The practical usefulness of quick intraoperative immunoradiometric measurements of intact (1-84) parathyroid hormone (iPTH) in the surgical management of primary hyperparathyroidism (HPTI) is here assessed. Fourty-two patients entered the study between March 1991 and January 1993. All patients showed a good decline of iPTH after diseased gland(s) removing and 41/42 patients presented undetectable or normal values of iPTH after a period of 10 to 110 minutes. No persistent or recurrent hyperparathyroidism was observed. Quick intraoperative measurements of iPTH are specially usefull when unilateral neck exploration is indicated.

The practical usefulness of quick intraoperative immunoradiometric measurements of intact (1–84) parathyroid hormone (iPTH) in the surgical management of primary hyperparathyroidism (HPT I) is here assessed. Fourty-two patients entered the study between March 1991 and January 1993. All patients showed a good decline of iPTH after diseased gland(s) removing and 41/42 patients presented undetectable or normal values of iPTH after a period of 10 to 110 minutes. No persistent or recurrent hyperparathyroidism was observed. Quick intraoperative measurements of iPTH are specially usefull when unilateral neck exploration is indicated.

A case of nosocomial meningitis due to aKlebsiella pneumoniae producing a CAZ-5 extendedspectrum β-lactamase and anEnterobacter aerogenes producing a derepressed cephalosporinase is reported. The intrathecal catheter incriminated was removed and a treatment with ceftazidime (4 g/24 h) and amikacin (1.5 g/24 h) was started. After 24 h ceftazidime was replaced by imipenem (2 then 4 g/24 h). This treatment failed to obtain cerebrospinal fluid sterilization; therefore the imipenem dosage was increased to 8 g/24 h and two intrathecal infusions of amikacin (50 mg) were carried out. Thereafter the patient recovered.

The effects of reversal of flunitrazepam-induced sedation with flumazenil on coronary hemodynamics, myocardial oxygen consumption (MVO2), and left ventricular (LV) performance were investigated, in a double-blind trial, in 12 patients with stable coronary artery disease undergoing cardiac catheterization. Coronary sinus blood flow was measured by continuous thermodilution. Arterial and coronary sinus blood were analyzed for oxygen and lactate contents. The determinants of LV performance were obtained from the cardiac output measured by thermodilution and from left heart catheterization data. To reverse flunitrazepam-induced sedation, patients were randomly allocated to receive placebo or flumazenil (by increment, up to 1 mg) at the end of procedure. In the placebo group, no significant hemodynamic changes were observed. In the flumazenil group, heart rate, cardiac index, maximum velocity of shortening, and relaxation time constant were not significantly altered. By contrast, mean aortic pressure and LV end-diastolic pressure (baselines: 90 +/- 5 and 7.3 +/- 4.1 mmHg, respectively) increased (9%, P less than 0.05 and 67%, P less than 0.05, respectively) after flumazenil administration, but these changes represented mainly a return toward presedation values. MVO2 and coronary resistance were not significantly altered, whereas CSBF increased slightly (baseline: 119 +/- 20 ml/min; increase 10%, P less than 0.05). No electrocardiographic evidence of myocardial ischemia was observed during the study. These data show that reversal of benzodiazepine effects with flumazenil is not associated with a major alteration of LV systolic function, relaxation, or coronary hemodynamics in patients with coronary artery disease. Nevertheless, it should be cautiously used when LV end-diastolic pressure is increased at the time of its administration.

Various laboratory investigations were assessed with respect to their accuracy in detecting myocardial contusion in patients with blunt chest trauma. All patients, aged between 18 and 50 years, admitted to the intensive care unit for flail chest, sternal fracture, pulmonary contusion, pleural or mediastinal lesion not requiring surgery, were included over a twelve month period. A complete cardiac assessment was carried out, including a physical examination, electrocardiogram, chest X-ray, enzyme assay (ALAT, ASAT, LDH, CPK and MB isoenzyme), two-dimensional echocardiography (2D-EC), thallium-201 scintigraphy. Myocardial contusion was diagnosed when an area of decreased or absent thallium-201 uptake was found in the scintigraphy. These latter results were compared with those obtained with the other investigations. Sixteen patients, mean age 34 years, were included; two who died before the end of the investigations were excluded. 2D-EC provided the most useful data (pericardial effusions in a third of the cases). The physical examination, enzyme assays, and chest films were of low value. The investigations carried out six months after the initial trauma showed that long term follow-up was not required. All patients were asymptomatic ten months after their trauma Although the diagnosis of myocardial contusion was made in half the cases using thallium-201 scintigraphy, 2D-EC provided reliable data and had the advantage to be carried out at the patient's bedside.

