Background and objective: The efficiency of intraoperative autotransfusion in scoliosis surgery is poorly known but needs to be evaluated, not least because of the large blood losses in these patients. This is a retrospective analysis of transfusion requirements of 43 such patients. Methods: Records from 43 patients were studied. During surgery, the shed blood was salvaged and washed in an autotransfusion device (AT1000 Auto-transfusion Unit«) and a suspension of red cells was reinfused. Results: Fifty-eight per cent of the intraoperative blood loss was salvaged. The total blood loss during the patients' hospital stay was calculated from the haemoglobin balance, 24% of this loss was salvaged by the device. Moreover, 36 of the patients needed allogeneic blood transfusion. Conclusion: The efficiency of the autotransfusion device was relatively low in relation to the total extravasation, mainly because the postoperative blood loss is substantial.

Cerebral injuty remains a major cause of morbidity and mortality after cardiac surgery. Previous studies have mainly focused on preoperative risk factors and intraoperative events but cerebral complications may also occur in the postoperative period. Cognitive impairment is common after cardiac surgery but the consequences of this complication for activities of daily life are less known. Safe driving involves a complex set of skills requiring preserved cognitive function. A substantial number of patients with heart disease are active drivers. The impact of postoperative cognitive dysfunction on driving performance, however, has not previously been investigated in this large patient group.

In this thesis pre-, intra- and postoperative risk factors for focal cerebral complications were determined and the onset time of cerebral symptoms were evaluated in two cohorts of cardiac surgical patients, comprising 2480 and 3282 patients respectively. Data analysed were drafted from a clinical register and the surgical database of Linköping University Hospital Heart Center. Cerebral complication was delayed, i.e occurred after a free interval, in about one third of patients suggesting causes other than intraoperative events. Different risk factors were found for early and delayed cerebral complications suggesting different mechanisms of cerebral injury. Advanced age, preoperative hypertension, aortic surgery, prolonged cardiopulmonary bypass (CPB) time, intraoperative hypotension after completion of CPB, and arrhytlunia in the early postoperative period increased the risk for early cerebral complication. Female gender, diabetes, previous cerebrovascular disease, combined coronary artery bypass grafting (CABG) and valve surgery and arrhythmia on the thoracic ward increased the risk for delayed cerebral complication. Cognitive function and driving performance were evaluated in 27 patients before and 4-6 weeks after CABG. The patients underwent neuropsychological testing, an on-road driving test and a test in an advanced driving simulator. Twenty patients scheduled for percutaneous coronary intervention (PCI) served as controls. Complete data were obtained in 23 and 19 patients respectively. Furthermore cognitive function and driving performance in on-road driving of the 44 patients with complete tests before intervention were compared with controls of similar age without heart symptoms. Cognitive function and driving performance were already impaired in patients with coronary artery disease before intervention when compared with controls. After surgery 48% of the patients showed cognjtive decline compared to 10% after PCI. These patients also scored less in the on-road driving test to a greater extent than did patients without postoperative cognitive decline.

Objective: To find out if there is a correlation between AB0 type and the amount of blood lost at operation. Design: Retrospective study. Setting: One county and one university hospital, Sweden. Subjects: 540 patients who underwent primary prosthetic hip replacement under regional anaesthesia. Albumin (n = 298) or dextran (n = 242) were used as plasma substitutes. Main outcome measures: Estimated blood loss and number of units of red cell concentrates transfused. Results: The characteristics of the study groups were similar. In patients given albumin, the mean (SD) intraoperative loss with blood group 0 (n = 100) was 718 (413) ml and 2.7 (1.9) red cell units were given. Those with other blood groups (n = 198) lost 713 (469) ml and were given 2.5 (2.0) units. In patients given dextran with blood group 0 (n = 82), the intraoperative blood loss was 650 (337) ml, the postoperative loss 480 (222) ml and they received 2.1 (2.1) units. The corresponding values in the patients with other blood groups (n = 160) were 665 (351), 498 (208) and 2.5 (2.1) units. Conclusion: Blood group 0 was not associated with increased blood loss.

Background. The outcome of different treatment strategies for postoperative pain has been an issue of controversy. Apart from efficacy and effectiveness a policy decision should also consider cost-effectiveness. Since economic analyses on postoperative pain treatment are rare we developed a decision model in a pilot cost-effectiveness analysis (CEA) comparing epidural analgesia (EDA) and patient-controlled intravenous analgesia (PCIA) after major abdominal surgery in routine care. Methods. Using a decision-tree model, treatment with EDA (ropivacaine and morphine) was compared with PCIA (morphine). Effects and costs of treatment were established. The number of pain-free days at rest (pain intensity <30 using visual analogue scale 1-100 mm) was the primary measure of effect. An incremental cost-effectiveness ratio (ICER) was calculated as the difference in direct costs divided by the difference in effect. A database on 644 patients collected for the purpose of quality control during the period of 1997 to 1999 was the main data source. Sensitivity analysis was used to test uncertain data. Results. EDA was more effective in terms of pain-free days but more expensive. The additional cost for each pain-free day was 5652 Euros. Conclusion. It is a judgement of value if the additional cost is reasonable. When the cost of around 55 000 Euros per gained life-year with full health for other interventions is debated, our result indicates poor cost-effectiveness for EDA. Before any conclusion can be drawn concerning policy recommendations the difference in costs has to be related to other outcome measures as length of hospital stay, morbidity and mortality are required. © The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved.

The  common  method  for  postoperative  pain  control  after  major  abdominal surgery in routine care is epidural analgesia (EDA) using a combination of local anaesthetics  with  opiate  and  patient-controlled   intravenous  analgesia  using opiate (PCIA). It is a matter of dispute which method is better and should be favoured in different clinical situations. The superior analgesic effect of epidural analgesia reported in clinical trials has been difficult to transform into clinical practice.  In a large number  of patients  the epidural  analgesia  is discontinued earlier  than planned  because  of technical  difficulties.  The influence  of better analgesic effect on outcome in terms of mortality and morbidity has also been an issue  of  controversy.  There  are  no  clear  recommendations  which  treatment should  be  selected  in  specific  situations.  According  to  the  guidelines  of  the Swedish  Society  of Anaesthesiology  both  EDA  and  PCIA  can  be chosen  in several  situations.  Apart  from  efficacy  and  effectiveness  a  policy  decision should    also    consider    cost-effectiveness.    Since    economic    analyses    on postoperative pain treatment are rare an analysis of costs and consequences of planned  and discontinued  treatment  is of interest  when  comparing  these  two strategies. The aim of this report is to estimate cost-effectiveness  of treatment with EDA and PCIA under clinical circumstances by a decision analytic model using a clinical database as datasource.

