Arrêt de la sédation en neuroréanimation [Sedation interruption in neurointensive care].

The reasons for sedation in neurointensive care can be divided into two main groups: (i) general indications, as for other intensive care patients, such as to allow the necessary treatments (therapeutic facilitation), controlling the states of agitations em leader; (ii) specific indications due to the neuro-physiologic effect of the sedatives: facilitation of the control of the intracranial pressure and lowering of the cortical excitability during the epileptic fits and thereby helping the recovery of the cerebral tissue and diminishing the secondary brain insults. It is important to remember that sedation is usually combined with the administration of opioids, which can potentiate the effect of the sedative drugs. The interruption of the sedation can be long- or short-termed. The definitive interruption is possible once the clinical and cerebral state of the patient does not justify any sedation, whereas the brief interruption allows a neurological reassessment. The amount of literature on sedation in intensive care is opposed to the few studies on neurointensive care: in January 2003, the American Society of Intensive Care has published recommendations for this topic without mentioning the interruption of sedation in neurointensive care patients. The aim of this article is to review the literature about the effects of the interruption of the sedation in neurointensive care patients

Hypocaloric feeding: pros and cons.

PURPOSE OF REVIEW: Since the 1980s, hypocaloric feeding has been regularly proposed in the critically ill, although there is no clear definition available, nor evidence-based strategy to support it. We aim to define hypocaloric feeding based on indirect calorimetric data and to discuss patient-relevant clinical outcomes resulting from hypocaloric feeding. RECENT FINDINGS: Overfeeding and underfeeding both have proven deleterious effects and should be avoided, which requires determination of the patient's total energy requirement. Indirect calorimetry appears as the only precise method to determine such requirements in clinical settings. We define hypocaloric feeding as the delivery of 0.5-0.9 times the resting energy expenditure, isocaloric feeding as 1.1-1.3 times the resting energy expenditure, whereas hypercaloric feeding delivers more than 1.5 times the resting energy expenditure. Whether the patients are lean or obese, all the available predictive equations of energy requirements are grossly inaccurate in more than 30% of cases. SUMMARY: There is growing evidence that negative energy balances are associated with poor intensive-care-unit and hospital outcome. Using an evidence-based approach, hypocaloric feeding in the critically ill cannot be supported either. Whether the cutoff of tolerance for introducing feeding is 24 h or more is not yet defined and still awaits a prospective trial

Anaesthesia for procedures in the intensive care unit.

Taking in charge severely ill patients in the intensive care environment to manage complex procedures is a performance requiring highly specific knowledge. Close collaboration between anaesthetists and intensive care specialists is likely to improve the safety and quality of medical care. Three forms of anaesthetic care should be considered in clinical practice: sedation and analgesia; monitored anaesthetic care; and general anaesthesia or conduction block anaesthesia. Even in the field of sedation and analgesia, the anaesthesiologist can offer expertise on new anaesthetic techniques like: the most recent concepts of balanced anaesthesia in terms of pharmacokinetics and dynamics, favouring the use of short-acting agents and of sedative-opioid combinations. New modes of administration and monitoring intravenous anaesthesia have been developed, with potential application in the intensive care unit. These include the use of target-controlled administration of intravenous drugs, and of electroencephalographic signals to monitor the level of sedation

Monitoring the clinical introduction of a glutamine and antioxidant solution in critically ill trauma and burn patients.

Enteral glutamine supplementation and antioxidants have been shown to be beneficial in some categories of critically ill patients. This study investigated the impact on organ function and clinical outcome of an enteral solution enriched with glutamine and antioxidant micronutrients in patients with trauma and with burns. This was a prospective study of a historical control group including critically ill, burned and major trauma patients (n = 86, 40 patients with burns and 46 with trauma, 43 in each group) on admission to an intensive care unit in a university hospital (matching for severity, age, and sex). The intervention aimed to deliver a 500-mL enteral solution containing 30 g of glutamine per day, selenium, zinc, and vitamin E (Gln-AOX) for a maximum of 10 d, in addition to control treatment consisting of enteral nutrition in all patients and intravenous trace elements in all burn patients. Patients were comparable at baseline, except for more inhalation injuries in the burn-Gln-AOX group (P = 0.10) and greater neurologic impairment in the trauma-Gln-AOX group (P = 0.022). Intestinal tolerance was good. The full 500-mL dose was rarely delivered, resulting in a low mean glutamine daily dose (22 g for burn patients and 16 g for trauma patients). In burn patients intravenous trace element delivery was superior to the enteral dose. The evolution of the Sequential Organ Failure Assessment score and other outcome variables did not differ significantly between groups. C-reactive protein decreased faster in the Gln-AOX group. The Gln-AOX supplement was well tolerated in critically ill, injured patients, but did not improve outcome significantly. The delivery of glutamine below the 0.5-g/kg recommended dose in association with high intravenous trace element substitution doses in burn patients are likely to have blunted the impact by not reaching an efficient treatment dose. Further trials testing higher doses of Gln are required

