In a small investigation into patient-controlled sedation healthy volunteers (n=10) were asked to anaesthetise themselves using target-controlled propofol infusion. The authors were evaluating their own pharmacokinetic-based microprocessor controlled TCI system, where infusion is started with a target blood propofol concentration of 1 µg/ml. Double button-presses by the patient increase this target concentration up to a maximum of 3 µg/ml in steps of 0.2, with a lockout period of 2 minutes; failure to successfully double-press the button within 6 min lowers the target concentration to a minimum of 0.2 µg/ml.

Eight of the ten patients (no confidence interval given) were not over-sedated despite actively trying to anaesthetise themselves. (One became unresponsive, and another responded only to ear-pinching). The authors contrast these findings with the much larger study of Thorpe et al [Anaesthesia 1997 52 1144-50] (n=100), where 11% were oversedated on a system with no lockout period.

This small study again alerts us to the problems we might expect to encounter with patient-controlled conscious sedation.
 

The same authors (with one addition) studied the same volunteers (who had aged slightly), and looked at psychomotor function associated with propofol anaesthesia (administered by 'Diprifusor'). This topic is of no little significance, with the widespread use of day-case anaesthesia, although one suspects that few anaesthetists would be rash enough not to forbid their patients from driving in the twenty four hours following anaesthesia!

The authors relate psychomotor impairment associated with propofol infusion to the benchmark of impairment associated with alcohol intake. Tests used were:

• Computerised choice reaction time (response to 1 of five choices when a circle changed colour);
• Dual-task tracking with secondary reaction time (moving a cursor and then responding to a secondary stimulus);
• Within-list recognition (noting a word repetition).

The two reaction times increased progressively with increasing predicted blood levels of propofol; within-list recognition worsened with increasing propofol levels, but not significantly so!

Of importance is that psychomotor impairment at the lowest propofol infusion rate (0.2 µg/ml) is no worse than the effect of alcohol at blood levels of 20mg/100ml (The lowest European "maximum permissible level", in force in Sweden).

The small study size, and the baseline 'wellness' of the subjects makes extrapolation to real patients of dubious value.
 

In a study of propofol versus isoflurane for maintenance of anaesthesia (in thirty patients undergoing embolisation of cerebral AV malformations), propofol was found to significantly lower the percentage of polymorphonuclear leukocytes with respiratory burst activity, both compared with control values before surgery (to 54% below baseline at 4 hours), and compared with isoflurane anaesthesia (where the decrease was only 18%). Although phagocytosis of E. coli was also slightly lower in both groups during anaesthesia, there was no difference between the propofol and isoflurane groups (findings which differ from previously-published in vitro studies, which showed more suppression of phagocytosis by propofol).

Although the study has potentially worrisome implications (particularly for patients in ICU on long-term propofol infusions), it is difficult to deduce from some impairment of white-cell function that propofol necessarily has a negative effect on clinical outcome!