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Objectives Regional anesthesia for patients undergoing carotid endarterectomy is associated with improved intraoperative hemodynamic stability compared with general anesthesia. The authors hypothesized that the reported advantages might be related to attenuated ipsilateral baroreflex control of blood pressure, caused by chemical denervation of the carotid bulb baroreceptor nerve fibers. Design A prospective cohort study. Setting Single-center university hospital. Participants The study included 46 patients undergoing carotid endarterectomy using superficial cervical block. Interventions A noninvasive computational periprocedural measurement of baroreceptor sensitivity was performed in all patients. Two groups were formed, depending on the patients’ subjective response to surgical stimulation regarding the necessity of additional intraoperative local anesthesia (LA) administration on the carotid bulb. Group A (block alone) included 23 patients who required no additional anesthesia, and group B (block + LA) consisted of 23 patients who required additional anesthesia. Measurements and Main Results Baroreceptor sensitivity showed no significant change after application of the block in both groups (group A: median [IQR], 5.19 [3.07-8.54] v 4.96 [3.1-9.07]; p = 0.20) (group B: median [IQR], 4.47 [3.36-8.09] v 4.53 [3.29-8.01]; p = 0.55). There was a significant decrease in baroreceptor sensitivity in group B after intraoperative LA administration (median [IQR], 4.53 [3.29-8.01] v 3.31 [2.26-7.31]; p = 0.04). Conclusions Standard superficial cervical plexus block did not impair local baroreceptor function, and, therefore, it was not related to improved cerebral perfusion in awake patients undergoing carotid endarterectomy. However, direct infiltration of the carotid bulb was associated with the expected attenuation of baroreflex sensitivity.

IntroductionPostoperative pancreatic fistula (POPF) is still the most frequently occurring and clinically relevant complication after distal pancreatectomy (DP). Preoperative endoscopic injection of botulinum toxin (BTX) into the sphincter of Oddi represents an innovative approach to prevent POPF. The aim of this project (PREBOTPilot) is to generate the first randomised controlled trial data on the safety, feasibility and efficacy of preoperative endoscopic BTX injection into the sphincter of Oddi to prevent clinically relevant POPF following DP.Methods and analysisPREBOTPilot is an investigator-initiated, single-centre, randomised, controlled, open-label, phase II clinical trial with two parallel study groups and an exploratory study design. 60 patients scheduled for DP will be randomised to intervention and control group. In the intervention group, patients will undergo preoperative endoscopic injection of BTX into the sphincter of Oddi, whereas in the control group no preoperative endoscopy will be performed. The combined primary endpoint is the occurrence of clinically relevant POPF and/or death within 30 days after DP. The secondary endpoints comprise further postoperative outcome parameters and quality of life up to 3 months after DP as well as safety and feasibility of the procedure. Statistical analysis is based on the modified intention-to-treat population, excluding patients without status post DP. For safety analysis, rates of adverse events (AEs) and serious AEs will be calculated with 95% CIs for group comparisons.Ethics, funding and disseminationPREBOTPilot has been approved by the German Federal Institute for Drugs and Medical Devices (reference number 4043654) and the Ethics Committee of Heidelberg University (reference number AFmo-523/2019). This trial is supported by the German Federal Ministry of Education and Research (BMBF). The results of the trial will be presented at national and international conferences and published in a peer-reviewed journal.Trial registration numberDRKS00020401.

Summary Liver transplant recipients are at a significant risk for invasive fungal infections (IFI). This retrospective study evaluated the impact of the pretransplant model for end stage liver disease (MELD) on the incidence of posttransplant IFI in a single centre. From 2004 to 2008, 385 liver transplantations were included, from which 210 transplantations were conducted allocated by Child Turcotte Pugh and 175 were allocated by MELD score. Both groups differed regarding the age of transplant recipients (50.1 ± 10.7 vs. 52.5 ± 9.9, P = 0.036), pretransplant MELD score (16.43 ± 8.33 vs. 18.29 ± 9.05), rate of re-transplantations, duration of surgery, demand in blood transfusions and rates of renal impairments. In the MELD era, higher incidences of IFI (pre-MELD 11.9%, MELD 24.0%, P

Background In the pathogenesis of sepsis, inflammation-induced changes in coagulation play a pivotal role. Methods In total, 90 patients (30 patients with septic shock, 30 surgical patients following major abdominal surgery and 30 healthy volunteers) were enrolled. Blood samples from patients with septic shock were collected at the time of sepsis diagnosis as well as 24 h, 4 days, 7 days, 14 days and 28 days later. Samples from surgical patients with a post-surgical inflammatory response were collected three times (before surgery, immediately after surgery and 24 h after surgery) and once from healthy volunteers. Thromboelastometry (ROTEM ®), as well as whole blood impedance aggregometry (Multiplate®) were performed. Additionally, plasma concentrations of interleukin-6 and tumour necrosis factor-alpha were measured using enzyme-linked immunosorbent assay kits. Results Thromboelastometry lysis index was shown to be a reliable biomarker for septic shock. Furthermore, in septic patients with overt disseminated intravascular coagulation, thromboelastometry revealed signs indicating a hypocoagulable status, whereas patients without overt disseminated intravascular coagulation were found to be hypercoagulable. Platelet aggregation capability, as assessed by whole blood impedance aggregometry, was significantly reduced in septic patients with overt disseminated intravascular coagulation, whereas it was comparable with healthy volunteers and in septic patients without overt disseminated intravascular coagulation. Conclusion Viscoelastic and aggregometric point-of-care testing was shown to be potentially useful for bedside diagnosis of sepsis. Moreover, viscoelastic and aggregometric point-of-care testing was able to determine the phase of septic coagulopathy (hypercoagulability vs. hypocoagulability) and therefore identified patients at high risk for overt disseminated intravascular coagulation.