Glucose control after severe brain injury.

PURPOSE OF REVIEW: A substantial body of evidence supports the use of intensive insulin therapy in general critical care practice, particularly in surgical intensive care unit patients. The impact of intensive insulin therapy on the outcome of critically ill neurological patients, however, is still controversial. While avoidance of hyperglycemia is recommended in neurointensive care, no recommendations exist regarding the optimal target for systemic glucose control after severe brain injury. RECENT FINDINGS: An increase in brain metabolic demand leading to a deficiency in cerebral extracellular glucose has been observed in critically ill neurological patients and correlates with poor outcome. In this setting, a reduction of systemic glucose below 6 mmol/l with exogenous insulin has been found to exacerbate brain metabolic distress. Recent studies have confirmed these findings while showing intensive insulin therapy to have no substantial benefit on the outcome of critically ill neurological patients. SUMMARY: Questions persist regarding the optimal target for glucose control after severe brain injury. Further studies are needed to analyze the impact of intensive insulin therapy on brain glucose metabolism and outcome of critically ill neurological patients. According to the available evidence, a less restrictive target for systemic glucose control (6-10 mmol/l) may be more appropriate

Segmental body composition assessed by bioelectrical impedance analysis and DEXA in humans.

The present study assessed the relative contribution of each body segment to whole body fat-free mass (FFM) and impedance and explored the use of segmental bioelectrical impedance analysis to estimate segmental tissue composition. Multiple frequencies of whole body and segmental impedances were measured in 51 normal and overweight women. Segmental tissue composition was independently assessed by dual-energy X-ray absorptiometry. The sum of the segmental impedance values corresponded to the whole body value (100.5 +/- 1.9% at 50 kHz). The arms and legs contributed to 47.6 and 43.0%, respectively, of whole body impedance at 50 kHz, whereas they represented only 10.6 and 34.8% of total FFM, as determined by dual-energy X-ray absorptiometry. The trunk averaged 10.0% of total impedance but represented 48.2% of FFM. For each segment, there was an excellent correlation between the specific impedance index (length2/impedance) and FFM (r = 0.55, 0.62, and 0.64 for arm, trunk, and leg, respectively). The specific resistivity was in a similar range for the limbs (159 +/- 23 cm for the arm and 193 +/- 39 cm for the leg at 50 kHz) but was higher for the trunk (457 +/- 71 cm). This study shows the potential interest of segmental body composition by bioelectrical impedance analysis and provides specific segmental body composition equations for use in normal and overweight women

Effects of beta-blockade on energy metabolism following burns.

The purpose of this study was to compare the effects of propranolol administered either by i.v. infusion or by prolonged oral administration (4 days) during the first 3 weeks following burns. The resting metabolic rate (RMR) of 10 non-infected fasting burned patients (TBSA: 28 per cent, range 18-37 per cent) was determined four times consecutively by indirect calorimetry (open circuit hood system) following: (1) i.v. physiological saline; (2) i.v. propranolol infusion (2 micrograms/kg/min following a bolus of 80 micrograms/kg); (3) oral propranolol (40 mg q.i.d. during 4 +/- 1 days); and (4) in control patients. All patients showed large increases in both RMR (144 +/- 2 per cent of reference values) and in urinary catecholamine excretion (three to four times as compared to control values). The infusion of propranolol induced a significant decrease in RMR to 135 +/- 2 per cent and oral propranolol to 129 +/- 3 per cent of reference values. A decrease in lipid oxidation but no change in carbohydrate and protein oxidation were observed during propranolol administration. It is concluded that the decrease in RMR induced by propranolol was not influenced by the route of administration. The magnitude of the decrease in energy expenditure suggests that beta-adrenergic hyperactivity represents only one of the mediators of the hypermetabolic response to burn injury