[Does research in anesthesia-intensive care improve our practice?].
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Biomedical subjects
Publications and source records attributed to B Riou.
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Every scientific article has to undergo a critical reading before its conclusions can be accepted. This article discusses the tools for assessing the scientific value of a study. A sequence of methodological criteria allows quality evaluation of an article and its classification in a scale of level of proof.
OBJECTIVE: To analyse pre and peroperative variables for predicting mortality after abdominal aortic surgery. STUDY DESIGN: Prospective study. PATIENTS: We prospectively included 658 consecutive patients undergoing abdominal aortic surgery from January 1993 to July 1997. METHODS: Age, gender, hypertension, history of myocardial infarction or coronary revascularization, angina pectoris, diabetes, arrhythmia, cardiac insufficiency, serum creatinine > 150 mumol.L-1, beta-blockers therapy, calcium channel inhibitors, angiotensin converting enzyme inhibitors were preoperative analysed variable. Type of aortic disease (anuerysms versus aortic occlusion), duration of surgery, blood loss, type of laparotomy (medium versus lombotomy) were peroperative analysed variables. Haemoglobinemia was monitored during surgery and patients were transfused if haemoglobinaemia < 80 g.L-1. RESULTS: Thirty-three patients died after aortic surgery (5%). In multivariate analysis, angina pectoris (OR = 5.47, P < 0.001), chronic obstructive bronchopulmonary disease (OR = 2.27, P = 0.05) and duration of surgery (OR = 1.60, P < 0.001) were the independent predictive factors of mortality. Age, blood loss were predictive factors only in univariate analysis. CONCLUSION: Angina pectoris and COBP were the two independent preoperative factors of mortality. The duration of surgery was the only peroperative factor. Well monitored blood loss was not a predictive factor.
BACKGROUND: The additive effect of non-steroidal anti-inflammatory drugs administered with propacetamol after major orthopaedic surgery has not been studied. Thus, we performed a prospective, placebo-controlled study to assess the analgesic effects of ketoprofen in patients undergoing spinal fusion surgery and receiving propacetamol. METHODS: Fifty patients undergoing spinal fusion surgery received either 100 mg of ketoprofen every 8 h or a placebo, postoperatively. All patients received propacetamol and morphine (intravenous titration followed by patient-controlled analgesia (PCA) over 24 h). Pain was assessed using a visual analogue pain scale (VASpi). Data are mean+/-SD. RESULTS: During morphine titration, ketoprofen did not significantly reduce the dose of morphine (8+/-6 vs 11+/-4 mg, NS) whereas it significantly decreased VASpi (P<0.001). During PCA, ketoprofen significantly reduced morphine consumption (25+/-17 vs 38+/-20 mg, P=0.04) and VASpi (P=0.002). The total postoperative morphine consumption was significantly (33%) reduced with ketoprofen. CONCLUSION: Ketoprofen reduced morphine requirements and improved postoperative analgesia in patients undergoing major spinal surgery and receiving propacetamol.
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BACKGROUND: Maintenance of airway patency and oxygenation are the main objectives of face-mask ventilation. Because the incidence of difficult mask ventilation (DMV) and the factors associated with it are not well known, we undertook this prospective study. METHODS: Difficult mask ventilation was defined as the inability of an unassisted anesthesiologist to maintain the measured oxygen saturation as measured by pulse oximetry > 92% or to prevent or reverse signs of inadequate ventilation during positive-pressure mask ventilation under general anesthesia. A univariate analysis was performed to identify potential factors predicting DMV, followed by a multivariate analysis, and odds ratio and 95% confidence interval were calculated. RESULTS: A total of 1,502 patients were prospectively included. DMV was reported in 75 patients (5%; 95% confidence interval, 3.9-6.1%), with one case of impossible ventilation. DMV was anticipated by the anesthesiologist in only 13 patients (17% of the DMV cases). Body mass index, age, macroglossia, beard, lack of teeth, history of snoring, increased Mallampati grade, and lower thyromental distance were identified in the univariate analysis as potential DMV risk factors. Using a multivariate analysis, five criteria were recognized as independent factors for a DMV (age older than 55 yr, body mass index > 26 kg/m2, beard, lack of teeth, history of snoring), the presence of two indicating high likelihood of DMV (sensitivity, 0.72; specificity, 0.73). CONCLUSION: In a general adult population, DMV was reported in 5% of the patients. A simple DMV risk score was established. Being able to more accurately predict DMV may improve the safety of airway management.