Using   a   decision-tree,   treatment   with   EDA   was   compared   with   PCIA (morphine) by describing the possible clinical pathways for the successful and early-terminated treatments. The length of treatment was 3 days. A database on 644 patients collected for the purpose of quality control during 1997-99 was the main data source. By using the model costs and effects were established. The effects were expressed as number of pain-free days and the costs in Swedish krona (SEK). Number of pain-free days at rest (pain intensity<30 using visual analogue  scale  1-100  mm)  was  the  primary  measure  of  effect.  The  cost- effectiveness,  the average cost for reaching a particular outcome with a given treatment, is expressed as cost-effectiveness ratio (CER). When decision has to be  taken  to  replace  a  treatment  with  a  more  expensive  and  more  effective treatment, an estimate of the additional resources that have to be used to obtain the additional benefit is needed. That is the incremental cost-effectiveness ratio (ICER).

The result of the main analysis is that the cost for each pain-free day is 6.489 SEK for treatment with EDA and 2.602 SEK for PCIA. The incremental cost- effectiveness  ratio  is  50.215  SEK.  This  is  the  additional  cost  for  each  of additional  pain-free  day in a situation  when treatment  strategy  from PCIA is converted to EDA. The sensitivity analysis of our result shows that the result of the cost analysis is robust. However changes in assumptions of effect size have substantial impact on the result*.

*  See  an  English  version  of  the  report.  Bartha  E,  Carlsson  P,  Kalman  S. Evaluation  of  costs  and  effects  of  epidural  analgesia  and  patient-controlled intravenous  analgesia after major abdominal  surgery. Br J Anaesth. 2005 Oct 28; [Epub ahead of print]

Sepsis and septic shock are important causes of morbidity and mortality in the intensive care unit (ICU). Mortality rates in septic shock are estimated to be 40-50%, in spite of modem intensive care. Death is commonly caused by cardiovascular collapse and multiple organ dysfunction syndrome (MODS). Hepatic dysfunction is a common component of MODS, and can have a major impact on prognosis and survival. Sepsis is, among other derangements, also accompanied by disturbed tissue water homeostasis with increased extravasation of water resulting in tissue edema.

Hyaluronan is an interstitial macromolecule that participates in the regulation of tissue hydration. It is normally present in small concentrations in the blood, and is rapidly cleared from the blood by the liver endothelial cells. The synthesis of hyaluronan can be stimulated by inflammatory mediators. Thus sepsis and hyaluronan turnover could interact in many ways. The aim of the present investigations was to study possible changes in circulating hyaluronan concentrations in relation to sepsis and septic shock.

Plasma levels of hyaluronan were studied in 44 patients with infections and septic shock. Increased plasma concentrations were found, and the increase correlated to disease severity and outcome. In experimentally induced sepsis in pigs, an increase in circulating concentrations was found, and a relation to hemodynamic instability and outcome was seen. A moderate increase in blood hyaluronan concentrations was seen after surgical trauma in both humans and pigs. Crystalloid infusion therapy also caused a small increase in plasma hyaluronan concentrations in healthy volunteers, probably through an increased washout of interstitial hyaluronan. The hepatic turnover of hyaluronan was studied in septic shock patients. Low extraction ratios at high circulating concentrations were found, suggesting a reduced capacity of hepatic uptake and an increased inflow to the circulation. The kinetics of plasma turnover of hyaluronan were studied in septic and non-septic ICU patients. A prolonged half-life was seen among the septic patients, suggesting a reduced clearance capacity.

In conclusion, sepsis is accompanied by increased circulating hyaluronan concentrations. The magnitude of the increase seems to correlate to disease severity and outcome. The cause of this increase is suggested to be both reduced hepatic uptake function, and increased input to the circulation. The relative contributions of these mechanisms, and the possible clinical utility of plasma hyaluronan measurements, remain to be determined.

Pre-eclampsia is a serious multi-system disorder with general endothelial disease, often with a component of hepatic dysfunction. The pathogenesis of pre-eclampsia is not fully understood, and no specific diagnostic tests are available for early and reliable diagnosis, or for monitoring of the disease process. Hyaluronan is an extracellular matrix polysaccharide present at low concentrations in plasma. Normally, it is rapidly eliminated from the blood by the liver. Increased concentrations of circulating hyaluronan are seen in conditions with impaired hepatic function such as liver cirrhosis, and hyaluronan concentrations have previously been used to evaluate hepatic function in other diseases. In the present study, 11 pregnant women admitted to the intensive care unit with severe pre-eclampsia or eclampsia were studied. As control 31 healthy pregnant women, 18 undergoing vaginal delivery and 13 caesarean section, were included. Plasma hyaluronan was measured before and after delivery. Increased concentrations of plasma hyaluronan were found in the pre-eclampsia group both before (171 (75-586) ╡g/L (p < 0.01) and after delivery (215 (124-768) ╡g/L (p < 0.001) (median and inter-quartile range), as compared to both caesarean section (13 (7-28) ╡g/L before and 28 (18-48) ╡g/L after delivery) and vaginal delivery healthy controls (12 (8-24) ╡g/L before and 30 (13-63) ╡g/L after delivery). In the control groups, a small increase in plasma hyaluronan was seen after delivery, after both caesarean section (p < 0.05) and vaginal delivery (p < 0.01). In conclusion, plasma hyaluronan is increased in severe pre-eclampsia and eclampsia. The cause of the increase is unknown.

Background: Intravascular volume expansion is followed by loss of fluid from the circulation. The extravasation of albumin in this readjustment is insufficiently known. Methods: Twelve male volunteers participated, each in three separate sessions, in a controlled, randomised, open fashion. They received one of the following: albumin 40g/L,(7.1mL/kg, i.e. 500mL per 70kg), Ringer's acetate (21.4mL/kg), or dextran 30g/L (7.1mL/kg). The fluids were infused during 30min and the subjects were followed for 180min. ECG, arterial oxygen saturation and non-invasive arterial pressure were recorded. Haemoglobin, haematocrit, serum albumin and osmolality, plasma colloid osmotic pressure and hyaluronan concentration were determined in venous samples. Results: The serum albumin concentration decreased (P < 0.05, ANOVA) following Ringer's acetate or dextran, whereas serum osmolality was unchanged in all groups. The colloid osmotic pressure decreased (P<0.05) after the Ringer solution. The blood volume increase was estimated from the decrease in haemoglobin concentration and did not differ between the three fluids. The cumulated extravasation of albumin was largest following albumin (10.4 ▒ 5.4g, mean ▒ SD), less following dextran (5.6 ▒ 5.0 g) and negligible in the Ringer group (0.5 ▒ 10.0 g, P < 0.05 against albumin). However, the Ringer solution increased the plasma concentration of hyaluronan drastically. Conclusions: Infusion of hypotonic colloidal solutions entails net loss of albumin from the vascular space. This is not the case after Ringer's acetate. Increased interstitial hydration from the latter fluid is followed by lymphatic wash out of hyaluronan. ⌐ Acta Anaesthesiologica Scandinavica.

