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B Bassoul

Publications and source records attributed to B Bassoul.

At least 19 recordsLinked to original sources
PubMed2006

[Postoperative pneumonia: nosocomial, predictable, iatrogenic, preventable or not?].

We report the case of a 52-year-old man, ASA 3-4, malnourished, heavy smoker and drinker at the stage of chronic obstructive pulmonary disease and cirrhosis. The postoperative course of a cervical cancer surgery was complicated by a pneumonia with fatal outcome in the intensive care unit. Taking into account the patient's history and surgical requirements, this nosocomial infection did not appear easily preventable. The multiple risk factors and the few preventive measures usable were analyzed. In this context, the media and legal trend to make the doctors responsible for the nosocomial infections should be revised.

Alcoholism↗
PubMed2003

[Orbital haemorrhage after medial canthus episclera (sub-Tenon's) anaesthesia].

Medial canthus episclera (sub-Tenon's) anaesthesia is a technique proposed as a suitable alternative to the more classical peribulbar block because of the greater reliability and more constancy in effectiveness. We report two cases of retrobulbar haematoma after sub-Tenon's anaesthesia, one with central retina artery compression needed anterior room punction. Sub-Tenon's anaesthesia, like peribulbar anaesthesia, can give also retrobulbar haemorrhage if the insertion of the needle is not limited to the anterior orbit.

Aged↗
PubMed1994

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.

Anesthesia↗
PubMed1994

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)

Animals↗
PubMed1994

[Block of the sciatic nerve].

Sciatic nerve blocks were seldom used until recently. They apply to most surgical procedures on the lower limb and are often combined with a "3 in 1" block. However they can be used alone for foot surgery or postoperative analgesia. Nerve stimulators make their realization easier and more reliable. Sciatic nerve block can be obtained by different techniques. The choice of which being helped by some guidelines according to the patients characteristics and the surgical site.

Anesthetics, Local↗
PubMed1993

Lemakalim, a potassium channel agonist, reverses electrophysiological impairments induced by a large dose of bupivacaine in anaesthetized dogs.

We have examined the ability of lemakalim to correct bupivacaine-induced cardiac electrophysiological impairment in an experimental electrophysiological model in closed-chest dogs. Two groups (n = 6) of pentobarbitone-anaesthetized dogs were given atropine 0.2 mg kg-1 i.v., and bupivacine 4 mg kg-1 i.v. over 10 s. Group 2 received also lemakalim 0.03 mg kg-1 i.v. Bupivacaine induced bradycardia, prolonged PR and His-ventricle (HV) intervals, QRS duration, QTc and JTc intervals, decreased left ventricular (LV) dP/dt max and increased LV end-diastolic pressure. Lemakalim reversed bupivacaine-induced PR, HV, QRS, QTc and JTc prolongation, and did not worsen bupivacaine-induced bradycardia and haemodynamic depression. We conclude that lemakalim can antagonize the main deleterious electrophysiological effects induced by a large dose of bupivacaine in anaesthetized dogs.

Anesthesia, General↗
PubMed1993

[Tetraplegia and functional surgery of the upper limb: what anesthesia for what surgery?].

Surgical rehabilitation of the upper limb in quadriplegia aims to restore prehension function. Surgical restoration always involves active extension of both elbow and wrist. Anesthesia, which first aim is to allow adequate surgical conditions, must adapt to the patient's disability. In this particular setting, regional anesthesia and especially brachial plexus block techniques represents our priority choice.

Anesthesia, Conduction↗
PubMed1992

Experimental evidence in favor of role of intracellular actions of bupivacaine in myocardial depression.

