Staff attitudes toward a surgical checklist were mostly positive 1 year after their introduction in two large hospitals in central Sweden.

SummaryClassically haemodilution is regarded as causing coagulopathy. However, haemodilution with saline seems to cause a hypercoagulable state both in vivo and in vitro. The aim of the present study was to measure the effect of mild to severe haemodilution using thrombelastography. Blood samples were taken in 12 healthy volunteers and divided into seven aliquots. One aliquot was undiluted and acted as control. The other six were diluted with normal saline, Ringer Acetate, 4% albumin, Dextran 70, 6% and 10% hydroxyethylstarch to 10%, 20%, 40%, 50% and 60% dilution. The dilution was checked by measuring the haemoglobin concentration. Each aliquot was placed in a temperature-controlled thrombelastography channel. Increased coagulation activity, as measured by thrombelastography changes, was detected at low and medium levels of dilution with all the tested solutions. At more than 40% dilution, coagulation returned to normal while in the case of dextran and hydroxyethylstarch coagulopathy developed. For crystalloids and albumin, dilution had to exceed 50% before coagulation was impaired. If these findings can be reproduced in vivo, they may have implications for transfusion practice and prophylaxis against thrombosis.Keywords Coagulation: haemodilution; thrombelastography. Correspondence to: Dr K. Ekseth E-mail: kare.ekseth@rikshospitalet.no Accepted: 14 May 2002 Haemodilution is common following blood loss. Traditionally the focus during haemodilution has been on the oxygen carrying capacity of blood [1], and haemodilution has generally been regarded as a cause of hypocoagulation. However, in 1950 Tocantins et al. reported that moderate blood dilution with normal saline caused accelerated coagulation. Numerous reports describing alterations of coagulation during haemodilution followed [2][3][4][5][6]. During normovolaemic haemodilution in patients under anaesthesia, abnormal haemostasis develops before impaired global tissue oxygenation [7].Thrombelastography was developed as a research tool [8] but has been developed into a clinically useful coagulation monitor [9]. Thrombelastography can be used at the bedside and can detect impaired coagulation as well as hypercoagulable states. By using thrombelastography, Tuman et al. found increased coagulability with progressive blood loss, even when losses were replaced by crystalloids and packed red cells [3].Therefore the aim of the present investigation was to use thrombelastography in vitro to find the level of dilution required to cause hypercoagulation with commonly used crystalloids and colloids. We also wanted to determine whether the degree of dilution influenced coagulation. MethodsThe thrombelastograph (Haemoscope Corp., 5693 West Howard Street ⁄ Niles, IL 60714, USA) consists of a heated (37°C) cuvette containing 0.36 ml of whole blood. A pin suspended by a torsion wire is lowered into the blood. The cuvette oscillates on its vertical axis through 4.0-4.5 degrees. While the blood remains liquid, Anaesthesia, 2002Anaesthesia, , 57, pages 1102Anaesthesia, -1...

The concentration of propofol in and surrounding the human brain during propofol anaesthesia is unknown. We measured simultaneously the concentration of propofol in cerebrospinal fluid (CSF) from an indwelling intraventricular catheter and the concentration in arterial blood in five neurosurgical patients before, during induction (at 2.5 and 5 min) and during a maintenance propofol infusion (at 15 and 30 min). After induction of anaesthesia with propofol 2 mg kg-1, anaesthesia was maintained with an infusion of 8 mg kg-1 h-1 for 15 min and then reduced to 6 mg kg-1 h-1. The plasma concentration of propofol increased rapidly during induction and reached a plateau concentration of mean 2.24 (SD 0.66) micrograms ml-1 after 5 min. The concentration of propofol in CSF showed a slower increase during induction and remained almost constant at 35.5 (19.6) ng ml-1 at 15-30 min after induction. The CSF concentration of propofol that we measured was 1.6% of the plasma concentration and consistent with the high protein binding of the drug in plasma.

Our study indicates that there is a dose-dependency for the incidence of HES-induced pruritus, and that in some cases the pruritus may be severe and long-lasting.

Summary This study compares the induction and recovery characteristics, haemodynamic changes and side effects of propofol, thiopentone and midazolam when used as the anaesthetic agents for cardioversion. Recovery after midazolam was significantly longer (p < 0.05) than with either thiopentone or propofol. There was no difference in the recovery times between thiopentone and propofol. There was a significant decrease in mean arterial pressure 2 minutes after induction with propofol and midazolam. Three patients each in the thiopentone and propofol groups needed assisted ventilation because of apnvea, and four patients each in the propofol and midazolam groups had low Spo2 values (<95%). Flumazenil was used to reverse the effects of midazolam in eight patients and five of these were still drowsy 4 hours after the procedure. This study indicates that thiopentone is the most satisfactory agent for anaesthesia for cardioversion.