Background: Propofol is known to interact with the γ-aminobutyric acid_A (GABA_A) receptor, however, activating the receptor alone is not sufficient for producing anaesthesia.

Methods: To compare propofol and GABA, their interaction with the GABA_A receptor β subunit and actin were studied in three cellular fractions of cultured rat neurons using Western blot technique.

Results: Propofol tyrosine phosphorylated the GABA_A receptor β₂ (MW 54 and 56 kDa) and β₃ (MW 57 kDa) subtypes. The increase was shown in both the cytoskeleton (β₂₍₅₄₎ and β₂₍₅₆₎ subtypes) and the cell membrane (β₂₍₅₄₎ and β₃ subtypes). Concurrently the 56 kDa β₂ subtype was reduced in the cytosol. Propofol, but not GABA, also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. Without extracellular calcium available, the amount of actin decreased in the cytoskeleton, but tyrosine phosphorylation was unchanged. GABA caused increased tyrosine phosphorylation of β₂₍₅₆₎ and β₃ subtypes in the membrane and both β₂ subtypes in the cytoskeleton but no cytosolic tyrosine phosphorylation.

Conclusion: The difference between propofol and GABA at the GABA_A receptor was shown to take place in the membrane, where the β₂₍₅₄₎ was increased by propofol and instead the β₂₍₅₆₎ subtype was increased by GABA. Only propofol also tyrosine phosphorylated actin in the cell membrane and cytoskeletal fraction. This interaction between the GABA_A receptor and actin might explain the difference between anaesthesia and physiological neuronal inhibition.

Background: The cellular effects of anesthetics is poorly known. The GABA_A receptor has been suggested as the main target for most anesthetics. In previous studies we have shown that propofol tyresine phosphorylates the GABA_A receptor ß subunit, increases intracellular calcium and changes the actin morphology of neurons.

Aim: To investigate the effects of the volatile anesthetics sevoflurane, isoflurane and nitmus oxide on changes in [Ca²⁺]_i tyrosine phosphorylation and actin morphology in cultured rat neurons.

Methods: Western blotting (WB) was used to visualize tyrosine phosphorylated proteins. Fluorescence microscopy after rhodamine-phalloidin labelling of actin was used to calculate the number of actin ring structures eaused by sevoflurane. Intracellular calcium was measured with the calcium-binding probe Fura-2 on single cells.

Results: A protein of approx. 60 kDa increased dose-dependently in tyresine phosphorylation by sevoflurane in the membrane and cytoskeletal fractions, and was simultaneausly reduced in the cytosol. Isoflurane instead increased the tyresine phosphorylation of the same protein in the cytosol with only a slight increase in the membrane and no changes in the cytoskeletal fraction. Nitrous oxide did not cause any changes campared to air in the cytosol and was not detectable in the membrane. However, in the cytoskeletal fraction, the increase in tyrosine phosphorylation was high compared to air. Sevoflurane but not nitrous oxide or air increased the [Ca^2+]_i· Sevoflurane also eaused actin ring structures with a maximum after 20 minutes.

Conclusion: Sevoflurane, isoflurane and nitrous oxide all have different signal pathways. The 60 kDa protein is probably the GABA_A receptor ß subunit. According to the changes in tyrosine phosphorylation, changes in actin morphology and intracellular calcium, sevoflurane behaves most like the intravenous anesthetic propofol.

Background: Propofol is known to interact with the γ-aminobutyric acidA (GABA_A) receptor, however, activating the receptor alone is not sufficient for producing anaesthesia. Propofol tyresine phosphorylates the GABAA receptor and reorganises the actin cytoskeleton, eausing ring structures and rnembrane ruffles. Propofol, but not GABA, the endogenous tigand for the GABAA receptor, tyresine phosphorylates actin, both in the membrane and cytoskeletal fractions of the neuron.

Aim: How does propofol cause the actin reorganisation and is this a specific effect of propofol? Is the small membrane associated G-protein rho involved in the signal cascade towards the actin reorganisation?

Methods: Westem blotting (WB) was used to visualize tyresine phosphorylated immunoprecipitated proteins and changes in actin between the different cellularcompartments after inhibition with rho (C₃ exotoxin) and rho kinase (ROK) (HA-1077) inhibitors. Fluoreseenee mireoscopy after rhodamine-phalloidin labelling of actin was used to calculate the number of actin ring structures caused by propofol or GABA, in same experiments combined with pre-incubation with C₃ exotoxin, HA- 1077 or the tyrosine kinase inhibitor Herbimycin A. Propofol-stimulated cells were studied with confocal microscopy.

Results: Propofol eaused an increased tyresine phosphorylation, that was reduced by C₃ exotoxin, of a 160 kDa protein after two minutes stimulation. The 160 kDa protein is still unidentified. The actin ring structures caused by propofol was shown with confocal microscopy to go almost through the entire cell. The amount of rings were reduced by C3 exatoxin as well as HA-1077. Furthermore, w hen a tyrosine kinase bioeker was used no ring structures were formed. However, GABA did not produce any ring structures. When the actin content of the cellular campartments were analysed, C3 exatoxin treated cells showed an increased amount of actin in the cytoskeletal fraction, simultaneausly with a decrease in both the membrane and the cytosol fractions. The ROK bioeker on ly eaused a reduction of actin in the cytosol/membrane fractions, but no increase was observed in the cytoskeleton.

Conclusion: Propofol, but not GABA, eauses actin ring structures in neurons. Propofol uses the rho and rho kinase pathway to reorganize the actin cytoskeleton into ring structures, which is also dependent on a tyresine klnase. Propofol also eauses an unidentified rho dependent 160 kDa protein to be tyresine phosphorylated. The activation eaused by propofol of rho and rho kinase causes actin to be moved from the cytoskeleton to the cell membrane and cytosol. This reorganisation of actin might influence the GABA_A receptor by keeping it open, thus allowing the cell to be hyperpolarized for longer time, and consequently maintain anaesthesia.

