Good measures for self-report of pain in children are important, particularly as other informants tend to underestimate children's pain. This paper describes the development of a new computer-assisted approach to assessment of pain in children. The child can represent a range of different types of pains on body maps, and use two scales to indicate the size of the pain and the ‘throb’ or intensity. Facial expressions of associated emotions can also be incorporated into the figure. A series of ‘pain pages’ is included in the program. The pages allow changes in pain to be tracked over time, building up a cumulative record. The child can also report on different experiences and give retrospective accounts. Potential applications are suggested, for example in facilitating communication with children who find it difficult to give a clear verbal account of their pain, due to emotional difficulties, language or disability. Research directions are outlined.

To elucidate if an effect of propofol on endothelium-dependent relaxation could contribute to propofol-induced vasodilation, smooth muscle relaxation of isolated human omental artery and vein segments precontracted by endothelin-1 were measured. Substance P induced a concentration-dependent relaxation (mean ±SEM) in both artery (63 ± 8.4% of precontraction, n=9) and vein (60 ± 11%, n=7). The relaxation was enhanced by 10−6 M propofol (artery, 72 a 9.5%, n=9; vein, 81 ± 12%, n=7) but not affected by 10−7, 10−5 and 10−4 M propofol. In the presence of Nω-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor), 10−6 M propofol still enhanced the substance P-induced relaxation in arteries but not veins, whereas 10−4 M propofol inhibited the relaxation in both arteries (rightward shift of the concentration-response curve) and veins (28 ± 7.5%, n=8). In the presence of potassium chloride (to prevent hyperpolarization), the enhancement of substance P-induced relaxation by 10−6 M propofol was abolished in both arteries and veins whereas 10−5 and 10−4 M propofol reduced the relaxation in arteries (38 ± 13% at 10−5 M, n=6; 30 ± 11% at 10−4 M, n=6) but not in veins. These results demonstrate that propofol, at lower, clinically relevant concentrations, promotes endothelium-dependent relaxation mediated via hyperpolarization in human omental arteries and via both nitric oxide and hyperpolarization in human omental veins.

The aim of the present multiple cross-over study was to compare the effects of biphasic positive airway pressure (BIPAP) ventilation with synchronized intermittent mandatory ventilation combined with pressure support ventilation (S-IMV/PSV) in sedated and awake patients after coronary artery bypass grafting (CABG) surgery. Twenty-four patients with no evidence of preoperative respiratory dysfunction and an uncomplicated intraoperative course were investigated. The patients were randomly assigned to one of two groups starting with either BIPAP or S-IMV/PSV mode. Haemodynamic measurements and blood gas analyses were performed during sedation with 2.0 mg kg−1 h−1 propofol in the primary mode, after switching to the alternative ventilatory mode, and in the primary mode again. The same sequence of measurements was repeated in awake patients who had reached extubation criteria. In awake patients, PSV was performed instead of S-IMV. Statistical analysis of data was performed using non-parametric tests. Inspiratory peak pressure increased significantly during S-IMV/PSV in sedated patients in both groups. Other ventilatory parameters did not differ significantly between BIPAP and S-IMV/PSV in both groups. Similarly, haemodynamic parameters and blood-gas analyses did not vary with the ventilatory mode. Our results demonstrate that BIPAP ventilation has comparable effects on haemodynamics and pulmonary gas exchange compared with S-IMV/PSV and PSV when used for short-term ventilatory support in patients after cardiac surgery.

At clinically relevant concentrations, volatile anaesthetic agents influence neutrophil function. Our hypothesis was that sevoflurane would inhibit neutrophil apoptosis and consequently influence the postoperative pro-inflammatory state. In order to identify selectively the effect of the anaesthetic agent sevoflurane, we studied patients undergoing minimally stimulating (cataract) surgery randomly allocated to receive either sevoflurane (n=11) or local anaesthesia (n=12). Venous blood samples were taken immediately prior to anaesthesia and at 1, 8 and 24 h thereafter. The rate of neutrophil apoptosis, plasma concentration of cytokines and differential white cell count were measured. The rates of neutrophil apoptosis and plasma concentrations of IL-1β, TNF-α and IL-8 at each time point were similar in the two groups. IL-6 concentrations increased significantly and to a similar extent compared to preanaesthetic levels at 8 and 24 h. This study demonstrates that sevoflurane does not influence the rate of neutrophil apoptosis, cytokine concentrations and neutrophil count following cataract surgery.

Thirty-six unpremedicated women due for gynaecological surgery were examined for time-dependent prolongation of the QT interval in the electrocardiogram (ECG) before and after induction of anaesthesia using either sevoflurane or propofol. The conventional inhalational technique to induce anaesthesia with sevoflurane. ECG recordings were taken before, 2, 5 and 10 min after drug administration. Sevoflurane significantly lengthened (P < 0.001) the heart rate corrected QT interval within 10 min from 434±5ms to 459±6ms (mean ±SEM). Already after 2 min of sevoflurane application a trend towards prolongation was visible. The critical value of 440ms in the rate-corrected QT interval was exceeded in four patients in the sevoflurane group (n=18) but in only in one patient in the propofol group (n=18). Rate-corrected QT interval prolongation caused by sevoflurane needs to be recognized early in order to prevent the critical ventricular tachycardia torsade de pointes