Background: The safety and efficacy of subcutaneous immunotherapy (SCIT) with the high-dose hypoallergenic preparations Allergovit® have been well documented in several randomised clinical trials. The following study aimed to confirm these results in daily practice.

Background: Opinions about satisfaction with care are rarely obtained from disabled children and their carers, and few studies of this type exist in the area of pediatric anesthesia. We specifically aimed to assess groups of children with disabilities and Down syndrome and aimed to identify factors influencing satisfaction in these groups. Methods: We assessed two groups of children using the Paediatric Perianesthesia Questionnaire (PPQ). Families with Down syndrome children (Down syndrome group, DSG) were approached via a Down syndrome family support magazine, and families with disabled children were enrolled in hospitals. Two hundred and fifteen disabled children (125 from the journal, 90 from the hospitals) were compared to matching controls without disabilities. Controls were drawn randomly using computer-generated tables of random numbers using data from the PPQ validation, to match cases for confounding variables. Results: Satisfaction was lower in both groups with disabilities (P < 0.05) (lowest in the DSG), fewer would choose the hospital or anesthetic department again. In both of the disabled groups, negative comments were related to the anesthetists' behavior during the consultation, the content of the consultation, and how anxiety was dealt with. Ninety five percent in the DSG reported that the anesthetist had not mentioned or enquired about atlantoaxial instability. Satisfaction was lower than the rest of the respective group if memories of the disclosure of the disabling condition were negative (P = 0.006) or if potential offensive terms had been used during the consultation (P < 0.001). Conclusions: This is the first study to assess families with disabled children for satisfaction with anesthesia. Our findings suggest that parents of children with disabilities are less satisfied with their anesthetic care than parents of children without disabilities. Potential bias comes from the self-selection of the DSG and the recall period in this group.

Background Securing the airway by means of endotracheal intubation (ETI) represents a fundamental skill for anaesthesiologists in emergency situations. This study aimed to evaluate the time needed by first-year anaesthesiology residents to perform 200 ETIs and assessed the associated success rates and number of attempts until successful ETI. Methods This prospective single centre study evaluated the number of working days, the success rate, the attempts needed until successful ETI in consecutive blocks of 25 ETI procedures and the related difficulties and complications. Results From 2007 to 2010, 21 residents were evaluated consecutively. These residents needed a mean (mean ± standard deviation) of 15.6 ± 3.0 days for 25 ETIs. Out of all residents 52% reached the target value of 200 ETIs after 50.2 ± 14.8 weeks of total working time. The ETI success rate after the first 25 ETIs increased steadily to the results after 200 ETIs (ETI success rate within one ETI attempt: 67% vs. 83%, P = 0.0001; ETI success rate within all ETI attempts: 82% vs. 92%, P = 0.0001). The number of attempts required until successful ETI decreased from 1.6 ± 0.8 after the first 25 ETIs to 1.3 ± 0.6 after 200 ETIs (P = 0.0001). Conclusion The increasing rate of relative ETI success and the decreasing rate of necessary attempts for successful airway management suggest a steadily increasing gain in ETI experience. The complications that developed during the first 200 ETI procedures justify supervision by a specialist in the field or a senior physician. Moreover, these results may influence the minimum requirement for qualification in anaesthesiology and emergency medicine.

