[Circulatory arrest. Diagnostic orientation and emergency treatment].
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Biomedical subjects
Publications and source records attributed to F Bonnet.
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The effects of apnea testing-induced respiratory acidosis on left ventricular function (LVF) are still controversial. The aim of the study was to assess LVF during apnea testing using transesophageal echocardiography (TEE). Twenty consecutive patients suspected of brain death, hemodynamically stable, and considered as potential organ donors were prospectively studied. A 20-min apnea test was performed after obtaining a PaCO2 > 35 mmHg and 20 min of FIO2 1 ventilation. LVF was assessed using TEE with a CFM 750 (Diasonic) connected to a 5 MHz probe. Heart rate (HR), mean arterial pressure (MAP), left ventricle end-diastolic and systolic area (LVEDA, LVESA), and LVF assessed by fractional area changes (FAC), systolic wall motion (SWM) scores, and blood gases were recorded at baseline, and after 5, 10, 15, and 20 min of apnea testing. In 19 patients, no spontaneous respiratory movement occurred during the standard 20-min period. In one patient (No. 15), the apnea test had to be stopped after 10 min because of hypoxia. HR, LVEDA, LVESA, and SWM were not significantly modified during the study. There was a progressive statistically significant decrease in MAP during apnea (from 77 +/- 10 to 63 +/- 11 mmHg), associated with a statistically significant increase in FAC at 20 min (from 48 +/- 13 to 56 +/- 8%). PaCO2 progressively rose (from 40 +/- 3 to 95 +/- 11 mmHg), associated with a decrease in pH (from 7.42 +/- 0.06 to 7.09 +/- 0.08). At the same time, PaO2 decreased slightly in all patients, but values remained well above hypoxic levels, except for one patient. Despite severe respiratory acidosis the increase in FAC suggests that apnea testing is well tolerated for brain death assessment.
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Proteoglycans in male reproductive tract have been mainly characterized in testicular extracellular matrix and somatic cells. Heparan sulfate, chondroitin sulfate and hybrid chondroitin/heparan sulfate proteoglycans coexist within the testes. Their biological roles are not currently established, however, the molecular characterization of some of them is indicative that they might be involved in various regulatory processes during spermatogenesis.
The amino acid sequence of neuropolypeptide h3 from Homo sapiens brain has been determined. It revealed that h3 is the exact counterpart of the 21-kDa protein from Bos taurus brain and the 23-kDa protein from Rattus norvegicus brain: The three proteins belong to the same 21-23-kDa protein family. Multiple tissue Northern blots showed that the mRNA encoding the 21-23-kDa protein is expressed in different amounts according to tissues and species; it is particularly abundant in Rattus norvegicus testis.
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The diagnosis of aortic injury after blunt chest trauma is of utmost importance to emergency physicians. We present a case in which transesophageal echocardiography was successful in diagnosing a transectional intimal tear on the posterior wall of the ascending aorta. Potential usefulness of transesophageal echocardiography is discussed.
In order to assess the quality of sleep in surgical patients the amount of self-rated postoperative insomnia and its predisposing factors, we conducted a three-fold questionnaire * survey in 176 consecutive patients undergoing elective orthopaedic, vascular or abdominal surgery. The first questionnaire was completed the day preceding surgery, the second at the day of discharge and the third two weeks later. This survey concerned the patient's general status, his usual sleep profile and factors which could interfere with sleep (hypnotics, pain, environmental factors) throughout the study period. It allowed quantification of these parameters and the assessment of their time-course. Perioperative insomnia appeared to be a long-lasting phenomenon which persisted after discharge. Factor analysis and multiple regression models showed that postoperative, self-rated insomnia was multifactorial and mainly explained by the amount of postoperative pain (p = 0.035).
Alpha 2 adrenergic agonists stimulate specific receptors in the dorsal horn of the spinal cord leading to blockade of potassium and calcium channels. Presynaptic alpha 2 receptors inhibit the release of substance P and other neuropeptides which stimulate transmission of nociceptive stimulations. Post-synaptic alpha 2 receptors hyperpolarize neurons membranes and decrease the activity of nociceptive neurons. In addition, alpha 2 adrenergic agonists have a synergistic action with opioid and cholinergic agonists.
Pain is a major factor of respiratory decompensation after chest trauma. General and/or regional analgesia improve alveolar ventilation, make physiotherapy easier and often avoid mechanical ventilation. Concerning regional techniques, epidural, intercostal and interpleural routes have their respective indications and contraindications, benefits and risks. When suitable, epidural analgesia appears to be the preferable technique.
Mechanisms of the analgesic actions of alpha 2-adrenergic agonists are likely related to various modulating systems of nociceptive neurotransmission, especially those dependent on opiate receptors. Analgesic action of alpha 2-adrenergic agonists implies alpha 2-adrenergic receptors, strategically located on the dorsal horn neurones of the spinal cord to inhibit the release of substance P in response to peripheral stimuli. However, these receptors are included in the control that supraspinal sites exert via the descending medullospinal noradrenergic pathway. Because of its high lipophilic structure, alpha 2-adrenergic agonist can easily penetrate into the central nervous system, reproducing the effects of activation of medullospinal noradrenergic pathway. Alpha 2-adrenergic agonists have been found to be efficient in human pain treatment after systemic, spinal or troncular administration, but there were few randomized clinical studies comparing analgesia potency and adverse effects of either systemic or regional administrations. Clonidine added to local anaesthetic agents increases the analgesic effects in a greater extent than systemic administration of similar dose, probably because this effect depends on the local clonidine concentration. Extradural administration of clonidine is also more efficient than systemic administration, at least when high doses are injected. This superiority is questionable when low-dose clonidine is used. Adverse effects are quite similar in both systemic and spinal routes. Invasiveness of extradural route may be considered in regard to the gain which may be expected in analgesia efficiency.
