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F d'Athis

Publications and source records attributed to F d'Athis.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Sedation with propofol and fentanyl in patients under intensive care].

This study investigated the efficacy of a constant rate infusion of propofol and fentanyl in thirty patients requiring artificial ventilation for more than 24 h. A loading dose, which differed according to the patient's age, was administered over a 30 min period: 2.5 mg.kg-1 for patients less than 50 (G1) (n = 9), 2 mg.kg-1 for patients between 50 and 60 years old (G2) (n = 9), and 1.5 mg.kg-1 for patients over 60 (G3) (n = 12). This was followed by an infusion of 3 mg.kg-1.h-1 in G1 and G2, and 2 mg.kg-1.h-1 in G3. A 1 microgram.kg-1.h-1 infusion of fentanyl was also given. The degree of sedation was assessed with the Ramsay scale before starting, after induction, and every four hours thereafter. When this proved to be insufficient, the dose of propofol was increased by 0.5 mg.kg-1.h-1 as well as that of fentanyl by 0.5 microgram.kg-1.h-1. Heart rate, mean arterial blood pressure, blood propofol, creatinine, transaminase and lipid levels, and urine output were measured before, during, and after the infusion. The blood propofol level increased during the infusion, being correlated to the doses given (r = 0.64, p less than 0.001). Sedation lasted 91.7 +/- 57.7 h. After stopping the infusion of propofol, mean recovery times were 7.5 +/- 5.9 min (G1), 11.4 +/- 11.4 min, and 14.4 +/- 13.5 min (G3) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Nicardipine vs trinitrin for controlled hypotension in maxillo-facial surgery].

In this study we examined perioperative blood losses during maxillo-facial surgery comparing 2 techniques for controlled hypotension using nitroglycerin (NTG) and nicardipine (NICAR). 37 ASA I and II patients electively scheduled for rhinoseptoplasties under general anaesthesia were randomly divided into 2 groups. General anaesthesia was induced with intravenous thiopental and vecuronium following a neuroleptanalgesia consisting of fentanyl (0.053 +/- 0.004 microgram.kg-1.min-1) IV and droperidol (1.98 +/- 0.35 microgram.kg-1.min-1) IV given in bolus doses. The patients were intubated and ventilated (N2O in O2) to maintain normocarbia. Controlled hypotension to maintain a mean arterial pressure (MAP) between 50 and 55 mmHg was induced using an IV infusion of NTG 6 micrograms.kg-1.min-1 in group I and NICAR 10 micrograms.kg-1.min-1 over 10 minutes followed by an infusion at 4 mg.kg-1.min-1 for group II. Measurements of heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), MAP using an automated blood-pressure cuff and end tidal carbon dioxide (ETCO2) were recorded prior to induction (PREIND), intraoperatively (PEROP) at 15, 30, 40 and 120 minutes post-induction, and at 15, 30 and 60 minutes postoperatively (POSTOP). Blood loss, graded as minimal or frank, was assessed by the surgeon during the operative period, post-extubation and 3 days postoperatively at dressing removal. The surgeon was unaware of the randomization schedule. Student's test was applied for statistical analysis of measured variables and Fisher's test for qualitative parameters. No statistically significant differences were noted between both groups with respect to demographic data, duration of surgery and total doses of anaesthetic agents (Table I).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Brachial plexus block with bupivacaine: effects of added alpha-adrenergic agonists: comparison between clonidine and epinephrine.

The effects of clonidine and epinephrine, administered into the brachial plexus sheath, were evaluated in 60 patients who underwent surgery of the upper limb. All patients received 40 to 50 ml of 0.25% bupivacaine, injected into the brachial plexus sheath, using the supraclavicular technique. The patients were randomly allocated to two groups so that 30 patients received 150 micrograms clonidine hydrochloride (Group I), and 30 received 200 micrograms epinephrine (Group II). The quality and the duration of analgesia were assessed as well as the possible side-effects. The block produced with the addition of clonidine was longer (994.2 +/- 34.2 vs 728.3 +/- 35.8 min) and superior to that with epinephrine (P less than 0.001). No major side-effects were recorded. We conclude that the injection of clonidine into the brachial plexus sheath is an attractive alternative to epinephrine to prolong the duration of analgesia following upper limb surgery under conduction anaesthesia.

Adult↗
PubMed1991

[Fibrinolytic activity in traumatic hemothorax fluids].

Twenty-nine patients, 15 to 85-year-old (mean: 50 years) who presented with a pleural effusion after trauma were studied. The blood content of pleural fluid was confirmed by thoracocentesis. None of the patients had been taking anticoagulant drugs during the fortnight preceding the trauma. Thoracocentesis was always carried out less than 90 min after the trauma. The following parameters were measured in the haemothorax liquid samples: clotting fibrinogen fraction (Fg C), fibrin degradation D-dimers, functional plasminogen, alpha 2-antiplasmin, alpha 2-macroglobulin, plasminogen tissue activator (tPA Ag), type 1 tPA plasma inhibitor (PAI), and haematocrit. Haemothorax liquid haematocrit values ranged from 13 to 35% (25 +/- 7%, with a mean peripheral venous haematocrit of 34 +/- 6%). Only three patients had some Fg C (0.05-0.13 g.l-1). The D-dimer level was very high (0.23 +/- 0.22 g.l-1). The other factors involved in fibrinolysis were also present. Moreover, there was a statistically significant inverse correlation between D-dimer and alpha 2-macroglobulin levels (r = -0.64, p less than 0.0025). These data suggest two possible mechanisms to explain the fibrinogen levels: coagulation is activated, followed by an important fibrinolytic reaction elicited by the large amounts of plasminogen and tPA present in the haemothorax liquid.