BACKGROUND: Traumatic aortic injury is a frequent cause of death after blunt trauma, but few patients survive to reach a trauma center. The role of transesophageal echocardiography (TEE) in the diagnosis of traumatic aortic injury remains debated. METHODS: Over a 9-yr period, 209 blunt trauma patients (mean age, 34 +/- 13 yr) were suspected of having traumatic aortic injury because of enlarged mediastinum and/or sudden deceleration, and underwent TEE and angiography (aortography and/or contrast-enhanced computed tomography. RESULTS: Traumatic aortic injury was diagnosed in 42 patients (20%). Angiography (aortography and/or contrast-enhanced computed tomography) was less accurate (sensitivity, 83%; specificity, 100%) than TEE (sensitivity, 98%; specificity, 100%) for the diagnosis of aortic injury because it failed to diagnose most minor injuries (intramural hematoma or limited intimal flap, n = 7). However, when considering only patients with major aortic injury (n = 33; i.e., those who might need surgery), angiography (sensitivity, 97%; specificity, 100%) and TEE (sensitivity, 97%; specificity, 100%) were equivalent. CONCLUSION: Transesophageal echocardiography is an accurate method for diagnosis of traumatic aortic injury. Nevertheless, the clinical implications of limited aortic injuries diagnosed by the technique have yet to be determined.
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Bronchial fibrescopy in intensive therapy patients raises the problem of oxygenation during the procedure. The Fibroxy mask allows fibrescopy with simultaneous O2 administration and manual or mechanical ventilation. This study, which included ten patients, assessed the benefits of this device. During fibrescopy, the heart rate, the mean arterial blood pressure, and the arterial oxygen saturation (SpO2) remained unchanged and only one short episode of desaturation occurred. The satisfaction index was high. However, this mask did not fit closely to the patient's face, and an additional assistant was required for efficient ventilation. Moreover, end-tidal CO2 could not be monitored satisfactorily. After some improvements, this device seems to be of value for bronchial fibrescopy in intensive therapy unit.
The aim of the study was to determine diaphragm performance and cross-bridge properties in rats bearing a growth hormone (GH)-secreting tumour. The tumour was induced by subcutaneous injection of GH-hypersecreting cells (GC cells) into the flank. Eighteen weeks after GC cell injection, rats developed a GH-secreting tumour (45.4+/-5.1 g) and the GH plasma level reached 5,408+/-648 microg x L(-1) in GH rats versus 7.2+/-2.2 microg x L(-1) in control rats (p<0.001). Diaphragm mechanics and cross-bridge properties were studied by applying the equations of A. Huxley in isolated diaphragm strips (control rats: n=12; GH rats n=20). In comparison to control rats, the total tension and total number of cross-bridges x mm(-2) in GH rats were lower in both twitch and tetanus (p<0.001). A linear relationship was observed between total tension and total cross-bridge number (r=0.94; p<0.001). Conversely, the cross-bridge single force and peak mechanical efficiency did not differ between control and GH rats, in either twitch or tetanus modes. In conclusion, the diaphragm strength was significantly lower in rats bearing growth hormone secreting tumours, and this was essentially determined by the lower cross-bridge number x mm(-2) without change in cross-bridge single force.
