G. François

Development and validation of a perioperative satisfaction questionnaire.

Background:Satisfaction is considered a valuable measure of outcome of healthcare processes. Only a few anesthesia-related validated questionnaires are reported. Because their scope is restricted to specific clinical contexts, their use remains limited. The objective of the current study was to develop and validate a self-reported questionnaire, Evaluation du Vécu de l’Anesthésie Générale (EVAN-G), assessing the satisfaction of the perioperative period surrounding general anesthesia. Methods:Development of the EVAN-G questionnaire comprised a phase of item generation and a phase of psychometric validation. The patient sample was generated to be proportionally matched to the population of patients undergoing general anesthesia in France. The structure of the questionnaire was identified studying interitem, item–dimension, and interdimension correlations and factor analyses. Data were concurrently gathered to assess external validity. The discriminant validity was determined by comparison of scores across well known patient groups. Reliability was assessed by computation of Cronbach α coefficients and by test–retest. Results:Eight hundred seventy-four patients were recruited in eight anesthesia departments. The EVAN-G includes 26 items; six specific scores and one global index score are available. Correlations between EVAN-G scores and other concurrent measures supported convergent validity. The EVAN-G correlated poorly with age, American Society of Anesthesiologists physical status, total anesthesia time, and number of previous anesthesias. Significantly higher satisfaction was reported by patients older than 65 yr, belonging to the laryngeal mask group. Reliability and reproducibility were shown. Conclusion:The EVAN-G adds important information oriented toward patients’ perceptions. The authors’ approach provides a novel, valid, and reliable tool that may be used in anesthesia practice.

Influence of body temperature, with or without sedation, on energy expenditure in severe head-injured patients.

OBJECTIVE To quantify the effect of body temperature and sepsis on energy expenditure in head-injured patients. DESIGN Prospective, nonrandomized, observational study. SETTING Neurosurgical intensive care unit. PATIENTS Severe head-injured patients. INTERVENTIONS Use of an indirect calorimeter to measure energy expenditure. MEASUREMENTS AND MAIN RESULTS Mean arterial pressure (MAP), heart rate (HR), body temperature, and mean hourly energy expenditure were recorded. Twenty-four patients had 1,919 hourly measures of the above parameters. The measurement periods were divided into four groups, according to the anesthetic agents used for sedation: fentanyl and midazolam (group FM); fentanyl, midazolam, and curarization (group C); thiopental (group T); and no sedation (group NS). The energy expenditure/basal energy expenditure ratio (EE/BEE) was significantly lower in group T (1.20 +/- 0.15) than in group FM (1.32 +/- 0.24) or group C (1.32 +/- 0.20) and was significantly higher in group NS (1.60 +/- 0.33). There was a significant correlation between body temperature and EE/BEE (p < .0001, r2 = .27) only in sedated patients. Using the equation of the regression line to correct energy expenditure for differences in body temperatures between groups, the difference in energy expenditure between groups with sedation disappeared. This finding suggested that the low energy expenditure under thiopental was due only to hypothermia. Sepsis significantly increased energy expenditure independently of fever. There was a weak but statistically significant correlation between energy expenditure and HR (p<.01, r2 = .13) but not between energy expenditure and MAP. CONCLUSIONS Sedation had a major effect on energy expenditure. In sedated patients, body temperature was the main determinant of energy expenditure; the anesthetic agent used had little influence on the level of energy expenditure. Sepsis increased energy expenditure independently of fever, probably through hormonal changes.