Adolescent↗
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

[Pharmacokinetics and changes in the physical properties of blood and urine after administration of dextran 60000].

A study was carried out to assess the changes induced by an infusion of dextran, molecular weight 60,000 daltons, in blood and urine. Plasma and urine dextran and serum protein concentrations, haematocrit, blood and urine viscosities, and blood oncotic pressure were measured in 10 consecutive male patients. Fifteen min after administration of 20 ml dextran 1000 (Promit), they were each given 500 ml (30 g) dextran 60 (Hemodex) over 30 min for plasma volume expansion. The measurements were carried out at the end of the infusion, and then at regular intervals over a 48 h period. The highest dextran blood concentrations were found at the end of the infusion, decreasing thereafter with a distribution half-life of 1.83 +/- 0.64 h, and an elimination half-life of 25.5 +/- 7.6 h. Haematocrit values decreased by 12%, and serum protein concentrations by 9.5%, after the end of the infusion. These changes remained significant for 9 h; they were probably due to the dilution effect of 500 ml of dextran. Colloid osmotic pressure was not significantly altered (20.7 +/- 4.7 mmHg vs. 23.1 +/- 5.1 mmHg 48 h after the end of the infusion). The colloid osmotic pressure due to dextran 60 compensated for the fall in protein concentration. A decrease in blood viscosity was found at different shear rates, despite dextran 60 being highly viscous. This could also be explained by a dilution effect. The highest degree of urinary excretion occurred 30 min after the end of the infusion, and lasted for 3 h. Forty-five percent of the total dextran dose had been excreted by the 48th hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Humidification of the respiratory tract in anesthesia].

The upper airways humidify, warm and purify the air breathed in. When these are bypassed by an endotracheal intubation catheter, cold dry air goes straight to the bronchi; this leads to local and generalized changes, which are all the more pronounced the longer the intubation lasts. Drying of the tracheobronchial mucosa leads to an early decrease in mucus production, with an increase in its viscosity, a progressive arrest of ciliary function with, finally, a destruction of the vibratory cilia. These lesions create a build-up of thick mucus which hinders humidification of the gas flow and increases bronchial resistances. The disturbed VA/Q relationship leads to a decreased secretion of surfactant. The usual loss of water by way of the lungs is about 30 mg.l-1 of air. Evaporation of this water uses up calories. Most authors suggest that, so as to compensate for the heat and water loss, inhaled gases should be warmed to between 25 and 30 degrees C and be saturated with water to 100%, i.e. 23-30 mg water per litre of air. The water and heat loss can be reduced by using either partial or total rebreathing of expired gases, or a device for heat and moisture exchange, or a humidifier. The most efficient circuits are those which include a soda lime canister. They can be made even more efficient by using different devices. Although this humidification is sufficient for large tidal volumes and a surrounding temperature greater than 22 degrees C, it is not enough for Bain's circuit.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1988

[How should a toxic accident be treated?].

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.

Anesthetics, Local↗
PubMed1988

[Cardiac toxicity of bupivacaine and diazepam. Experimental study in the anesthetized dog].

The use of diazepam has been suggested for the treatment of convulsions resulting from accidental high plasma levels of local anaesthetics. However, it has been reported that this drug may increase the cardiac effects of bupivacaine in dogs. The present study aimed to assess the effects of diazepam on the electrophysiological signs of a high-dose intravenous bolus of bupivacaine in fourteen dogs, divided into two groups, and anaesthetized with thiopentone and ventilated. All the animals were given a bolus dose of 4 mg.kg-1 bupivacaine. Immediately afterwards, group I (n = 7) received 0.8 ml.kg-1 normal saline solution and group II (n = 7) was given 4 mg.kg-1 diazepam over 1 min. The parameters measured on lead II of the electrocardiogram were: cycle length (R-R interval), QRS length (QRS) and QT interval corrected for heart rate (cQT). Intranodal (AH) and His-Purkinje (HV) conduction times were measured with recording bipolar stimulation electrodes (USCI 6F). Mean aortic pressure (Pao) was measured via a femoral arterial line. In the two groups, the parameters were recorded before and 2, 5, 10 and 15 min after the bupivacaine bolus. Arterial blood samples for measurement of bupivacaine and diazepam serum levels were obtained before and 3, 15 and 30 min after the bupivacaine bolus. There was no significant difference between the two groups in the electrophysiological or haemodynamic parameters at any time. However, the increase in HV and QRS length was a little higher in group I than in group II.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1988

Rapid pre-operative immunotherapy in a patient allergic to muscle relaxants.

Allergic reactions to muscle relaxants are not uncommon. Although, in most instances, divalent quaternary ammonium salts are involved in these reactions, some monovalent quaternary ammonium compounds can trigger IgE-mediated reactions. A woman who suffered from several episodes of anaphylaxis with divalent (suxamethonium) and monovalent quaternary ammonium salts (tiemonium) needed surgery. Regional anaesthesia was contra-indicated owing to a possible intolerance to local anaesthetics. Investigation confirmed an allergy to monovalent quaternary ammonium salts. Rapid immunotherapy was started with a monovalent quaternary ammonium salt (tiemonium) and subsequently followed by a general anaesthesia using vecuronium. The patient did not develop anaphylactic symptoms.

Adult↗