Various laboratory investigations were assessed with respect to their accuracy in detecting myocardial contusion in patients with blunt chest trauma. All patients, aged between 18 and 50 years, admitted to the intensive care unit for flail chest, sternal fracture, pulmonary contusion, pleural or mediastinal lesion not requiring surgery, were included over a twelve month period. A complete cardiac assessment was carried out, including a physical examination, electrocardiogram, chest X-ray, enzyme assay (ALAT, ASAT, LDH, CPK and MB isoenzyme), two-dimensional echocardiography (2D-EC), thallium-201 scintigraphy. Myocardial contusion was diagnosed when an area of drecreased or absent thallium-201 uptake was found in the scintigraphy. These latter results were compared with those obtained with the other investigations. Sixteen patients, mean age 34 years, were included ; two who died before the end of the investigations were excluded. 2D-EC provided the most useful data (pericardial effusions in a third of the cases). The physical examination, enzyme assays, and chest films were of low value. The investigations carried out six months after the initial trauma showed that long term follow-up was not required. All patients were asymptomatic ten months after their trauma. Although the diagnosis of myocardial contusion was made in half the cases using thallium-201 scintigraphy, 2D-EC provided reliable data and had the advantage to be carried out at the patient's bedside.

Thirty one epidural analgesias were performed in 23 ASA 1 or 2 infants ranged in age from 2 days to 1 year for orthopedic operation; 20 G needles were used for epidural puncture (25 with Potts-Cournand needles, 6 with Tuohy needles). A mixture of 0.5 mg.kg-1 0.5% bupivacaine, 0.5 mg.kg-1 1% etidocaine and 0.05 mg.kg-1 of morphine was administered. The same anesthetic mixture (without morphine) was injected by a catheter during the first 30 hours after the procedure to provide post-operative analgesia. Adequate, complete sensory blockade was obtained in every case (mean level T6). Five accidental dural punctures occurred with Potts-Cournand needles, none were observed with Tuohy needles. Hemodynamic and respiratory parameters did not show significant variations.

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.

Une jeune fille de 15 ans, sans antécédents notables, est admise dans le service de réanimation 90 minutes après l'absorption d'environ 2,5 g de cyanure de potassium. Elle présente un tableau clinique d'intoxication cyanhydrique grave associant un coma profond, une défaillance hémodynamique et une acidose métabolique sévère. Le traitement éliminateur et chélateur par lavage gastrique et perfusion de 4 g d'hydroxocobalamine associée à 8 g d'hyposulfite de sodium est mis en route dans des délais brefs, en liaison avec une thérapeutique symptomatique : ventilation mécanique à Fio2 100 %, alcalinisation et administration de bêtamimétiques. Le traitement permet une amélioration clinique rapide. La malade sort de réanimation au quatrième jour avec pour séquelles une détérioration intellectuelle modérée un mois après l'intoxication. La survie malgré un taux sanguin de cyanure très élevé (494 μmol · l−1 à l'admission) est à mettre sur le compte des thérapeutiques symptomatiques et spécifiques rapidement mises en œuvre.

Les modifications hémodynamiques et adrénergiques provoquées par l'administration de flumazénil après une anesthésie ayant comporté du flunitrazépam ont été étudiées chez 20 patients, lors d'un essai contrôlé, randomisé, en double aveugle contre placebo. Tous ces patients bénéficiaient d'une intervention orthopédique de courte durée (< 90 min) sous anesthésie générale associant du flunitrazépam pour l'induction (30 à 40 μg · kg−1), du N2O, de l'halothane et de l'alfentanil pour l'entretien. Quinze minutes après l'arrêt de l'anesthésie par inhalation, les patients recevaient soit du placebo soit du flumazénil (1 mg) selon le tirage au sort. La pression artérielle, la fréquence cardiaque, le niveau de conscience et les prélèvements sanguins pour le dosage de la noradrénaline plasmatique ont été obtenus avant réversion, puis de façon répétée pendant 30 minutes après la réversion. L'administration de flumazénil a provoqué dans tous les cas un réveil immédiat et complet alors que le réveil a été lent et progressif dans le groupe placebo. Aucune modification hémodynamique n'a été observée dans les deux groupes. En revanche les concentrations de noradrénaline plasmatique ont significativement augmenté dans les deux groupes. En conclusion cette étude montre que le flumazénil n'aggrave pas les modifications circulatoires ou adrénergiques habituellement observées lors de la période de réveil.

Reversal of benzodiazepine-induced sedation by flumazenil has been reported to produce no or minor hemodynamic alterations although some adverse responses have been observed. To better delineate circulatory and adrenergic modifications induced by flumazenil, 20 consenting patients scheduled for short orthopedic procedures were included in a double blind controlled study. Anesthesia consisted in flunitrazepam (30 to 40 micrograms.kg-1) plus halothane (0.5 vol. % in N2O-O2, 60-40 vol. %) and alfentanil. At the end of surgery, patients received 15 minutes after discontinuation of halothane and N2O, either flumazenil (1 mg) or placebo according th randomization. Heart rate and blood pressure were obtained before reversal and repeatedly for 30 minutes following flumazenil or placebo. Level of consciousness was also assessed and blood samples were withdrawn for subsequent determination of plasma levels of norepinephrine. Flumazenil administration induced in all cases an immediate and total reversion of sedation while recovery was slow in the placebo group. No significant changes in heart rate and blood pressure values were found in both groups. By contrast, plasma levels of norepinephrine were significantly increased in all patients. It is concluded that reversal of benzodiazepine-induced sedation or anesthesia is not associated with significant variations of usual hemodynamic or adrenergic responses.

Schoeffler, P.*; Pichard, E.**; Ramboatiana, R.***; Joyon, D.*; Haberer, J. P.* Author Information