Bupivacaine is more cardiodepressant than lidocaine. Nevertheless, the marked depression of contractility induced by bupivacaine cannot be completely explained by its electrophysiologic properties alone. Biophysical differences such as the greater lipid solubility of bupivacaine versus lidocaine must be taken into consideration. Perhaps more bupivacaine enters the cardiac cells and interacts with contractile processes. To test this hypothesis, the entry of lidocaine into the cells was facilitated by a membrane-permeant lipophilic anion, tetraphenylboron. We compared the spontaneous atrial rate and the contractile force of rabbit right atria bathing in solutions containing either 0.5 microgram/mL lidocaine or bupivacaine. Group 1 (n = 8) served to test the stability of the preparation. In group 2 (n = 6), tetraphenylboron (17 micrograms/mL) was added to Tyrode's solution; atrial rate was decreased by 8% and contractile force by 1.7%. In group 3 (n = 6), bupivacaine (0.5 microgram/mL) was added; bupivacaine decreased atrial rate by 11.3% and markedly depressed contractile force by 68.3%. In group 4 (n = 6), lidocaine (0.5 microgram/mL) was added; lidocaine did not change atrial rate but decreased contractile force by 6.0%. In group 5 (n = 6), both lidocaine and tetraphenylboron were added; atrial rate was decreased by 15.5% and contractile force was markedly depressed by 81.1%. In group 6 (n = 6), 0.2 mM adenosine triphosphate, tetraphenylboron, and then lidocaine were added; the addition of adenosine triphosphate partially counteracted the cardiodepressant effects of the combination of lidocaine and tetraphenylboron. Atrial rate was decreased by 10.4% and contractile force was depressed by 13.6%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Reversal of electrophysiologic and hemodynamic effects induced by high dose of bupivacaine by the combination of clonidine and dobutamine in anesthetized dogs.

The ability of clonidine and dobutamine to correct bupivacaine-induced cardiac electrophysiologic and hemodynamic impairment was evaluated in an experimental electrophysiologic model on closed-chest dogs. Five groups (n = 6) of pentobarbital-anesthetized dogs were given atropine (0.2 mg/kg IV). Group 1 was given a saline solution; all other dogs were given bupivacaine (4 mg/kg IV) over a 10-s period. Group 2 was given only bupivacaine. Group 3 was given clonidine (0.01 mg/kg IV) over a 1-min period. Group 4 was given a dobutamine infusion at 5 micrograms.kg-1.min-1. Group 5 was given the combination of clonidine and dobutamine. Bupivacaine induced bradycardia, prolonged atrioventricular conduction time (PR interval), atrioventricular node conduction time (AH interval), His-Purkinje conduction time (HV interval), and QRS duration. Bupivacaine decreased left ventricular (LV) dP/dt max and increased LV end-diastolic pressure (LVEDP). Clonidine improved QRS duration and HV interval but enhanced AH interval, bradycardia, and hemodynamic depression induced by bupivacaine. Dobutamine infusion improved LV dP/dt max but did not modify bupivacaine-induced ventricular electrophysiologic impairment. The combination of clonidine and dobutamine corrected not only the electrophysiologic impairment induced by bupivacaine but also the hemodynamic depression. As the HV interval and the QRS duration could be correlated with ventricular conduction velocities, we conclude that (a) clonidine reversed the slowing of ventricular conduction velocities induced by bupivacaine, and (b) the combination of clonidine and dobutamine was able to correct the cardiac disturbances induced by bupivacaine in anesthetized dogs.

Animals↗
PubMed1991

[Non-analgesic effects of opioids].

The aim of the regional administration of opioids is to provide an efficient and prolonged analgesia. Then, opiates can be useful for postoperative analgesia and for the treatment of chronic pain of malignant origin. Analgesia is correlated with several adverse effects of which the most frequent are nausea and itching and the most severe is respiratory depression. Beside the adverse effects, other properties of opiates could be responsible of favourable effects which can be taken in advantage in specific indications. In the postoperative period, epidurally administered opioid can attenuate the neuroendocrine and metabolic responses to surgery and pain. This effect is responsible of a reduction of the resistance to insulin and of a better nutritional balance, especially after major abdominal surgical procedures. Opioids also act by a reduction of the motor functions of the bowel, which perhaps could reduce the incidence of anastomotic breakdowns. Finally, other effects have been reported, as anecdotes, such as the treatment of spasm after bilateral replantation of the ureters, neurologic bladder dysfunctions and enuresis. Spinal administration of opioids has also been used as a treatment of premature ejaculation.