Energy expenditure and withdrawal of sedation in severe head-injured patients

ObjectivesTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity. DesignProspective, descriptive study. SettingNeurosurgical intensive care unit (ICU) in a university hospital. PatientsFifteen severe head-injured patients with tracheostomies and who were mechanically ventilated and sedated at the time of the study. InterventionsNone. Measurements and Main ResultsVo2 and energy expenditure were measured, using indirect calorimetry during and after discontinuation of sedation. After the measurement period, the patients were divided into two groups. Group 1 included patients who were completely weaned from sedation; group 2 included patients who had to be sedated again using predetermined criteria. In both groups, energy expenditure was close to basal energy expenditure during sedation, and increased to 150% of basal energy expenditure during the recovery period, with maximum hourly values 80% above basal energy expenditure. In group 1, Vo2 and energy expenditure changed from 284 ± 44 mL/min and 1833 ± 261 kcal/day during sedation to 390 ± 85 mL/min and 2512 ± 486 kcal/day for the period without sedation. During this period, there was a significant correlation between Vo2 and mean arterial pressure. For the recovery period, there was no difference in mean or maximum Vo2 between the two groups of patients. At 24 and 48 hrs after cessation of sedation, Vo2 and energy expenditure decreased to 30% above basal energy expenditure. These changes may be due to the recovery of muscular activity, weaning from mechanical ventilation, or an increase in the amount of circulating catecholamines. ConclusionIn severe head-injured patients, during the first 12 hrs after the discontinuation of sedation, the patients experienced a large increase in Vo2, energy expenditure, and mean arterial pressure. Although these changes have no prognostic value in our study, they have potential deleterious effects in head-injured patients. Methods that blunt these changes which have proven efficacious in anesthesia may be effective for intensive care patients. (Crit Care Med 1994; 22:1114–1119)

The Effect of Hemodilution on Cerebral Blood Flow Velocity in Anesthetized Patients

Transcranial Doppler is used to estimate changes in cerebral blood flow, but the effect of hemodilution on cerebral blood flow velocity (CBFV) in anesthetized patients has not been evaluated.The aim of this study was to measure the effect of isovolemic hemodilution on CBFV and lumbar cerebrospinal fluid pressure (PCSF) in anesthetized patients without change in other physiological variables that may affect CBFV. Patients under-going hemodilution were compared with a control group undergoing no hemodilution. With hemodilution, hematocrit decreased from 38% +/- 3% to 30% +/- 2%, arterial oxygen content (CaO2) decreased from 17.5 +/- 1.3 to 13.9 +/- 0.9 mL/dL, and CBFV increased from 50 +/- 10 to 58 +/- 10 cm/s. An equivalent of cerebral arterial O2 transport calculated as CaO2 x CBFV did not significantly change. Over the same time interval, there were no changes in the control group. There was no statistically significant change in PCSF, pulsatility index, PaCO (2), blood pressure, heart rate, or body temperature in either group. We conclude that CBFV reflects cerebral blood flow changes after hemodilution. Implications: Hemodilution increases cerebral blood flow but may change the cerebral artery diameter, which could confound perioperative measurement of cerebral blood flow velocity. This study found transcranial Doppler ultrasonography to accurately assess the effects of hemodilution on the cerebral circulation, but the hematocrit should be taken into account to fully understand perioperative cerebral blood flow velocity changes. (Anesth Analg 1998;86:320-4)

Metabolic and hemodynamic changes during recovery and tracheal extubation in neurosurgical patients: immediate versus delayed recovery.

UNLABELLED Delayed recovery has been advocated to limit the postoperative stress linked to awakening from anesthesia, but data on this subject are lacking. In this study, we measured oxygen consumption (V(O2)) and plasma catecholamine concentrations as markers of postoperative stress. We tested the hypothesis that delayed recovery and extubation would attenuate metabolic changes after intracranial surgery. Thirty patients were included in a prospective, open study and were randomized into two groups. In Group I, the patients were tracheally extubated as soon as possible after surgery. In Group II, the patients were sedated with propofol for 2 h after surgery. V(O2), catecholamine concentration, mean arterial pressure (MAP), and heart rate (HR) were measured during anesthesia, at extubation, and 30 min after extubation. V(O2) and noradrenaline on extubation and mean V(O2) during recovery were significantly higher in Group II than in Group I (V(O2) for Group I: preextubation 215 +/- 46 mL/min, recovery 198 +/- 38 mL/min; for Group II: preextubation 320 +/- 75 mL/min, recovery 268 +/- 49 mL/min; noradrenaline on extubation for Group I: 207 +/- 76 pg/mL, for Group II: 374 +/- 236 pg/ mL). Extubation induced a significant increase in MAP. MAP, HR, and adrenaline values were not statistically different between groups. In conclusion, delayed recovery after neurosurgery cannot be recommended as a mechanism of limiting the metabolic and hemodynamic consequences from emergence from general anesthesia. IMPLICATIONS In this study, we tested the hypothesis that delayed recovery after neurosurgery would attenuate the consequences of recovery from general anesthesia. As markers of stress, oxygen consumption and noradrenaline blood levels were higher after delayed versus early recovery. Thus, delayed recovery cannot be recommended as a mechanism of limiting the metabolic and hemodynamic consequences from emergence after neurosurgery.