To evaluate the effectiveness and safety of infrahepatic inferior vena cava (IVC) clamping for reduction of central venous pressure (CVP) and blood loss during hepatic resection.Low CVP during parenchymal transection has been widely accepted to reduce intraoperative hemorrhage via the hepatic veins and is commonly achieved by anesthesiological interventions such as fluid restriction. We hypothesized that infrahepatic clamping of the IVC may lower the intraoperative blood loss more effectively and, moreover, prevent potential adverse effects of fluid restriction such as hemodynamic instability.Patients scheduled for elective hepatic resection were enrolled and allocated randomly to CVP reduction by infrahepatic IVC clamping or anesthesiological interventions including primarily fluid restriction with additional use of diuretics, nitro compounds, and opioids (control group). The primary efficacy endpoint was total intraoperative blood loss. Analyses were done following intention-to-treat principles. The protocol was submitted to the clinicaltrials.gov registry (NCT00732979).From April 2007 to December 2009, a total of 152 patients were randomized and 128 were eligible for final analyses. Baseline data were similar between both study groups. Despite higher CVP values during resection (4.0 ± 3.2 vs. 2.6 ± 1.8 mm Hg; P = 0.003), infrahepatic IVC clamping significantly reduced total intraoperative blood loss [550 (350.0-1150) mL vs. 900 (500-1500) mL; P = 0.02] and blood loss during parenchymal transection [150 (85-500) mL vs. 400 (200-700) mL; P = 0.006] compared with the control group. Postoperative mortality [4 (6.1%) vs. 2 (3.2%); P = 0.42] and total morbidity rates [38 (58.5%) vs. 37 (58.7%); P = 0.97] were comparable between both study groups. Although intraoperative hemodynamic instability occurred less frequently in patients with infrahepatic IVC clamping [0 vs. 4 (6.3%); P = 0.04], the incidence of pulmonary embolism was increased in this study arm [4 (6.1%) vs. 0; P = 0.04].Infrahepatic IVC clamping is associated with significantly less intraoperative blood loss and may reduce the incidence of intraoperative hemodynamic instability. The potential association with postoperative pulmonary embolism represents a significant concern.

Surgical intensive care units (ICU) play a pivotal role in perioperative care of patients undergoing major abdominal surgery. Differences in quality of care provided by medical staff in ICUs may be linked to improved outcome. This review aims to elucidate the relationship between quality of care at various ICUs and patient outcome, with the ultimate aim of identifying key measures for achieving optimal outcome.We reviewed the literature in PubMed to identify current ICU structural and process concepts and variations before evaluating their respective impact on quality of care and outcome in major abdominal surgery.ICU leadership, nurse and physician staffing, and provision of an intermediate care unit are important structural components that impact on patients' outcome. A "mixed ICU" model, with intensivists primarily caring for the patients in close cooperation with the primary physician, seems to be the most effective ICU model. Surgeons' involvement in intensive care is essential, and a close cooperation between surgeons and anesthesiologists is vital for good outcome. Current general process concepts include early mobilization, enteral feeding, and optimal perioperative fluid management. To decrease failure-to-rescue rates, procedure-specific intensive care processes are particularly focused on the early detection, assessment, and timely and consistent treatment of complications.Several structures and processes in the ICU have an impact on outcome in major abdominal surgery. ICU structures and care processes connected with optimal outcome could be transmitted to other centers to improve outcome, independent of procedure volume.

Background Recent evidence suggests that the endothelial glycocalix plays an important role in lethal outcomes following sepsis. We therefore tested if the endothelial glycocalix is shed in patients with sepsis compared with patients after major abdominal surgery and healthy volunteers. Material and Methods A total of 150 individuals were tested for levels of inflammatory markers (intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], interleukin-6 [IL-6]) and glycocalix markers (syndecan-1, heparan sulfate). Three groups consisted of patients with severe sepsis or septic shock, patients after major abdominal surgery without systemic inflammatory response syndrome, and healthy volunteers. Blood was drawn, at the time of diagnosis or surgery, and 6, 24, and 48 h later. We correlated these markers to each other and to clinically used inflammation markers. Results Levels of inflammatory markers were markedly higher in patients with sepsis compared with patients after major abdominal surgery and healthy volunteers. After major abdominal surgery, glycocalix markers in human plasma were at levels comparable to patients with sepsis. In patients with sepsis, levels of IL-6 correlated with syndecan-1, ICAM-1, VCAM-1, and lactate, while ICAM-1 furthermore correlated with CRP and lactate levels. Conclusion High levels of glycocalix markers indicated that significant flaking of the endothelial glycocalix occurred in patients with sepsis, and to a lesser extent in patients after major abdominal surgery. This novel finding could explain the nonspecific capillary leaking syndrome of patients with sepsis and after major abdominal surgery, and may identify new targets for treating those patient populations.

Background Severe sepsis, septic shock, and resulting organ failure appear as the most common cause of death in intensive care medicine. Inflammatory mediators (interleukin-6/IL-6), cell adhesion molecules (intercellular adhesion molecule-1/ICAM-1, vascular cell adhesion molecule-1/VCAM-1), and redox active substances (manganese superoxide dismutase/MnSOD, macrophage migration inhibitory factor/MIF) must be considered to be central hubs in the inflammatory process. However, their exact pathophysiologic function and prognostic value are still poorly understood. Materials and Methods In total, 133 individuals (87 patients with severe sepsis or septic shock, 28 postoperative patients after major abdominal surgery, 18 healthy volunteers) were enrolled in the study. Blood samples from septic patients were collected within 24 h after the time of sepsis diagnosis, and 48 and 120 h later; samples from healthy volunteers were collected once, and samples from postoperative patients once immediately after surgery. In all patients we measured plasma levels of IL-6, sICAM-1, sVCAM-1, MnSOD, and MIF using enzyme linked immunosorbent assay (ELISA) kits. Results Healthy volunteers and postoperative patients showed comparable levels of cell adhesion molecules. Furthermore, their redox system was activated in a comparable manner, whereas in postoperative patients IL-6 was significantly elevated. Plasma levels of inflammatory mediators, cell adhesion molecules and redox active substances were significantly elevated in septic patients. In patients with sepsis who had died, plasma levels of MIF and MnSOD were significantly elevated in comparison with survivors. Conclusions Our results therefore demonstrate that redox active substances may play an important role in the septic inflammatory response. MIF and MnSOD appear to be early predictors for survival in septic patients.

