Comparison of the anaesthetic requirement with target-controlled infusion of propofol to insert the laryngeal tube vs. the laryngeal mask.

BACKGROUND AND OBJECTIVE: The target effect-site concentration of propofol to insert a laryngeal mask airway was recently reported as almost 5 microg mL(-1). The present study aimed to determine the target effect-site concentration with target-controlled infusion of propofol to place classical larnygeal mask airway or current laryngeal tube in adult patients. METHODS: We included 40 patients scheduled for short gynaecological and radiological procedures under general anaesthesia in a randomized, double-blind manner using the Dixon's up-and-down statistical method. Monitoring included standard cardiorespiratory monitors, and bispectral index monitoring was used for all patients. Anaesthesia was conducted with a target-controlled infusion system: Diprifusor. The initial target plasma concentration of propofol was 5 microg mL(-1), and was changed stepwise by 0.5 microg mL(-1) increments according to Dixon's up-and-down method. Criteria for acceptable insertion were: Muzi's score < or = 2, and mean arterial blood pressure, heart rate or bispectral index variation <20% the baseline values. RESULTS: Target effect-site concentration of propofol required to insert laryngeal tube was 6.3 +/- 0.3 microg mL(-1) with Dixon method and ED50 was 6.1 microg mL(-1) (5.9-6.4) with logistic regression method. In the case of larnygeal mask airway they were 7.3 +/- 0.2 microg mL(-1) (Dixon method) and 7.3 microg mL(-1) (7.1-7.5; with logistic regression) respectively (P < 0.05). ED95 (logistic regression) was 6.8 microg mL(-1) (5.9-7.6) for laryngeal tube and 7.7 microg mL(-1) (7.3-8.0) for larnygeal mask airway (P < 0.05). Haemodynamic incidents were 55% in the larnygeal mask airway group vs. 30% in the laryngeal tube group (P < 0.05). CONCLUSIONS: The target effect-site concentration of propofol for insertion of laryngeal tube was lower than for larnygeal mask airway (P < 0.05), with a consequent reduction of the propofol induced haemodynamic side-effects.

[Low doses ketamine: antihyperalgesic drug, non-analgesic]. / Kétamine à faibles doses: antihyperalgésique, non analgésique.

Recent data in animal experiments as in clinical trials have clearly reported that pain modulation is related to an equilibrium between antinociceptive and pronociceptive systems. Therefore, the apparent pain level could not only be a consequence of a nociceptive input increase but could also result from a pain sensitization process. Glutamate, via NMDA receptors, plays a major role in the development of such a neuronal plasticity in the central nervous system, leading to a pain hypersensitivity that could facilitate chronic pain development. By an action on NMDA receptors opioids also induce, in a dose dependent manner, an enhancement of this postoperative hypersensitivity. "Antihyperalgesic" doses of ketamine, an NMDA receptor antagonist, were able to decrease this central sensitization not only in painful animal but also in human volunteers exposed to different pain models, or in the postoperative period. Many studies have reported that ketamine effects are elicited when this drug is administered the following manner: peroperative bolus (0.1 to 0.5 mg/kg), followed by a constant infusion rate (1 to 2 microg/kg per min) during the peroperative period and for 48 to 72 hours after anaesthesia. Those ketamine doses improved postoperative pain management by reducing hyperalgesia due to both surgical trauma and high peroperative opioid doses. This antihyperalgesic action of ketamine also limited the postoperative morphine tolerance leading to a decrease in analgesic consumption and an increase in the analgesia quality.