Propofol, an intravenous anaesthetic, has been shown to interact with the β-subunit of the γ-amino butyric acid_A (GABA_A) receptor and also to cause changes in [Ca²⁺]_i. The GABA_A receptor, a suggested target for anaesthetics, is known to be regulated by kinases. We have investigated if tyrosine kinase is involved in the intracellular signal system used by propofol to cause anaesthesia. We used primary cell cultured neurones from newborn rats, pre-incubated with or without a tyrosine kinase inhibitor before propofol stimulation. The effect of propofol on tyrosine phosphorylation and changes in [Ca²⁺]_i were investigated. Propofol (3 μg mL⁻¹, 16.8 μM) increased intracellular calcium levels by 122 ± 34% (mean ± SEM) when applied to neurones in calcium free medium. This rise in [Ca²⁺]_i was lowered by 68% when the cells were pre-incubated with the tyrosine kinase inhibitor herbimycin A before exposure to propofol (P < 0.05). Propofol caused an increase (33 ± 10%) in tyrosine phosphorylation, with maximum at 120 s, of the β-subunit of the GABA_A-receptor. This tyrosine phosphorylation was decreased after pre-treatment with herbimycin A (44 ± 7%, P < 0.05), and was not affected by the absence of exogenous calcium in the medium. Tyrosine kinase participates in the propofol signalling system by inducing the release of calcium from intracellular stores and by modulating the β-subunit of the GABA_A-receptor.

The anaesthetic propofol interacts with the GABAA receptor, but its cellular signalling pathways are not fully understood. Propofol causes reorganisation of the actin cytoskeleton into ring structures in neurons. Is this reorganisation a specific effect of propofol as apposed to GABA, and which cellular pathways are involved? We used fluorescence-marked actin in cultured rat neurons to evaluate the percentage of actin rings caused by propofol or GABA in combination with rho, rho kinase (ROK), PI3-kinase or tyrosine kinase inhibitors, with or without the presence of extracellular calcium. Confocal microscopy was performed on propofol-stimulated cells and changes in actin between cellular compartments were studied with Western blot. Propofol (3 μg·ml-1), but not GABA (5 μM), caused transcellular actin ring formation, that was dependent on influx of extracellular calcium and blocked by rho, ROK, PI3-kinase or tyrosine kinase inhibitors. Propofol uses rho/ROK to translocate actin from the cytoskeleton to the membrane and its actin ring formation is dependent on an interaction site close to the GABA site on the GABAA receptor. GABA does not cause actin rings, implying that this is a specific effect of propofol.

Aims of the study: 1. to compare ropivacaine, a new long-acting amino-amide local anaesthetic drug, and bupivacaine (with/without adrenaline) concerning dermal analgesia and local vascular effects, 2. to design a suitable test procedure to evaluate changes in skin blood flow after intradermal injection of local anaesthetics, 3. to evaluate changes in skin blood flow of various concentrations of ropivacaine with/without adrenaline, 4. to investigate the influence of ropivacaine, bupivacaine, lidocaine, mepivacaine and prilocaine on the production of oxygen metabolites in human polymorphonuclear leukocytes (PMNL) (intra- and extracellular reactions), and 5. to examine the neural blocking characteristics on sensory, motor and sympathetic pathways using ropivacaine for epidural analgesia.

72 male patients scheduled for transurethral surgery and 50 male volunteers participated in this work. Heparinized blood was obtained from a total of 29 healthy adult blood donors.

Dermal analgesia was evaluated by pin-prick, skin colour changes by visual inspection, skin blood flow by laser Doppler flowmetry, sensory blockade by pin-prick, motor blockade by a modified Bromage scale, sympathetic blockade by assessments of skin resistance level (SRL) and response (SRR), skin temperature and skin blood flow (laser Doppler flowmetry). Production of oxygen metabolites by PMNLs was measured by luminal-enhanced chemiluminescence (intra- and extracellular reactions).

Ropivacaine produced significantly longer duration of dermal analgesia, following intradermal injection (0.1 ml, 30-G needle), compared with bupivacaine, in comparable concentrations. Addition of adrenaline increased the duration of both local anaesthetics. Local blanching was more frequent for plain solutions of ropivacaine.

The effect of drugs on local circulation may well be studied by intradennal injection (0.1 ml, 30-G needle, volar surface, forearms) and recording of changes in skin blood flow (laser Doppler flowmetry). The intradennal injection of a local anaesthetic drug may produce not only a further increase but also a decrease in skin blood flow, if the effect of an intradermal saline injection, causing a very reproducible flow increase, is considered in the evaluation of the net circulatory effect of the tested drug.

Intradermal injection of lidocaine 1% and bupivacaine 0.75% produced an increase in skin blood flow. Ropivacaine 1% produced a flow similar to saline, while a decrease was seen for ropivacaine 0.75%. Ropivacaine0.5%, 0.375%, 0.25%, 0.125% and 0.063% showed a gradual further reduction in flow, where 0.063% produced a flow similar to adrenaline-injection (5 Jlg/ml) and almost as low as at the untreated control sites. The combination of ropivacaine 1%, 0.5% , 0.25% and adrenaline did not accentuate but instead decreased the vasoconstrictive effect of adrenaline.

By and large a decrease in response of chemiluminescence for PMNLs was seen with the higher concentrations of the various local anaesthetics. Lidocaine showed a minor decrease even at lower concentrations. Ropivacaine 1000 J.Lg/ml showed a depression of both intra- and extracellular responses that was similar to, and even somewhat more pronounced than lidocaine 1000 J.Lg/ml. This effect could be of great interest e.g. for local antiinflammatory effects by topical administration, but it has to be further investigated. A marked increase for prilocaine (1000 Jlg/ml) in intracellular response accompanied with a reduction in extracellular response was noted.

Ropivacaine (0.5%, 0.75% with/without adrenaline) 20 ml administered epidurally provided a good sensory blockade and a motor blockade satisfactory for transurethral surgery. The maximum sensory level of analgesia was high, median Th 2-3. The majority of patients had a marked or complete sympathetic blockade in the lower limbs. Besides mild or moderate hypotension, which responded well to treatment with ephedrine, no other serious adverse reactions were seen, Addition of adrenaline did not provide any significant prolongation of the epidural blockade, and did not alter the influence upon the sympathetic blockade nor the hemodynamic changes during onset.

Background: Release of biochemical markers of myocardial injury unrelated to permanent myocardial damage has been claimed to explain a major proportion of elevations seen after cardiac surgery. However, little is known about the magnitude of this unspecific release. The aim of this study was to shed light on this issue by serial measurements in patients without permanent myocardial injury after coronary surgery.

Methods: The unique release kinetics of troponin-T were employed to identify patients with no or minimal permanent myocardial injury. 302 patients undergoing CABG procedures (employing cardiopuhnonary bypass, crystalloid cardioplegia and retransfusion of shed mediastinal blood) were studied.

Results: 90 patients were found to have normalized troponin-T levels no later than the fourth postoperative day indicating that early elevation of biochemical markers was explained almost purely by unspecific release. In this subgroup troponin-T (2.03±1.36 µg/L; range 0.35-8.99 µg/L) peaked at the 3 hour recording and CK-MB (28.3±10.7 µg/L; range 11.9-86 µg/L) peaked at the 8 hour recording after unclamping the aorta.