Increased patients' serum anticholinergic activity (SAA) is described as a marker of cognitive dysfunction and can be influenced by different exogenous and endogenous factors. The role of cortisol in relation to SAA and cognition in perioperative conditions has not been investigated so far. In 30 men scheduled for urological surgery, the authors determined SAA and cortisol levels in blood and CSF and conducted neuropsychological testing in two subgroups with comparable pre- and intraoperative characteristics, one group with low SAA (mean=2.4 [SD=0.9], n=23) and the other with high SAA (mean=5.1 [SD=2.4], n=7) values. Increased SAA was associated with two times the number of anticholinergic medications but not with patients' age, medical history or impaired cognition. A significant linear correlation was detected between anticholinergic activities and cortisol levels. Thus, endogenous factors such as patients' stress levels should be taken into account for interpretation of the role of SAA.

It is difficult to substantiate the clinical diagnosis of postoperative delirium with objective parameters in intensive care units (ICU). The purpose of this study was to analyze (1) whether the bilateral bispectral (BIS) index, (2) cortisol as a stress marker, and (3) interleukin-6 as a marker of inflammation were different in delirious patients as compared to nondelirious ones after cardiac surgery. On the first postoperative day, delirium was analyzed in 114 patients by using the confusion assessment method for ICU (CAM-ICU). Bilateral BIS data were determined; immediately thereafter plasma samples were drawn to analyze patients’ blood characteristics. The current ICU medication, hemodynamic characteristics, SOFA and APACHE II scores, and artificial ventilation were noted. Delirium was detected at 19.1 ± 4.8 h after the end of surgery in 32 of 114 patients (28%). Delirious patients were significantly older than nondelirious ones and were artificially ventilated 4.7-fold more often during the testing. In delirious patients, plasma cortisol and interleukin-6 levels were higher (p = 0.01). The mean BIS index was significantly lower in delirious patients (72.6 (69.6–89.1); median [interquartile range (IQR), 25th–75th percentiles] than in nondelirious patients, 84.8 (76.8–89.9). BIS EEG raw data analysis detected significant lower relative alpha and higher theta power. A significant correlation was found between plasma cortisol levels and BIS index. Early postoperative delirium after cardiac surgery was characterized by increased stress levels and inflammatory reaction. BIS index measurements showed lower cortical activity in delirious patients with a low sensitivity (27%) and high specificity (96%).

In recent years delirium in the intensive care unit (ICU) has internationally become a matter of rising concern for intensive care physicians. Due to the design of highly sophisticated ventilators the practice of deep sedation is nowadays mostly obsolete. To assess a ventilated ICU patient for delirium easy to handle bedside tests have been developed which permit a psychiatric scoring. The significance of ICU delirium is equivalent to organ failure and has been proven to be an independent prognostic factor for mortality and length of ICU and hospital stay. The pathophysiology and risk factors of ICU delirium are still insufficiently understood in detail. A certain constellation of pre-existing patient-related conditions, the current diagnosis and surgical procedure and administered medication entail a higher risk for the occurrence of ICU delirium. A favored hypothesis is that an imbalance of the neurotransmitters acetylcholine and dopamine serotonin results in an unpredictable neurotransmission. Currently, the administration of neuroleptics, enforced physiotherapy, re-orientation measures and appropriate pain treatment are the basis of the therapeutic approach.

In acute lung injury (ALI) pulmonary hyporesponsiveness to inhaled nitric oxide (iNO) still represents an unresolved clinical challenge. In septic ALI-patients the incidence of hyporesponsiveness to iNO is increased; therefore, endotoxemia appears to play a major role. Experimental data suggest that endotoxemia, e.g., induced by lipopolysaccharides (LPS), contribute to the hyporesponsiveness to iNO. Guanosine 3',5'-cyclic monophosphate (cGMP) is metabolized by phosphodiesterases (PDE). The role of PDE in reduced pulmonary vascular response in experimental endotoxemia is still not known. Here, we hypothesized that PDE activity modulates initial pulmonary responsiveness to iNO in ALI following systemic endotoxin exposure. Rats were treated with LPS or used as controls. Lungs were isolated-perfused 0-36 h after LPS injection and the synthetic thromboxane analogue U46619 was added to increase pulmonary artery pressure by 6-8 mmHg (n = 47). Then, the pulmonary vasodilatory response to 3 doses of iNO (0.4, 4 and 40 ppm) was measured. Furthermore, lungs were prepared as described previously, and 2, 10, and 18 h after LPS the change in pulmonary artery pressure in response to two different inhibitors of PDE, one of which is PDE sensitive (8-Br-cGMP) and one is PDE stable (8-pCPT-cGMP), was determined (n = 43). Serum nitrite/nitrate levels started to increase 4 h after LPS, with a maximum at 18 h. In contrast, decreased pulmonary vasoreactivity in response to iNO developed as early as 2 h later and remained depressed up to 18 h. The pulmonary vasoreactivity to the PDE-sensitive 8-Br-cGMP after LPS-stimulation was lower than that in lungs treated with the PDE-stable 8-pCPT-cGMP. In rats pretreated with LPS, hyporesponsiveness of pulmonary vessels to iNO is time-limited and associated with increased serum nitrite/nitrate levels, and appears to be attributed in part to increased pulmonary PDE activity.

