterious as previously suggested; (2) the parasympathetic system is not markedly implicated in the worsening of direct bupivacaine cardiotoxicity; and (3) the sympathetic nervous system acts only by inducing a less marked bradycardia, which slows ventricular conduction velocity in a use-dependent manner, facilitating reentrant arrhythmias.

[Do morphines improve the quality of analgesia with local anesthetics?]. / Les morphiniques améliorent-ils la qualité de l'analgésie aux anesthésiques locaux?

Use of opioids for regional anaesthesia aims to improve the quality and to enhance the duration of local anaesthetics-induced analgesia, and also to reduce the rate of adverse effects due to these agents. Experimental data give evidence for a synergistic effect between local anaesthetic and opiates at the spinal level (dorsal root entry zone). A lot of clinical studies have shown the improvement of analgesia when opioids are added to local anaesthetics, by the subarachnoid as well as by the epidural route. The most frequent associations in use are fentanyl-bupivacaine and morphine-bupivacaine. The efficacy of these associations by peripheral perinervous routes is more controversial. In any cases, one must be aware of the incidence of potential side-effects of opioids and, consequently, of the need for a close clinical monitoring of the patients, at least for the duration of action of the agent injected by the spinal or the epidural route.

[Convulsions and cardiac arrest after epidural anesthesia. Prevention and treatment]. / Convulsions et arrêt cardiaque après anesthésie péridurale. Prévention et traitement.

Seizures followed by cardiac arrest after obstetrical epidural anaesthesia are induced by either low cerebral perfusion due to cardiovascular collapse after too excessive sympathetic blockade or after accidental total spinal anaesthesia, or by toxic accident due to accidental intravascular administration of local anaesthetic drugs. In case of toxic accident, convulsions usually occur before haemodynamic changes. Whatever the mechanism of the accident, excessive sympathetic blockade or toxic accident, when epidural anaesthesia is performed with lidocaine, bradycardia with normal QRS complexes occurs. Respiratory depression has to be treated and ephedrine has to be administered. In contrast, when bupivacaine is used, in case of toxic accident, there are dysrhythmias or bradycardia but QRS complexes are widened. The treatment is firstly to oxygenate, to stop convulsions and then to intubate the trachea and to ventilate the lungs.

[Neurophysiological bases of preventive analgesia]. / Bases neurophysiologiques de l'analgésie préventive.

The key-question, when dealing with preemptive analgesia, its to know whether an analgesic intervention coming before surgery is as efficient, more efficient or less efficient than the same intervention following surgery. Surgical tissular damaging leads to a dual phenomenon of peripheral and central sensitization. The result is a state of neuronal hyperexcitability, so-called "wind-up phenomenon", which could partially explain postoperative painful states. Peripheral mechanisms involve many factors, especially prostaglandins that could be blocked by NSAIDs. Central mechanisms and neuroplasticity are analyzed, insisting on inter and intracellular biochemical events. The role of excitatory amino-acid is explained, especially of glutamic acid and the NMDA (N-methyl-D-aspartate) receptor at the spinal level.