Conclusions: A substantial early release of CK-MB and troponin-T occurred in patients with no or minimal permanent myocardial injury after CABG. The time frame when unspecific release was most pronounced is frequently studied to evaluate myocardial protective strategies or to compare different treatment modalities. Also, differences in unspecific release of biochemical markers can be expected depending on type of surgical procedure or coronary intervention. Therefore, further efforts to hring clarity about diagnostic pitfalls are warranted to prevent inappropriate comparisons and to improve our assessment of myocardial damage in association with revascularisation procedures.

Objective - ECG diagnosis of myocardial infarction after cardiac surgery is associated with major pitfalls and enzyme diagnosis is interfered by unspecific elevation unrelated to permanent myocardial injury. Sustained release of troponin-T is a marker of permanent myocardial injury if renal function is maintained. However, early identification of perioperative myocardial infarction is desirable and therefore the usefulness of creatine kinase monobasic (CK-MB) kinetics to detect myocardial injury early after coronary surgery was investigated.

Design - Two hundred and eighty-six patients undergoing coronary surgery were studied with respect to release of enzymes and troponin-T preoperatively and postoperatively 3 and 8 h after unclamping the aorta, and every morning postoperative days 1-4.

Results - CK-MB peak was found at 3 h ( n = 145), 8 h ( n = 103) and 16-20 h after unclamping ( n = 38). Depending on when the CK-MB peak was recorded different demographic and perioperative characteristics were found. A sustained release of troponin-T was characteristic for the group with the CK-MB peak at 16-20 h after unclamping.

Conclusion - If CK-MB is measured only once it may be advisable to do it on the first postoperative morning as these measurements provided the best discrimination between patients with and without sustained elevation of troponin-T. However, repeated sampling provides additional information that aids in the early identification of permanent myocardial injury particularly in patients with borderline elevations of CK-MB.

Objective - Biochemical markers of myocardial injury are frequently elevated after cardiac surgery. It is generally accepted that release unrelated to permanent myocardial damage explains a proportion of these elevations. However, little is known about the magnitude and temporal characteristics of this diagnostic noise. One way to address this issue would be to study a group without permanent myocardial injury. Design - The unique release kinetics of troponin-T (permanent myocardial injury causes a sustained release of structurally bound troponin) were used to identify patients with no or minimal permanent myocardial injury. Blood was sampled from patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB) before surgery, 3 and 8 h after unclamping the aorta, and each morning until postoperative day 4, for analysis of enzymes and troponin-T. From 302 consecutive patients a subgroup was identified that fulfilled the following criteria: (a) normalized troponin-T levels =postoperative day 4, (b) no ECG changes indicating myocardial injury. Results - Seventy-seven patients fulfilled the criteria above and in this subgroup troponin-T (2.08 ▒ 1.42 ╡g/ 1, range 0.35-8.99 ╡g/l) peaked at the 3 h recording and creatine kinase monobasic (CK-MB) (28.6 ▒ 11.3 ╡g/l, range 11.9-86.0 ╡g/l) peaked at the 8 h recording after unclamping the aorta. Conclusion - Substantial early elevations of plasma CK-MB and troponin-T occurred in patients with no or minimal permanent myocardial injury after CABG. Unspecific release was most pronounced during the timeframe that is usually studied to evaluate myocardial protective strategies or to compare revascularization procedures.

Context: Amino-terminal pro-brain-type natriuretic peptide is known to predict outcome in patients with heart failure, but its role in an intensive care setting is not yet fully established. Objective: To assess the incidence of elevated amino-terminal pro-brain natriuretic peptide (NT-pro-BNP) on admission to intensive care and its relation to death in the ICU and within 30 days. Design: Prospective, observational cohort study. Setting: A mixed noncardiothoracic tertiary ICU in Sweden. Patients and main outcome measures NT-pro-BNP was collected from 481 consecutive patients on admission to intensive care, in addition to data on patient characteristics and outcome. A receiver-operating characteristic curve was used to identify a discriminatory level of significance, a stepwise logistic regression analysis to correct for other clinical factors and a Kaplan-Meier analysis to assess survival. The correlation between Simplified Acute Physiology Score (SAPS) 3, Sequential Organ Failure Assessment score (SOFA) and NT-pro-BNP was analysed using Spearmans correlation test. Quartiles of NT-pro-BNP elevation were compared for baseline data and outcome using a logistic regression model. Results: An NT-pro-BNP more than 1380 ng l(-1) on admission was an independent predictor of death in the ICU and within 30 days [odds ratio (OR) 2.6; 95% confidence interval (CI), 1.5 to 4.4] and was present in 44% of patients. Thirty-three percent of patients with NT-pro-BNP more than 1380 ng l(-1), and 14.6% of patients below that threshold died within 30 days (log rank P 0.005). NT-pro-BNP correlated moderately with SAPS 3 and with SOFA on admission (Spearmans rho 0.5552 and 0.5129, respectively). In quartiles of NT-pro-BNP elevation on admission, severity of illness and mortality increased significantly (30-day mortality 36.1%; OR 3.9; 95% CI, 2.0 to 7.3 in the quartile with the highest values, vs. 12.8% in the lowest quartile). Conclusion: We conclude that NT-pro-BNP is commonly elevated on admission to intensive care, that it increases with severity of illness and that it is an independent predictor of mortality.

Aim of study: To evaluate the effects of different doses of clonidine administered systemically or spinally in combination with local anaesthetics on sensory and motor block intraoperatively, on pain relief postoperatively, and on the incidence of postoperative alcohol withdrawal syndrome (AWS) in alcohol abusers.

Patients and methods: A total 285 patients were included in five studies. In two studies, oral clonidine (150 and 300 µg) or intrathecal clonidine (100 and 150 µg) was combined with local anaesthetics to evaluate the quality of sensory and motor block and postoperative analgesia. In a third study, the ant-idelirious effect of a single dose of clonidine (150 µg) given orally or intrathecally before operation was studied in 45 heavy alcohol abusers (daily ethanol intake of at least 60 g). The combination oflow doses of clonidine (15 and 30 µg) intrathecally with low dose bupivacaine was investigated during ambulatory herniorrhaphy. In a combined spinal-epidural anaesthesia study, a moderate dose of postoperative epidural clonidine (40 µg/h) was studied with or without low dose intrathecal clonidine (15µg); plain local anaesthetic was used as control. Sensory block was assessed by pin-prick, light touch, thermotest and transcutaneous electric stimulation; motor block was estimated by a modified Bromage scale. Pain intensity according to a Visual Analogue Scale (VAS) and analgesic request were recorded. AWS was assessed by the criteria of the Diagnostic and Statistical Manual of Mental Disorders.