We have developed a questionnaire to assess patients' peri-anaesthetic satisfaction. We recruited 1398 patients and 59 health care professionals for construction and validation. Relevant items were rated for preferences. The resulting questions underwent a cognitive and a standard pretest. The resultant Heidelberg Peri-anaesthetic Questionnaire consists of 38 questions about five identified themes: trust and atmosphere; fear; discomfort; treatment by personnel; and information and waiting. Internal consistency was demonstrated for the sum score (Cronbach's alpha = 0.79) and the five factors (Cronbach's alpha = 0.42-0.79). Multivariate analysis found significant influences of age, school education, marital status and duration of anaesthesia. Dissatisfied patients had a median (IQR [range]) of 73% (66-76% [35-83]), and satisfied patients 92% (90-94% [88-100]) of the sum score. The Heidelberg Peri-anaesthetic Questionnaire offers a valid and reliable way to identify dissatisfied patients and generate quality improvement and also has use as a benchmark tool.

The pathogenesis and mechanisms of septic encephalopathy are not completely understood. We compared two different models of sepsis: lipopolysaccharide-induced endotoxemia and cecal ligation and puncture (CLP) bacteremia in rats with respect to changes in endothelial expression of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), platelet-endothelial cell adhesion molecule-1 (PECAM-1), and of cerebral albumin extravasation as a marker for capillary breakdown of the blood brain barrier.Male Wistar rats were divided into control, endotoxemia, or CLP-group. Mean arterial blood pressure was measured via femoral artery catheterization. Brain tissue for immunohistochemistry was harvested at 1 h, 6 h, and 24 h after induction of sepsis.The CLP-group showed a decrease in mean arterial pressure after 24 h in comparison with the sham-group (P0.05). Cerebral ICAM-1 expression was at its maximum 24 h after induction of sepsis, with the highest expression in the CLP-group. There was no difference in PECAM-1 expression between the groups. Cerebral albumin extravasation increased early after 6 h in both septic groups with a maximum at 24 h after induction of sepsis.These results suggest that there are early changes in the integrity of the blood-brain barrier in the central nervous system in an ongoing septic progress. This provides evidence that these changes are due to inflammatory mediators, and not to the presence of live bacteria. Increased ICAM-1 expression might be an early factor involved in these pathogenic events. Although the role of PECAM-1 cannot conclusively be determined, we were able to show its expression on cerebral endothelium in all groups.

Lethal sepsis occurs when an excessive inflammatory response evolves that cannot be controlled by physiologic anti-inflammatory mechanisms, such as the recently described cholinergic anti-inflammatory pathway. Here we studied whether the cholinergic anti-inflammatory pathway can be activated by pharmacologic cholinesterase inhibition in vivo.Prospective, randomized laboratory investigation that used an established murine sepsis model.Research laboratory in a university hospital.Female C57BL/6 mice.Sepsis in mice was induced by cecal ligation and puncture. Animals were treated immediately with intraperitoneal injections of nicotine (400 microg/kg), physostigmine (80 microg/kg), neostigmine (80 microg/kg), or solvent three times daily for 3 days.Treatment with physostigmine significantly reduced lethality (por = .01) as efficiently as direct stimulation of the cholinergic anti-inflammatory pathway with nicotine (por = .05). Administration of cholinesterase inhibitors significantly down-regulated the binding activity of nuclear factor-kappaB (por = .05) and significantly reduced the concentration of circulating proinflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 (por = .001), and pulmonary neutrophil invasion (por = .05). Animals treated with the peripheral cholinesterase inhibitor neostigmine showed no difference compared with physostigmine-treated animals.Our results demonstrate that cholinesterase inhibitors can be used successfully in the treatment of sepsis in a murine model and may be of interest for clinical use.

Alterations in microcirculatory permeability are a characteristic of early tissue injury. Moreover, tissue edema is an early indicator of tissue dysfunction, prior to organ failure, because tissue edema is associated with impaired gas exchange, arterial hypoxemia, and may also impair tissue oxygen distribution. As a result of increased microvascular permeability, plasma fluid is lost into the interstitial space, leading to hypovolemia. Currently, no effective pharmacological therapy is available to reduce increased permeability. High mortality rate in sepsis is still mainly associated with endothelial damage. In this regard platelets, besides leukocytes, play a major role for the development of microvascular hyperpermeability. This review considers endothelial cell dysfunction during endotoxemia including current insights into sepsis pathophysiology. New aspects of this complex pathogenesis are illustrated and their relevance for clinical sepsis therapy is emphasized.