We have compared the value of different variables used in the assessment of blood loss during progressive hypovolaemia and resuscitation under general anaesthesia in anaesthetized pigs. We measured mean arterial pressure (MAP), pulmonary capillary wedge pressure (PCWP), the negative component of the systolic arterial pressure variation (delta Down) and left ventricular end-diastolic area (LVEDa) using echocardiography. Blood was progressively withdrawn (up to 35 ml kg-1 in seven steps) and then reinfused after the same pattern. Regression coefficient (r) and normalized slope (nS) of the regression relationship between each variable and amount of blood loss were determined. The difference between the withdrawal and reinfusion curves was assessed by the area between the curves. We also estimated the minimal loss of blood volume which induced significant changes in each variable compared with that under control conditions during withdrawal of blood (minWBV) and maximal loss in blood volume which induced no significant changes in a variable compared with control conditions during retransfusion (maxRBV). During haemorrhage, MAP decreased (from mean 74 (SD 9) to 31 (5) mm Hg; P < 0.001), delta Down increased (from 1.2 (1.4) to 11.4 (4.2) mm Hg; P < 0.001), PCWP decreased (from 6.2 (2.1) to 0.3 (1.0) mm Hg; P < 0.001) and LVEDa decreased (from 13.8 (2.0) to 5.1 (2.0) cm2; P < 0.01). The highest r values were obtained with MAP and LVEDa, and the highest nS value with delta Down. The least difference between withdrawal and reinfusion was with LVEDa, the lowest values of minWBV were with PCWP and LVEDa, and the highest value of maxRBV was obtained with PCWP. During progressive haemorrhage under general anaesthesia, LVEDa was an accurate variable for assessment of blood volume loss, delta Down contributed no further information compared with MAP, and PCWP was the most reliable variable for assessing return to baseline blood volume.
Recording of cortical somatosensory evoked potentials (CSEP) enables monitoring of spinal cord function. We studied the effects of propofol, propofol-nitrous oxide or midazolam during sufentanil anaesthesia on CSEP monitoring during major spinal surgery. Thirty patients with normal preoperative CSEP were allocated randomly to one of the following anaesthesia regimens: propofol (2.5 mg kg-1 followed by 10-6 mg kg-1 h-1) with or without nitrous oxide, or midazolam (0.3 mg kg-1 followed by 0.15 mg kg-1 h-1) combined with sufentanil 0.5 microgram kg-1 h-1 in the propofol and midazolam groups, or 0.25 microgram kg-1 h-1 in the propofol-nitrous oxide group. CSEP were elicited by alternate right and left tibial posterior nerve stimulation and recorded before and after induction (15 min, 1, 2 and 3 h), and during skin closure. CSEP latencies were not significantly modified in the three groups. CSEP amplitude decreased significantly in the propofol-nitrous oxide group (from mean 2.0 (SEM 0.3) to 0.6 (0.1) microV; P < 0.05) but not in the propofol (from 1.8 (0.6) to 2.2 (0.3) microV) or midazolam (1.7 (0.5) to 1.6 (0.5) microV) groups. The time to the first postoperative voluntary motor response (recovery) delay was significantly greater in the midazolam group (115 (19) min) compared with the propofol and propofol-nitrous oxide groups (43 (8) and 41 (3) min, respectively). Consequently, the use of propofol without nitrous oxide can be recommended during spinal surgery when CSEP monitoring is required.
UNLABELLED: Minimum alveolar anesthetic concentrations (MAC) values of volatile anesthetics in cardiovascular diseases remain unknown. We determined MAC values of volatile anesthetics in spontaneously breathing normal and cardiomyopathic hamsters exposed to increasing (0.1%-0.3% steps) concentrations of halothane, isoflurane, sevoflurane, or desflurane (n = 30 in each group) using the tail-clamp technique. MAC values and their 95% confidence interval were calculated using logistic regression. In normal hamsters, inspired MAC values were: halothane 1.15% (1.10%-1.20%), isoflurane 1.62% (1.54%-1.69%), sevoflurane 2.31% (2.22%-2.40%), and desflurane 7.48% (7.30%-7.67%). In cardiomyopathic hamsters, they were: halothane 0.89% (0.83%-0.95%), isoflurane 1.39% (1.30%-1.47%), sevoflurane 2.00% (1.85%-2.15%), and desflurane 6.97% (6.77%-7.17%). Thus, MAC values of halothane, isoflurane, sevoflurane, and desflurane were reduced by 23% (P < 0.05), 14% (P < 0.05), 13% (P < 0.05), and 7% (P < 0.05), respectively in cardiomyopathic hamsters. IMPLICATIONS: Minimum alveolar anesthetic concentrations of volatile anesthetics were significantly lower in cardiomyopathic hamsters than in normal hamsters.