Results: Intraoperatively, high doses of oral or intrathecal clonidine added to local anaesthetics almost doubled the time of sensory and motor block, and it was possible to reduce the dose of local anaesthetics without diminishing of the quality of spinal anaesthesia. Low doses of clonidine (15 µg) in combination with a low dose of bupivacaine significantly increased the spread of analgesia (4 dermatomes) without significantly prolonging the motor block. The same dose of clonidine combined with a high dose of bupivacaine significantly prolonged the sensory- and motor block by 36% and 18%, respectively Postoperatively, both oral and intrathecal clonidine prolonged time to first analgesic request. V AS score was acceptably low in all study groups. However, a high dose (150 µg) of intrathecal clonidine reduced postoperative 24-hour morphine consumption by 40% compared with control, while morphine-sparing was 55% when a low dose (15 µg) of intrathecal clonidine was combined with epidural clonidine. In ambulatory practice, low doses of intrathecal clonidine decreased analgesic requirements at home for up to 24 h after operation. In comparison with diazepam premedication, clonidine 150 µg, intrathecally or orally, reduced the incidence and degree of postoperative AWS in alcohol-dependent men (from 80 to 10%). The major side-effects of clonidine were hypotension and sedation, especially after oral administration. This hypotensive effect was also found after epidural clonidine infusion.

Conclusion: Clonidine, as an adjuvant to local anaesthetics, provided a higher quality of anaesthesia and postoperative analgesia and prevented postoperative alcohol withdrawal syndrome in alcohol abusers. Side effects such as hypotension and pronounced sedation postoperatively should be kept in mind if high doses of clonidine are used.

Laser Doppler perfusion imaging (LDPI), is a further development in laser Doppler flowmetry (LDF). Its advantage is that it enables assessment of microvascular blood flow in a predefined skin area rather than, as for LDF, in one place. In many ways this method seems to be more promising than LDF in the assessment of burn wounds. However, several methodological issues that are inherent in the LDPI technique, and are relevant for the assessment of burn depth, must be clarified. These include the effect of scanning distance, curvature of the tissue, thickness of topical wound dressings, and pathophysiological effects of skin colour, blisters, and wound fluids. Furthermore, we soon realised that to examine the perfusion image generated by LDPI adequately the process of analysis was appreciably improved by the simultaneous use of digital photography. In the present investigation we used both in vitro and in vivo models and also examined burned patients, and found that the listed factors all significantly affected the LDPI output signal. However, if these factors are known to the examiner, most of them can be adjusted for. If the technique is further improved by minimizing such effects and by reducing the practical difficulties of applying it to a burned patient in the burns unit, the technique may find uses in everyday clinical decision-making.

Allogeneic blood transfusion, although often needed in major surgery with large per-and postoperative bleeding, is fraught with dangers such as clerical mishandling, immunosuppression and blood-borne infections. It is therefore important to find ways to avoid allogeneic blood transfusion by means of less bleeding, better tolerance of the bleeding or alternatives to allogeneic blood.

Aim of the study: To evaluate different methods of blood saving in total hip replacement (THR) surgery, their efficacy, and the possible risks, especially hyper- and hypocoagulation.

Patients and methods: A total of 179 patients and eight volunteers were included in five studies. All patients were operated by primary TI-IR. Blood loss, allogeneic transfusions, coagulation parameters (platelets, bleeding time, fibrinogen, APTT, PT, soluble fibrin, TAT), fibrinolysis parameters (D-dimer, tPA, PAT, PAP), functional coagulation analysis (Sonoclot, TEG) and frequency of deep vein thrombosis (ultrasonography) were investigated according to the different study regimes. Thitiy patients undergoing predonation of autologous blood (PAD) with or without autotransfusion were compared with a control group of 15 patients without blood saving treatment. Fatty patients undergoing immediate prcopcrative platelet rich plasma (PRP) harvest and autotransfusion were compared with 40 patients undergoing PAD and autotransfusion. The spontaneous and induced activation of the platelets in the blood of20 patients undergoing THR with or without additive PRP harvest were also studied with flow cytometry. The efficacy of tranexamic acid (TA) as a blood saving method was examined in a study including 40 patients. As Sonoclot coagulation analysis was the single most important coagulation analysis during the studies, a methodological examination including eight volunteers was done for the instrument.

Results and discussion: If no blood saving method is used there is a very strong possibility of allogeneic blood transfusion (100% of the patients studied needed blood). Autotransfusion is not sutlicient as a single transfusion reducing method (53% patients studied still needed blood). PAD+ autotransfusion gives sufficient reduction in allogeneic blood transfusion (5-27% of patients in tlte different studies needed blood) but needs prcopcrativc planning, and PAD is not accepted by Jehovah's Witnesses. PRP reduces allogeneic blood transfusion as effectively as predonation of two units of blood (15% of studied patients needed blood) and can replace PAD in unplanned operations and for Jehovah's Witnesses. The majority of platelets are in a resting state during THR and PRP harvest. PRP harvest did not affect the degree of platelet activation, but there were great individual differences between patients (spontaneous activated platelets, i.e. presenting P-Selektin during the operation, between 1 %-23%). Most of the platelets in the c-PRP were not activated at the time ofretransfusion but were easily activated upon stimulation with the physiological activator ADP. TA therapy started prcoperatively is easily performed and reduces bleeding by 35%, probably by significantly reducing induced fibrinolysis perioperatively. During primary THR surgety there was an early postoperative hypocoagulation during the first postoperative day, with a hypercoagulation later postoperativcly, and an observed maximal value about 7 to 10 days postopcrativcly that was still evident three weeks postopcratively. Per- and early postoperatively there was also a marked fibrinolysis that was normalized on day 1 postoperatively. Six of the 120 patients examined with ultrasonography had DVTs, all after the first week postoperatively. There were no differences in the frequency of detected DVTs, irrespective oftrcahnent with PAD, PRP or TA. Sonoclot coagulation analysis was found to be a valuable tool in detecting hypercoagulability but was restricted by a high variability. This variability can be lowered by a dual machine setting, repetitive analysis and directly analyzed arterial samples.

Conclusion: The combination ofperioperative autotransfusion and PAD is effective in preventing allogeneic blood transfusions during primary THR. PRP harvest is as effective as PAD and is useful for patients who cannot donate blood. A minor propotiion of the patient's platelets are activated during the surgery irrespective of whether or not there is PRP harvest. TA therapy started preoperatively reduces fibrinolysis during the day of surgery and reduces per-and postoperative bleeding by 35%. Primmy THR surgery gives rise to an initial hypocoagulation followed by a hypercoagulation with an observed maximal value about 7 to 10 days postoperatively which is still evident three weeks postoperatively. However, the observed frequency of thrombosis was low (5%) in the 120 patients examined with utrasonography. Sonoclot analysis is an efficient tool for following this hypercoagulation. The high variability of the method can be reduced with a dual machine setting, repetitive analysis and directly analyzed arterial samples.