Analgesics, Opioid↗
PubMed1990

[Do beta adrenergic receptor blockaders increase bupivacaine cardiotoxicity?].

Bupivacaine is known to impair the electrophysiology of the heart as well as haemodynamic parameters. Administration of calcium channel blockers prior to bupivacaine enhances its cardiotoxicity. This study assessed the effects of bupivacaine at toxic dose in dogs with previous beta-adrenergic receptor blockade. It included 12 dogs anaesthetized with thiopentone, allocated in a control group (n = 6) receiving a bolus of bupivacaine (4 mg.kg-1) and a study group (n = 6) treated with the sequence propranolol (0.2 mg.kg-1) and bupivacaine (4 mg.kg-1), 15 min later. Infranodal conduction (HV conduction times and QRS durations) was worsened in both groups. Previous propranolol administration had no potentiating effects on these parameters. Conversely the latter was responsible of a greater decrease in heart rate, and increase in atrio-ventricular conduction time (77.9% vs 18.7%, p less than 0.05), as well as a more severe hypotension. Moreover, 3 out of the 6 animals in the study group suffered a cardiac arrest between the 5th and the 10th min. It is concluded that in anaesthetized dogs the cardiac and circulatory effects of a toxic dose of bupivacaine are increased in case of preexisting blockade of beta adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1990

[Treatment of acute hepatic encephalopathy with flumazenil].

In animal studies as well as in a few cases in humans, the benzodiazepine antagonist flumazenil has been shown to reverse hepatic encephalopathy. The authors treated 3 patients with acute hepatic encephalopathy stage III or IV complicating cirrhosis. Two patients had an immediate recovery, maintained with a continuous infusion of flumazenil. In the third patient the clinical status dit not improve but the hepatic encephalopathy coexisted with major abnormalities in blood gases and electrolytes abnormalities, which could participate to the neurologic failure.

Acute Disease↗
PubMed1989

Is epidural anaesthesia using bupivacaine safe in patients with atrio-ventricular conduction defects?

Bupivacaine is known to interact with the conductive system of the heart, also when used in epidural anaesthesia. Ten patients, undergoing bupivacaine epidural anaesthesia for lower limb or pelvic surgery, who presented a history of cardiac conduction disturbances, were studied. The ECG was continuously monitored and a right ventricular bipolar electrode was used to monitor the following parameters: heart rate, QRS duration, QT, Atria-His and His-Ventricle intervals. No significant change was noticed, even in patients with a high grade conduction defect. The mean plasma level of bupivacaine was 0.33 +/- 0.23 micrograms/ml. Based on this experience, it seems that lumbar epidural anaesthesia with bupivacaine can be safely used in patients with asymptomatic AV conduction abnormalities.

Anesthesia, Epidural↗
PubMed1989

In vitro study on mechanisms of bupivacaine-induced depression of myocardial contractility.

Although several mechanisms have been proposed to explain bupivacaine cardiotoxicity, the predominant effect remains to be determined. In this study, we used an isolated rabbit right atrial model that reproduces the effects on inotropic and chronotropic functions induced by 0.5 micrograms/mL bupivacaine; then we tried to counteract these events by electrical stimulation or by addition of CaCl2 or adenosine triphosphate (ATP) to the bathing solution. Contractile force was dramatically depressed by bupivacaine alone (-68%), even when the preparation was paced (-59%). CaCl2 partially counteracted this decrease (-37%). Inotropic function was almost completely restored (-9%) when ATP was added before administration of bupivacaine. Inhibition of energy metabolism seems to be a major explanation for bupivacaine cardiotoxicity.

Adenosine Triphosphate↗