UNLABELLED: Dantrolene is used in patients with muscle spasticity and is the only known effective treatment for malignant hyperthermia. However, its effects on muscle relaxation and energetics are unknown and may have important consequences in diaphragmatic function. We studied the effects of dantrolene (10(-8) to 10(-4) M) on diaphragm muscle strips (n = 12) in the hamster in vitro (Krebs-Henseleit solution, 29 degrees C, 95% oxygen/5% carbon dioxide) in response to tetanic stimulation (50 Hz). We studied contraction and relaxation under isotonic and isometric conditions, as well as energetics. Data are mean +/- SD. Dantrolene induced a negative inotropic effect in the hamster diaphragm (active force at 10(-4) M: 34% +/- 7% of baseline; P < 0.05) but did not significantly modify the curvature of the force-velocity relationship. Dantrolene did not significantly modify isotonic relaxation. Dantrolene, up to 10(-5) M, did not significantly impair isometric relaxation. In conclusion, dantrolene induced a marked negative inotropic effect on diaphragm muscle without affecting myothermal efficiency and relaxation. IMPLICATIONS: Dantrolene induced a significant and concentration-dependent negative inotropic effect on diaphragm muscle but did not modify isotonic relaxation, which suggests no alteration of the calcium reuptake by the sarcoplasmic reticulum; up to 10(-5) M dantrolene did not alter isometric relaxation, i.e., myofilament calcium sensitivity. Dantrolene did not modify the energetics of diaphragm muscle.
UNLABELLED: Pericardial fluid can reflect the composition of cardiac interstitium in myocardial ischemia. This study investigated the hypothesis that pericardial cardiac troponin I (CTnI) measurements could be a more accurate marker of perioperative myocardial infarction (MI) than serum CTnI after coronary artery bypass grafting (CABG). Postoperative arterial and pericardial blood samples were taken in 102 subjects undergoing elective CABG allocated to one of three groups according to the 12-lead electrocardiogram (ECG) abnormalities observed during the first postoperative 24 h: Group 1 = normal ECG; Group 2 = nonspecific ECG abnormalities; and Group 3 = perioperative Q-wave MI. Peak pericardial CTnI concentrations were much higher than peak serum concentrations in all subjects and significantly greater in Group 3 than in Groups 1 and 2 (1,318 +/- 1,810 ng/mL vs 367 +/- 339 ng/mL and 558 +/- 608 ng/mL, respectively; P < 0.01). However, no significant difference between groups occurred at any time for pericardial/serum CTnI ratios, indicating that time courses of CTnI were not different in pericardial fluid and serum. A significant correlation was found between serum and pericardial CTnI concentrations (R = 0.70, P < 0.001). Pericardial CTnI was not more accurate than serum CTnI in predicting Q-wave MI as shown by the low value of the area under the receiver-operator characteristic curve (= 0.71). Peak and early pericardial CTnI were also not accurate in predicting an increase of serum CTnI greater than a cutoff value of 19 ng/mL. Thus, pericardial CTnI measurements were less useful than serum CTnI measurements in the diagnosis of perioperative MI after CABG. IMPLICATIONS: Although cardiac troponin I concentrations were much higher in pericardial fluid than in serum and significantly increased in subjects who experienced perioperative Q-wave myocardial infarction, pericardial cardiac troponin I measurements were of less value than serum cardiac troponin I measurements for the diagnosis of perioperative myocardial infarction after coronary artery bypass grafting and cannot be recommended in routine clinical practice.