Intraoperative autologous blood transfusion in intracranial surgery.

OBJECTIVE The purpose of this study was to evaluate the benefits of intraoperative autotransfusion of autologous blood on the conservation of allogenic blood, including cost-effectiveness and the consequences for hemoglobin level and coagulation tests. METHODS The Hoemonetics Cell Saver 4 autotransfusion system (Hoemonetics Corporation, MA) was used when the estimated blood loss was equal to or more than 500 ml. A total of 472 patients undergoing intracranial surgery were included in the study. RESULTS Ninety patients (19%) received transfusions either with autologous blood or allogenic blood. Fifty-five patients (61%) received only autologous blood transfusions, 10 patients (11%) received both autologous and allogenic blood transfusions, and 25 patients (28%) received only allogenic blood transfusions. The amount of autologous blood transfused was 600 +/- 590 ml (range, 230-3000 ml). The amount of allogenic blood transfused was 3 +/- 3 units (range, 2-15 units). Autologous blood represented 68% of all blood products transfused. Mild abnormalities during coagulation tests occurred without clinical bleeding. CONCLUSION Autologous blood transfusions were demonstrated to be safe in patients undergoing intracranial surgery and to be more cost-effective than allogenic blood transfusions. Intraoperative autologous blood transfusions may be used alone in more than half of the patients requiring transfusions during intracranial surgery and decrease the amount of allogenic blood used. Improvements in the monitoring for the need of performing this technique, as well as preoperative blood donations, would decrease the amount of allogenic blood transfused.

Anesthésie pour chirurgie vasculaire cérébrale anévrismale

: The two major neurological complications of subarachnoid haemorrhage (SAH) due to an intracranial aneurysm are rebleeding and delayed cerebral ischaemia related to cerebral vasospasm. The best way to prevent rebleeding is early surgery. Even when surgery is performed within the first 72 hours posthaemorrhage, the risk of cerebral ischaemia due to vasospasm is high. Conventional medical treatment of cerebral vasospasm includes haemodilution, hypervolaemia and increase of arterial blood pressure. Haemodilution is of limited value as the patients suffering from SAH have usually a low haematocrit. The effectiveness of hypervolaemia is controversial and it may worsen cerebral and pulmonary oedema. Systemic hypertension is an effective therapy of vasospasm, but which can only be used once the aneurysm is controlled. Nimodipine and nicardipine, two calcium antagonists, have a beneficial effect on neurologic outcome following SAH. Today, it is still debated whether the beneficial effect of nimodipine results from the vascular effect of the drug or from a direct cerebral cytoprotective mechanism. Early surgery implies that surgeons operate on brains in acute inflammatory state. Thus, it is mandatory to use peroperative techniques improving cerebral exposure. These techniques include infusion of mannitol, lumbar cerebrospinal fluid (CSF) drainage, administration of anaesthetic agents known to decrease cerebral blood flow (CBF) and hypocapnia. Usually, the effect of CSF drainage is very effective and sufficient by itself. The second objective in the peroperative period is to avoid ischaemia. In areas with decreased flow distal to vasospasm, autoregulation is impaired and CBF is directly dependent on cerebral perfusion pressure. Furthermore, the safe practice of transient clipping of vessels supplying the aneurysm has dramatically reduced the indications of controlled hypotension. During temporary clipping, some authors recommend a pharmacological brain protection using barbiturates, etomidate or propofol, but this practice has not been validated by randomized studies. However, it is generally agreed that the arterial pressure should be increased during temporary clipping to improve collateral blood flow and to maintain it after the aneurysm has been secured. To conclude, together with lumbar CSF drainage and transient clipping, the anaesthetic management of the patients should include: maintenance of the arterial blood pressure close to its preoperative level, maintenance of PaCO2 between 30 and 35 mmHg and of normovolaemia through replacement of fluid and blood losses. After completion of surgery, recovery from anaesthesia should be rapid to allow fast diagnosis of neurological complications. The monitoring of the status of consciousness is the key of the diagnosis of early postoperative complications.