Background Levels of pro- and anti-inflammatory cytokines have been determined in numerous investigations. However, measurements of isolated cytokines do not allow conclusions on the resulting immune state. The purpose of this study was to determine resulting immune functions in patients’ plasma. Additionally, similar measurements were performed with ultrafiltrate gained from continuous venovenous hemofiltration (CVVH). Materials and Methods Nine septic patients and six critically ill patients with renal dysfunction in a surgical intensive care unit were observed. Two immune functions were chosen for detailed investigation over a time period of 72 h. The ability of patients’ plasma to induce or suppress β 2 -integrin expression on neutrophils of healthy controls served as marker for leukocyte activation. Interleukin (IL)-6 production or inhibition in washed whole blood cells induced through patients’ plasma was used as a marker of cytokine secretion. Results Plasma from septic patients led to a constantly increased expression of β 2 -integrins on isolated, unstimulated neutrophils. At the same time, septic plasma permanently suppressed the production of IL-6 and IL-10 in stimulated whole blood. Ultrafiltrate from CVVH mirrors the equivalent immune response patterns found for plasma. We did not find significant differences pre- and postfilter or over the next 72 h in the potential to cause IL-6 and IL-10 production or β 2 -integrin expression. Conclusions Plasma from septic patients triggers an increased expression of adhesion molecules and inhibited secretion of IL-6 and IL-10 in stimulated whole blood cells compared with nonseptic critically ill patients. Moreover, CVVH withdraws triggering mediators from plasma in equally bioactive proportions.

To compare a modified pulmonary artery catheter (PAC) and pulse-contour analysis by the PiCCO (Pulsion Medical Systems, Munich, Germany) system for continuous assessment of cardiac output in patients with septic shock. In addition, to assess the relationships between an index of global end-diastolic volume (GEDV) derived by the PiCCO system with traditional PAC-derived indicators of filling: central venous pressure; pulmonary artery occlusion pressure; and right ventricular end-diastolic volume (RVEDV). Prospective cohort study. Surgical intensive care unit of a university hospital. 14 patients with septic shock. None. A significant correlation was found between continuous cardiac output by PAC (CCOPAC) and by pulse-contour analysis (r 2 = 0.714, p

Successful management of emergency patients with multiple trauma in the hospital resuscitation room depends on the immediate diagnosis and rapid treatment of the most life-threatening injuries. In order to reduce the time spent in the resuscitation room, an in-hospital algorithm was developed in an interdisciplinary team approach with respect to local structures. The aim of the study was to analyse whether this algorithm affects the interval between hospital admission and the completion of diagnostic procedures and the start of life-saving interventions. Moreover, in-hospital mortality was investigated before and after the algorithm was introduced.In this prospective study, all consecutive trauma patients in the resuscitation room were investigated before (group I, 01/04-10/04) and after (group II, 01/05-11/05) introduction of the algorithm. The times between hospital admission and the end of the diagnostic procedures (ultrasound [sono], chest X-ray [CF], and cranial computed tomography [CCT]), and between hospital admission and the start of life-saving interventions were registered and in-hospital mortality analysed.In the study period, 170 patients in group I and 199 patients in group II were investigated. Injury severity score (ISS) were comparable between the two groups. The intervals between admission and completion of diagnostic procedures were significantly lower after the algorithm was introduced (mean+/-S.D.): sono (11 +/- 10 min versus 7 +/- 6 min, p0.05), CF (21 +/- 12 min versus 12 +/- 9 min, p0.01), and CCT (55 +/- 27 min versus 32 +/- 14 min, p0.01). Moreover, the interval to the start of life-saving interventions was significantly shorter (126 +/- 90 min versus 51 +/- 20 min, p0.01). After introducing the algorithm, in-hospital mortality was reduced significantly from 33.3% to 16.7% (p0.05) in the most severely injured patients (ISSor=25).The introduction of an algorithm for early management of emergency patients significantly reduced the time spent in the resuscitation room. The periods to completion of sono, CF, and CCT, respectively, and the start of life-saving interventions were significantly shorter after introduction of the algorithm. Moreover, introduction of the algorithm reduced mortality in the most severely injured patients. Although further investigations are needed to evaluate the effects of the Heidelberg treatment algorithm in terms of outcome and mortality, the time reduction in the resuscitation room seems to be beneficial.