Background: Explicit recall (ER) is evident in approximately 0.2% of patients given general anaesthesia including muscle relaxants. This prospective study was performed to evaluate if cerebral monitoring using BIS to guide the conduction of anaesthesia could reduce this incidence significantly. Patients and methods: A prospective cohort of 4945 consecutive surgical patients requiring muscle relaxants and/or intubation were monitored with BIS and subsequently interviewed for ER on three occasions. BIS values between 40 and 60 were recommended. The results from the BIS-monitored group of patients was compared with a historical group of 7826 similar cases in a previous study when no cerebral monitoring was used. Results: Two patients in the BIS-monitored group, 0.04%, had ER as compared with 0.18% in the control group (P < 0.038). Both BIS-monitored patients with ER were aware during intubation when they had high BIS values (>60) for 4 min and more than 10 min, respectively. However, periods with high BIS = 4 min were also evident in other patients with no ER. Episodes with high BIS, 4 min or more, were found in 19% of the monitored patients during induction, and in 8% of cases during maintenance. Conclusions: The use of BIS monitoring during general anaesthesia requiring endotracheal intubation and/or muscle relaxants was associated with a significantly reduced incidence of awareness as compared with a historical control population.

Classically 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.

Pneumothorax is the term used for all conditions where air is present in the pleural cavity outside the confinement of the lung. Active treatment of pneumothorax often consists of the introduction of a pleural drain and the application of a continuous vacuum to keep the collapsing lung expanded until the lesion has healed. Traditional techniques for the application of vacuum do not permit quantification of aspirated air volumes during treatment and assessment of the correct time to stop treatment rests on a purely subjective basis. The patients require hospitalisation during treatment which is often painful. The decision to institute active treatment usually relies on estimation of the volume of the collapsed lung pertormed from a chest X-ray.

The aims of this study were to investigate if treatment using equipment permitting quantification of aspirated air volumes could reduce treatment time, if the treatment could be made less painful and if chest X-ray was a reliable method for estimating the size of the pneumothorax.

A new device for vacuum treatment of pneumothorax was developed and six studies in 289 cases of pneumothorax were undertaken.

The studies showed that when the new technique was applied in 124 cases of traumatic and spontaneous pneumothorax, treatment time was reduced significantly compared to when the traditional technique was used. In a placebo-controlled, randomised study in 22 patients suffering from spontaneous pneumothorax it was demonstrated that pain relief during treatment was improved by the use of an interpleural technique for analgesia employing the injection of a local anaesthetic agent into the pleural cavity. This technique using 20ml bupivacaine-epinephrine 0.5% injected at 8-hourly intervals for three days did not produce serum concentrations in the toxic range, but small haemodynamic changes were registered possibly caused by beta-adrenergic stimulation by the epinephrine. A study on 16 patients with spontaneous pneumothorax showed that estimation of the degree of lung collapse from chest X-ray was unreliable as this correlated poorly to an estimation made on the same patient using CT-scan.

To evaluate the value of routine application ofneuroprotection and the use of temporary clips (TCL) in every day aneurysm surgery 203 patients with a total of 236 aneurysms were included in the a perioperative moderate hypothermia (MHT, <34° C) protocol. Poor grade patients (Hunt & Hess IV-V) were excluded fi·om the study. Induction of MHT averaged 0.98+/-0.37 hours and was based on a protocol for administration of cold, intravenous crystalloid fluid and barbiturates. Blood pressure was stable throughout MHT. 40% of the patients needed inotropic support during the first 12 postoperative hours. Cardiac arrhythmia was infrequent and when occurring always of benign character. In 8%, pulmonary problems with central venous congestion and/or poor systemic oxygenation occurred.

In total, temporary clipping was used in 66 cases (mean occlusion time being 10.5 ±7.3 min), 50% of which had not been expected pre-operatively. Overall, 40 aneurysms (75% 1-12 mm in size) ruptured during dissection - corresponding to 20% of the cases without preplanned use of TCL.

Excluding biasing confounding factors, TCL did not affect the outcome following aneurismal surgery. The study lends support to the idea that TCL should be considered a routine method for all aneurysm surgery.

Patients undergoing major abdominal surgery were randomly given total intravenous anaesthesia based on propofol and fentanyl, anaesthesia based on propofol, fentanyl and nitrous oxide or anaesthesia based on isoflurane and fentanyl. Postoperative atelectasis demonstrated by computed tomography of the chest was found to a similar extent and a similar decrease in arterial oxygen pressure was seen in the groups. No correlation was seen between the size of atelectasis and postoperative oxygen pressure. Cardiovascular stability was equally well maintained during surgery, but the patients anaesthetized with propofol needed more ephedrine and glycopyrrolate to achieve stability. In all groups the Acute Physiology Score was normal by day I (range 1-7). A similar impairment of bowel function after operation was found, with passage of gas day 3 ( 1-6) and tolerance of enteral intake day 5 (1-10). Hospital stay 11 (6-45) days and incidence of complications were unaffected by anaesthetic technique. Early recovery was similar in the three groups, but patients anaesthetized with propofol reported fewer symptoms, better subjective control and a higher degree of socially orientation than patients anaesthetized with isoflurane. On the whole, the advantages with propofol compared to isoflurane were small, and the addition of nitrous oxide to propofol had no influence on. the results.

Laboratory tests on human leucocytes, cultured human glial cells and rat glial cells and neurons were performed with propofol in concentrations between 0.3 ~g·ml" and 50 ~g·ml" (1.7 to 280 ~M). Clinically relevant concentrations of propofol decreased random and chemotactic locomotion of leucocytes in an agarose assay. Concentration dependent and reversible effects of propofol were found on the actin distribution of the cytoskeleton in cultured cells. The maximal effect was seen after 20 min of incubation. Using a single cell microfluorometric method with Fura2 an increase in cytosolic free calcium in rat neurons was seen immediately after the addition of propofol, lasting 128±39 seconds and thereafter returning to normal. This effect was dual, 60-7 5% of the increase came from the extracellular buffer and the remaining part from intracellular stores. A rise in intracellular calcium can lead to changes in the cytoskeleton and to hyperpolarization of a neuron.