BACKGROUND: A decrease in hematocrit lengthens bleeding time. The authors studied the role of hematocrit variations in an experimental model of arterial thrombosis and bleeding. METHODS: The Folts model was used in 24 rabbits. After anesthesia was induced and common monitors were positioned, the right common carotid artery was exposed and a 60% stenosis was induced. A compression injury of the artery was then produced, which triggered a series of cyclic episodes of thrombosis and clot lysis (cyclic flow reductions [CFRs]). After counting the number of CFRs that occurred in 20 min (CFR1), the animals were assigned randomly to one of three groups (n = 8 in each group): control, hemodilution with rabbit homologous platelet-rich plasma, and hemodilution with gelatin solution and then reinfusion of the shed blood. The effect of hemodilution with replacement by platelet-rich plasma or by colloid was observed by recording the number of CFRs during another 20-min period (CFR2). A third period of observation (CFR3) followed shed blood reinfusion in the gelatin solution group. Ear immersion bleeding time was recorded after each CFR period. RESULTS: In the two experimental groups, the decrease in hematocrit (from 36 +/- 3% to 23 +/- 2% and from 38 +/- 3% to 23 +/- 2%, respectively; mean +/- SD) abolished CFRs (from a median of 4 to 0 and 7 to 0, respectively) and significantly lengthened bleeding time (from 76 +/- 24 s to 114 +/- 36 s and from 84 +/- 37 s to 127 +/- 29 s, respectively). Blood reinfusion in the group that received the gelatin solution caused CFR to reappear (CFR3 = 4). CONCLUSIONS: Decreases in hematocrit reduced the cyclic arterial thrombosis rate and increased the bleeding time in the rabbits in this study. Hematocrit normalization caused thrombosis to reappear.
BACKGROUND: Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations, but their interactions with dobutamine remain unknown. METHODS: The effects of halothane, isoflurane, sevoflurane, and desflurane (1 and 2 minimum alveolar concentration) on the inotropic responses induced by dobutamine (10(-8)-10(-4) M) were studied in rat left ventricular papillary muscles in vitro. Inotropic effects were studied under low (isotony) and high (isometry) loads. The authors also studied the lusitropic effects in isotonic (R1) and isometric (R2) conditions. Data are the mean percentage of baseline +/- SD. RESULTS: Dobutamine induced a positive inotropic effect (active isometric force: 185+/-36%, P < 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P < 0.001), but not under high load (R2: 95+/-21%, not significant). Halothane, isoflurane, and sevoflurane did not modify the positive inotropic effect of dobutamine. Even in the presence of alpha-adrenoceptor blockade, isoflurane did not potentiate the positive inotropic effect of dobutamine. Desflurane significantly enhanced the positive inotropic effect of dobutamine (active isometric force: 239+/-35%, P < 0.001), but this potentiation was abolished by pretreatment with reserpine. In contrast to halothane, isoflurane, sevoflurane, and desflurane did not significantly modify the lusitropic effects of dobutamine. CONCLUSIONS: Halogenated anesthetics, except desflurane, did not modify the positive inotropic effects of dobutamine. Desflurane enhanced the positive inotropic effect of dobutamine, but this effect was related to the desflurane-induced release in intramyocardial catecholamine stores.
The load dependence (LD) of relaxation was studied in the diaphragm of rabbits with congestive heart failure (CHF). CHF (n = 15) was induced by combined chronic volume and pressure overload. Aortic insufficiency was induced by forcing a catheter through the aortic sigmoid valves, followed 3 wk later by abdominal aortic stenosis. Six weeks after the first intervention, animals developed CHF. Sham-operated animals served as controls (C; n = 12). Diaphragm mechanics were studied in vitro on isolated strips, at 22 degrees C, in isotonic and isometric loading conditions. Contractility was lower in the CHF group, as reflected by lower total tension: 1.11 +/- 0.10 in CHF vs. 2.38 +/- 0.15 N/cm(2) in C in twitch (P < 0.001) and 2.46 +/- 0.22 in CHF vs. 4.90 +/- 0.25 N. cm(-2) in C in tetanus (P < 0.001). The index LD was used to quantify the load dependence of relaxation: LD is <1 in load-dependent muscles and tends toward 1 in load-independent muscles. LD was significantly higher in CHF than in C rabbits, in both twitch (0.99 +/- 0.01 vs. 0.75 +/- 0.03; P < 0. 001) and tetanus (0.95 +/- 0.02 vs. 0.84 +/- 0.02; P < 0.001). In the CHF rabbits' diaphragm, the fall in total tension was linearly related to the fall in load dependence of relaxation. The decrease in load dependence of relaxation in CHF animals suggests sarcoplasmic reticulum abnormalities. Impairment of the sarcoplasmic reticulum may also partly account for the decrease in contractile performance of diaphragm in CHF animals.