Inhalation of nitric oxide (NO) and inhibition of phosphodiesterase type 5 (PDE5) selectively dilate the pulmonary circulation in patients with acute lung injury (ALI) associated with pulmonary hypertension. PDE5 inhibitors administered at doses that decrease pulmonary artery pressures have been shown to worsen arterial oxygenation. We investigated the efficacy of doses of PDE5 inhibitors that do not reduce pulmonary artery pressure alone (subthreshold doses) to improve the response to inhaled NO in an animal model of ALI.Adult Sprague-Dawley rats were pre-treated with 0.5 mg/kg Escherichia coli 0111:B4 endotoxin and 16 to 18 h later, their lungs were isolated perfused and ventilated. The thromboxane mimetic U46619 was used to induce pulmonary hypertension. After the determination of subthreshold doses of two different PDE5 inhibitors, either 50 microg zaprinast or 10 ng sildenafil was added to the perfusate and the decrease of pulmonary artery pressure measured in the presence and absence of inhaled NO.In the presence of 4 or 10 ppm NO, zaprinast (-1.6 +/- 0.4 and -2.9 +/- 0.6 mmHg, respectively) and sildenafil (-1.9 +/- 0.4 and -2.4 + 0.3 mmHg, respectively) improved responsiveness to inhaled NO compared to lungs from rats treated with LPS only (0.7 +/- 0.1 and -1.0 +/- 0.1 mmHg, respectively; P0.05). Neither zaprinast nor sildenafil prolonged the pulmonary vasodilatory response to inhaled NO.Subthreshold doses of PDE5 inhibitors improved responsiveness to inhaled NO. Combining inhaled NO with subthreshold doses of PDE5 inhibitors may offer a therapeutic strategy with minimal side-effects in ALI associated with pulmonary hypertension.

Previous studies have suggested a possible link between cognitive impairment and anticholinergic burden as reflected by high serum anticholinergic activity (SAA). Thus, we hypothesized a close relationship between anticholinergic activity in cerebral spinal fluid (CSF) and blood. However, it has never been convincingly demonstrated that peripheral anticholinergic activity correlates with central anticholinergic levels in presurgical patients. Therefore, anticholinergic activity was measured in blood and CSF from 15 patients with admission scheduled for urological surgery to compare peripheral and central anticholinergic level. Blood and CSF probes were taken after routine premedication and before spinal anesthesia. Anticholinergic activity was determined by competitive radioreceptor binding assay for muscarinergic receptors. Correlation analysis was conducted for peripheral and central anticholinergic levels. The mean anticholinergic levels were 2.4+/-1.7 in the patients' blood and 5.9+/-2.1 pmol/mL of atropine equivalents in CSF. Interestingly, the anticholinergic activity in CSF was about 2.5-fold higher than in patients' blood. A significant linear correlation was detected between blood and CSF levels. Therefore we conclude that SAA levels adequately reflect central anticholinergic activity. When patients receiving or not receiving anticholinergic medication were compared, anticholinergic activity tended to increase in blood and CSF after receiving anticholinergic medication > or =4 weeks (p>0.05).

Patients with malignant diseases are increasingly being treated with multimodal therapeutical concepts based on the three major modalities surgery, radiotherapy and chemotherapy. The perioperative period is crucial within this multimodal concept as the prognosis of patients may be directly influenced by perioperative measures. In addition, it is of major importance to avoid complications in the perioperative phase, as these might worsen the prognosis of the patient and in order to prevent a delay in the beginning of planned adjuvant therapies. These aspects demonstrate the important role of anesthesia in the treatment of patients with cancer. Further studies defining the relevance of anesthesiologic measures in oncologic patients are needed.

Kontinuierliche Verbesserungen chirurgischer und auch anasthesiologischer Techniken haben zu einer wesentlichen Reduktion perioperativer Komplikationen gefuhrt. Der postoperative Verlauf viszeralchirurgischer Patienten, deren individuelle postoperative Rekonvaleszenz und letztendlich auch die Dauer des stationaren Aufenthaltes werden mehr und mehr durch das klinische Bild des postoperativen Ileus bestimmt. In der vorliegenden Arbeit werden die moglichen Einflussgrosen diskutiert. Daruber hinaus werden die Moglichkeiten der Pravention und Therapie des postoperativen Ileus kurz dargestellt.

The role of reactive carbonyl species, such as methylglyoxal (MG), has been overlooked within the context of the sepsis syndrome. The aims of this study were to assess the impact of MG formation in different inflammatory settings and to evaluate its use for early diagnosis as well as prognosis of the sepsis syndrome. In total, 120 patients in three groups were enrolled in this observational clinical pilot study. The three groups included patients with septic shock (n = 60), postoperative controls (n = 30), and healthy volunteers (n = 30). Plasma samples from patients with septic shock were collected at sepsis onset and after 24 hours and 4, 7, 14, and 28 days. Plasma samples from postoperative controls were collected prior to surgery, immediately following the end of the surgical procedure as well as 24 hours later and from healthy volunteers once. Plasma levels of MG were determined by high-performance liquid chromatography. Additionally, plasma levels of procalcitonin, C-reactive protein, soluble CD14 subtype, and interleukin-6 were determined. Patients with septic shock showed significantly higher plasma levels of MG at all measured times, compared with postoperative controls. MG was found to identify patients with septic shock more effectively—area under the curve (AUC): 0.993—than procalcitonin (AUC: 0.844), C-reactive protein (AUC: 0.791), soluble CD14 subtype (AUC: 0.832), and interleukin-6 (AUC: 0.898) as assessed by receiver operating characteristic (ROC) analysis. Moreover, plasma levels of MG in non-survivors were significantly higher than in survivors (sepsis onset: *P = 0.018 for 90-day survival; **P = 0.008 for 28-day survival). Plasma levels of MG proved to be an early predictor for survival in patients with septic shock (sepsis onset: ROC-AUC 0.710 for 28-day survival; ROC-AUC 0.686 for 90-day survival). MG was identified as a marker for monitoring the onset, development, and remission of sepsis and was found to be more useful than routine diagnostic markers. Further studies are required to determine the extent of MG modification in sepsis and whether targeting this pathway could be therapeutically beneficial to the patient. German Clinical Trials Register DRKS00000505 . Registered 8 November 2010.