Background. Total knee arthroplasty (TKA) is often carried out using a tourniquet and shed blood is collected in drains. Tranexamic acid decreases the external blood loss. Some blood loss may be concealed, and the overall effect of tranexamic acid on the haemoglobin (Hb) balance is not known. Methods. Patients with osteoarthrosis had unilateral cemented TKA using spinal anaesthesia. In a double-blind fashion, they received either placebo (n=24) or tranexamic acid 10 mg kg-1 (n=27) i.v. just before tourniquet release and 3 h later. The decrease in circulating Hb on the fifth day after surgery, after correction for Hb transfused, was used to calculate the loss of Hb in grams. This value was then expressed as ml of blood loss. Results. The groups had similar characteristics. The median volume of drainage fluid after placebo was 845 (interquartile range 523-990) ml and after tranexamic acid was 385 (331-586) ml (P<0.001). Placebo patients received 2 (0-2) units and tranexamic acid patients 0 (0-0) units of packed red cells (P<0.001). The estimated blood loss was 1426 (1135-1977) ml and 1045 (792-1292) ml, respectively (P<0.001). The hidden loss of blood (calculated as loss minus drainage volume) was 618 (330-1347) ml and 524 (330-9620) ml, respectively (P=0.41). Two patients in each group developed deep vein thrombosis. Conclusions. Tranexamic acid decreased total blood loss by nearly 30%, drainage volume by ~50% and drastically reduced transfusion. However, concealed loss was only marginally influenced by tranexamic acid and was at least as large as the drainage volume.

Central mechanisms related to referred muscle pain and temporal summation of muscular nociceptive activity are facilitated in fibromyalgia syndrome (FMS) patients. The present study assessed the effects of an NMDA-antagonist (ketamine) on these central mechanisms. FMS patients received either i.v. placebo or ketamine (0.3 mg/kg, Ketalar(«)) given over 30 min on two separate occasions. Habitual pain intensity was assessed on a visual analogue scale (VAS). Initially, 29 FMS patients received ketamine or isotonic saline to determine which patients were ketamine responders (>50% decrease in pain intensity at rest by active drug on two consecutive VAS assessments). Fifteen out of 17 ketamine-responders were included in the second part of the study. Before and after ketamine or placebo, experimental local and referred pain was induced by intramuscular (i.m.) infusion of hypertonic saline (0.7 ml, 5%) into the tibialis anterior (TA) muscle. The saline-induced pain intensity was assessed on an electronic VAS, and the distribution of pain drawn by the subject. In addition, the pain threshold (PT) to i.m. electrical stimulation was determined for single stimulus and five repeated (2 Hz, temporal summation) stimuli. The pressure PT of the TA muscle was determined, and the pressure PT and pressure pain tolerance threshold were determined at three bilaterally located tenderpoints (knee, epicondyle, and mid upper trapezius). VAS scores of pain at rest were progressively reduced during ketamine infusion compared with placebo infusion. Pain intensity (area under the VAS curve) to the post-drug infusion of hypertonic saline was reduced by ketamine (-18.4▒0.3% of pre-drug VAS area) compared with placebo (29.9▒18.8%, P<0.02). Local and referred pain areas were reduced by ketamine (-12.0▒14.6% of pre-drug pain areas) compared with placebo (126.3▒83.2%, P<0.03). Ketamine had no significant effect on the PT to single i.m. electrical stimulation. However, the span between the PT to single and repeated i.m. stimuli was significantly decreased by the ketamine (-42.3▒15.0% of pre-drug PT) compared with placebo (50.5▒49.2%, P<0.03) indicating a predominant effect on temporal summation. Mean pressure pain tolerance from the three paired tenderpoints was increased by ketamine (16.6▒6.2% of pre-drug thresholds) compared with placebo (-2.3▒4.9%, P<0.009). The pressure PT at the TA muscle was increased after ketamine (42.4▒9.2% of pre-drug PT) compared with placebo (7.0▒6.6%, P<0.011). The present study showed that mechanisms involved in referred pain, temporal summation, muscular hyperalgesia, and muscle pain at rest were attenuated by the NMDA-antagonist in FMS patients. It suggested a link between central hyperexcitability and the mechanisms for facilitated referred pain and temporal summation in a sub-group of the fibromyalgia syndrome patients. Whether this is specific for FMS patients or a general phenomena in painful musculoskeletal disorders is not known. Copyright (C) 2000 International Association for the Study of Pain. Published by Elsevier Science B.V.

Background: To assess the effects of treatment with nebulized corticosteroids immediately after chlorine gas injury. Methods: Eighteen anesthetized and mechanically ventilated pigs were exposed to chlorine gas (140 ppm for 10 minutes) and observed for 6 hours. Nine pigs were treated with nebulized beclomethasone-dipropionate 20 ╡g/kg (BDP group), and nine pigs were given no treatment (control group). Results: All animals developed severe pulmonary dysfunction. The initial decrease in PaO2 was similar in both groups, but BDP-treated animals improved whereas control animals deteriorated (p < 0.005, analysis of variance). Pulmonary vascular resistance increased in both groups but less in the BDP group (p < 0.01). Lung-thorax compliance was better preserved in the BDP group (p < 0.01), and oxygen delivery was significantly better in the BDP group (p < 0.01). One animal died in the BDP group, as did three animals in the control group. Conclusion: Immediate treatment with nebulized BDP improved pulmonary and cardiovascular function after experimental chlorine gas injury.

A new test for the assessment of psychomotor recovery - the perceptive accuracy test - was designed and tested in a group of volunteers. It was found to be reproducible and not associated with any significant learning. Two hundred patients (ASA I-ll) undergoing day care arlhroscopic surgery were then studied in order to determine which anaesthetic technique is associated with the best recovery profile. No pharmacological premedication was given to any of the patients. The methodology was standardized in all studies so that the anaesthetic technique was similar between the groups, except for the study dmgs. Postural stability was measured following the injection of midazolam intravenously, using computerized dynamic posturography, Recovery was assessed using a combination of tests including a recovery scale, psychomotor tests and assessment of mood. Discharge times and post-operative complications were also recorded. Results showed that induction of anaesthesia with propofol followed by maintenance with isoflurane in oxygen and air, and alfentanil as analgesic, were associated with a good recovery profile. Maintenance of anaesthesia with propofol instead of isoflurane proved to be a satisfactory alternative. Early recovery was more rapid in patients anaesthetized with desflurane, but this group had a worse overall mood score, and a higher incidence of minor postoperative complications compared to the group in which anaesthesia was based on isoflurane. Postural stability was affected at 45 min after midazolam administration. The perceptive accuracy test was found to be sensitive in the detection of residual effects of anaesthetics, it was not associated with significant 'learning', it was easy to use, and the results obtained were 'on-line' and did not require tedious calculations.

In summary, induction of anaesthesia with propofol followed by maintenance with isoflurane in oxygen and air, and alfentanil for analgesia is associated with rapid recovery, minimal post-operative complications and good overall mood scores. total intravenous anaesthesia based on propofol is a suitable alternative. Computerized dynamic posturography is a new method for studying balance disturbances. Perceptive accuracy test is sensitive in the detection of residual effects of anaesthetics but more studies are needed to describe its exact place amongst the battery of psychomotor tests.