The temporal fasciocutaneous scalp flap (TFSF) is used as mucosal reconstruction in 22 oropharyngeal and oral carcinomas. The anatomical basis of the flap and the clinical observations are described. The qualities of such a flap clearly appear: high liability and plasticity, perfectly adapted with oropharyngeal and oral mucosal loss. However attention must be payed to reconstruction of the anterior floor of the mouth which seems to be the limit of the rotation arc. Within these limits the TFSH has an inconspicuous donor site scar and low morbidity quite resumed by the hair regrowth on the intral-oral skin paddle.
The use of opioids for postoperative pain relief is associated with the occurrence of side effects whatever the technique of administration. One may consider different solutions to reduce these side effects, while maintaining an adequate analgesia level. Combination of different pharmacological types of analgesic agents is defined as "balanced analgesia". In this setting, non steroidal antiinflammatory drugs have been demonstrated to reduce opioids requirements during patient-controlled analgesia and to improve the quality of epidural analgesia. Alpha 2 adrenergic agonists, acting at the level of the dorsal horn of the spinal cord, also strengthen and prolong analgesia induced by epidural or spinal opioids. Finally, local anaesthetic solutions in low concentration may potentiate the analgesic effect of opioids, also improving the quality of analgesia. These different combinations have to be considered in view of the surgical procedure performed, the patient condition and the possibilities of monitoring in any given care unit.
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Two cases are reported of patients with phantom limb pain after lower limb amputation and requiring surgery of their stump. The stumps were revised and the remaining femoral shaft shortened. Both had spinal anaesthesia for this procedure, with an association of bupivacaine and 150 micrograms of clonidine. In one patient, the phantom pain did not resume for one month, and in the other for three days. The return of pain was preceded by the sensation of a phantom limb. These cases suggest that alpha 2 adrenergic agonists could play a major part in the treatment of phantom limb pain.
The benefits of transoesophageal echocardiography (TOE) were assessed prospectively in intensive care patients. The doctors carrying out TOE were not the same as those who ordered it. TOE was performed in 32 patients, all of whom but one were intubated and artificially ventilated, to elucidate the cause of circulatory shock, or to search for valvular vegetations or an intracardiac mass. TOE confirmed the diagnosis previously obtained with pulmonary arterial catheterization (10 patients), transthoracic echocardiography (3 patients) or ventriculography (1 patient) in 54% of cases. In 28% of cases, TOE invalidated the suspected diagnosis, and, in the remaining 28% of patients, TOE invalidated provided a previously unsuspected diagnosis. TOE was particularly useful in confirming the presence of valvular vegetations, endocarditis, or intracardiac thrombi, and to assess left ventricular function and preload in patients in shock. Like others, this study confirms the benefits of TOE in the intensive care setting.
Conflicting reports of MDR1 gene expression in human tumours are observed according to whether studies are performed at the mRNA or P-glycoprotein level. We have investigated this expression in 22 clinically drug-resistant sarcomas at the mRNA level by Northern blot (NB), Dot blot (DB), in situ hybridisation (ISH), and at the protein level by immunohistochemistry (IHC) using three monoclonal antibodies (MoAbs): C219, JSB1, MRK16. Increased MDR1 mRNA expression was detected by NB, DB, and ISH in 1/22 sarcoma (an Ewing's sarcoma). ISH was perfectly correlated with DB hybridisation and confirmed the expression of tumoral cells alone. Specific staining of 100% of tumoral cells was obtained with the three MoAbs in the same sarcoma. Expression in tumoral cells of 12 other sarcomas was detected with MRK16, and positive staining of stromal cells with both C219 (1/22) and MRK16 (8/22) was observed. This study confirms that MDR1 overexpression occurs in human sarcomas but is not the principal mechanism of drug-resistance. Furthermore, positivity with one antibody does not necessarily imply the presence of P glycoprotein (P-gp) and a disparity may exist between the levels of P-gp and its mRNA in the same sample. So care must be taken in interpreting results and more sensitive techniques such as the polymerase chain reaction (PCR) could prove useful.
Extradural clonidine produces analgesia, with sedation, hypotension and bradycardia, in postoperative patients. This study assessed if oral yohimbine would reverse these side effects. We studied 30 ASA I-II patients undergoing orthopaedic surgery. After operation they were allocated randomly to three groups to receive placebo, extradural clonidine 450 micrograms or extradural clonidine 450 micrograms plus oral yohimbine 16 mg. Pain score was measured on a visual analogue scale (VAS); sedation was assessed on a simple scale graded from 0 (awake and alert) to 3 (deeply sedated, awakening after tactile stimulations) and heart rate and arterial pressure were monitored for 5 h. Yohimbine reversed the sedation induced by extradural clonidine, but also shortened the duration of analgesia (31 (SD 15) min, 186 (72) min and 126 (52) min in the placebo, extradural clonidine and extradural clonidine+yohimbine groups, respectively) (P < 0.05), and did not reduce the hypotension and bradycardia related to clonidine administration. These results suggest that alpha 2 adrenoceptors are mediators of the sedation induced by clonidine and that the haemodynamic effects are not related to stimulation of supraspinal alpha 2 receptors.