Search

article; International audience; We report the case of an 82-year-old woman treated with biliary stents for an ampulloma of Vater's papilla, with recurrent stenosis of the common bile duct. She was hospitalized with a cholestasis. An endoscopic retrograde cholangiopancreatography (ERCP) was scheduled to change the biliary stent for a metallic one, under general anaesthesia, with oral intubation. The ERCP was performed initially without any complication, but as the metallic biliary stent was placed, an air embolism occurred and a cardiac arrest happened immediately. The etiologic diagnosis was quickly confirmed by an injected multislice body-scan, which showed liver, right heart and brain gas embolism. Cardiopulmonary resuscitation allowed a complete haemodynamic recovery but a poor neurological recovery. The patient was transferred in intensive care unit, were she died 12 days after, despite hyperbaric oxygen therapy and the disappearance of the air embolism on the following computed tomography scan. This case may be useful to recall the utility of a body-scan for the diagnosis, treatment and follow-up of an air embolism during ERCP.

The volume dependence of respiratory resistance (Rrs), usually observed during normal breathing, is expected to be accentuated during expiratory flow limitation (EFL). In order to quantify this dependence we studied the pressure, flow and volume data obtained from eight New Zealand rabbits, artificially ventilated at different levels of applied expiratory pressure (0-10 hPa), before and during histamine i.v. infusion. EFL was provoked by lowering the expiratory pressure and was detected by the application of an additional negative expiratory pressure and by forced oscillations. The analysis of respiratory system mechanics was performed by multiple regression, using the classical linear first-order model and also a nonlinear model, accounting for volume dependence of Rrs. Both models satisfactorily fitted the data in the absence of EFL. The nonlinear model proved to be more appropriate in the presence of EFL. The coefficient expressing the volume dependence of Rrs (Rvd) was significantly more negative during EFL. Rvd values were highly correlated with the fraction of the tidal volume left to be expired at the onset of EFL. A threshold Rvd value of -1,000 (hPa(.)s(.)l(-2)) detected EFL with high sensitivity and specificity. We conclude that a strongly negative volume dependence of Rrs is a reliable and noninvasive index of EFL during artificial ventilation.

Background alpha 2-Adrenoceptor agonists, known as antihypertensive agents, may be used during general anesthesia for their anesthetic sparing action and to reduce the occurrence of side effects. Previous studies have shown that the brain's noradrenergic nucleus, locus coeruleus, is an important target in mediating the hypnotic action of alpha 2 agonists. The authors studied the effects of recovery from halothane anesthesia on the electrical activity of locus coeruleus neurons to examine cellular substrates underlying the clinical effectiveness of alpha 2 agonists. Methods Experiments were performed in locally anesthetized rats, whose circulatory and acid-base stabilities were ensured by mechanical ventilation and volume infusion. Locus coeruleus neurons were recorded continuously while the rats were anesthetized with halothane (1%) and/or after the halothane was discontinued. Results Under the influence of halothane, locus coeruleus cells exhibited a slow, regular spontaneous discharge (1.95 +/- 0.23 Hz), and contralateral foot or tail pinch elicited a prominent, phasic activation in locus coeruleus neurons. Such phasic activation was blocked by local ejection of kynurenic acid, an excitatory amino acid antagonist, close to recorded neurons, but not by clonidine (up to 64 micrograms.kg-1). Thirty minutes after the halothane was discontinued, the mean firing rate of locus coeruleus neurons was increased by 87 +/- 20%. This excitation resulted from a prominent increase in bursting activity (21 +/- 5% of spikes in bursts vs. 4 +/- 1%) and was reversed by halothane readministration. This activation also was reduced by local ejection of kynurenic acid. Halothane discontinuance revealed the reactivity of locus coeruleus neurons to nonnoxious, sensory stimuli, and considerably reduced the apparent potency of intravenous administration of clonidine to inhibit locus coeruleus activity (effective dose for 50% of maximal effect (ED50), 25.48 +/- 8.26 micrograms.kg-1 vs. 4.81 +/- 0.80 micrograms.kg-1 under halothane). This decrease was caused by the persistence of bursting activity after the administration of clonidine, which was completely suppressed by readministration of halothane or local application of kynurenic acid. Conclusion The data demonstrate: (1) that halothane withdrawal increases locus coeruleus neuronal activity via excitatory amino acid input, and this withdrawal-induced activity is characterized by a prominent burst (phasic) discharge; (2) that sedative doses of clonidine inhibit the tonic component of locus coeruleus activity but not the phasic activation of locus coeruleus neurons; and (3) that readministration of halothane or local ejection of an excitatory amino acid antagonist fully suppresses the bursting activity unaffected by clonidine.

A 79 year old woman was admitted for an episode of left facial paralysis and dysarthria which lasted several minutes. Her history included hypertension which was being treated with valsartan. At admission, no cardiovascular or neurological abnormalities were detected by physical examination, ECG, and carotid ultrasonography, and …

Soixante-dix malades presentant une bronchopneumopathie chronique, hospitalises pour insuffisance respiratoire aigue (SaO2 inferieure ou egale a 70 p. 100; PaCO2 superieure a 60 mm Hg) ont subi, pendant la reanimation d’urgence, des enregistrements electroencephalographiques repetes en meme temps qu’un dosage des gaz du sang arteriel. Chez 19 d’entre eux, le liquide cephalorachidien a ete preleve simultanement pour determiner l’equilibre acido-basique, la PCO2, la PO2 et doser les electrolytes. Les traces electroencephalographiques sont groupes en 4 stades en allant des traces les moins accuses aux plus perturbes, le stade 0 representant la normalite. Certains aspects particuliers sont notes: ondes triphasiques, silences periodiques. Des correlations electrocliniques et electrobiologiques ont ete tentees. La degradation des traces EEG est parallele a la degradation de l’etat de conscience. Le stade 4 correspond au coma carus. II existe un retard de l’amelioration electrique par rapport a l’amelioration clinique. Aucune correlation nette n’a ete trouvee entre les stades EEG et les gaz ou les electrolytes du sang. Par contre, l’aggravation des stades EEG correspond a une chute significative (p