Summary We investigated the association of peri-operative myocardial ischaemia with activation of coagulation and endogenous fibrinolysis in patients undergoing vascular surgery. In 50 patients, continuous Holter monitoring was performed to assess peri-operative myocardial ischaemia and 12-lead electrocardiography was recorded preoperatively and 72 h postoperatively to assess myocardial infarction. Serial blood samples were drawn peri-operatively to determine the concentrations of fibrin monomers (for activation of coagulation), d-dimer (for endogenous fibrinolysis) and cardiac troponin T and I. Patients with myocardial ischaemia showed higher concentrations of fibrin monomers at 48 h, and higher concentrations of d-dimer preoperatively and at 24 and 48 h postoperatively. In patients with peri-operative myocardial ischaemia, strong positive correlations were observed between fibrin monomer and d-dimer concentrations at 15 min and 4 h postoperatively, and cardiac troponins at 15 min and at 4, 24, 48 and 72 h postoperatively. Early postoperative activation of coagulation and fibrinolysis is associated with peri-operative myocardial cell damage among patients who are at risk for, or have a history of, coronary artery disease plus peri-operative myocardial ischaemia.

Using magnetic resonance imaging techniques, we examined the time course of apparent diffusion coefficient (ADC), T2, and T2* relaxation times in 1-year-old rats after different forms of cerebral oligemia had been induced by (1) transient systemic hypotension, (2) permanent bilateral carotid artery occlusion (BCCAO), and (3) combined hypotension and BCCAO over a time period of 14 days after the oligemic event. These groups were compared with a group of sham-operated adult rats (controls, 4) to rule out a drift of the parameters over time. The animals were examined in a 2.35 T scanner. ADC, T2, and T2* were measured in both hemispheres of rat parietotemporal cerebral cortex, thalamic nuclei, and hippocampus 1 day before as well as on days 1, 3, 7, and 14 after sham operation and in different models of oligemia, respectively. Hypotension alone had no significant effect on MRI parameters in rat brain. After BCCAO, an increase in T2* was observed. If a permanent BCCAO was combined with transient hypotension, however, 84% of 1-year-old animals died within 14 days after surgery. In the surviving animals, significant changes in ADC, T2, and T2* were observed in the hippocampus and parietotemporal cerebral cortex. ADC showed a decrease on day 1 after oligemia, and an increase on days 3, 7, and 14. The T2* and T2 values were markedly increased on days 7 and 14 after surgery. In conclusion, only severe oligemia combining BCCAO and hypotension induces significant changes in tissue integrity (as shown by ADC) and in blood oxygenation levels in the subchronic period, whereas no significant changes were detected if permanent BCCAO or transient hypotension was applied separately.

Compared with bupivacaine, acute myotoxicity of ropivacaine is less severe. Thus, in this study we compared the long term myotoxic effects of both drugs in a clinically relevant setting. Femoral nerve catheters were inserted in anesthetized pigs, and either 20 mL of bupivacaine (5 mg/mL) or ropivacaine (7.5 mg/mL) was injected. Subsequently, bupivacaine (2.5 mg/mL) and ropivacaine (3.75 mg/mL) were continuously infused (8 mL/h) over 6 h. Control animals were treated with corresponding volumes of normal saline. After 7 and 28 days, respectively, muscle samples were dissected at the former injection sites, and histological patterns of muscle damage were blindly scored (0 = no damage to 3 = marked lesions/myonecrosis) and compared. No morphological tissue changes were detected in control animals. In the observed period, both local anesthetics induced morphologically identical patterns of calcific myonecrosis, formation of scar tissue, and a marked rate of fiber regeneration. However, bupivacaine's effects were constantly more pronounced than those of ropivacaine. These data show that both drugs induce irreversible skeletal muscle damage in a clinically relevant model, and confirm the exceeding rate of myotoxicity of bupivacaine. However, the clinical impact of these long term myotoxic effects still has to be assessed.In a period of 4 wk after peripheral nerve block, both long-acting local anesthetics, bupivacaine and ropivacaine, produced calcific myonecrosis suggestive of irreversible skeletal muscle damage. In comparison with ropivacaine, however, the extent of bupivacaine-induced muscle lesions was significantly larger.

ObjectivesWe sought to evaluate the efficacy of recombinant human antithrombin III for restoration of heparin responsiveness in heparin-resistant patients scheduled for cardiac surgery.MethodsThis was a multicenter, randomized, double-blind, placebo-controlled study in heparin-resistant patients undergoing elective cardiac surgery. Patients were considered heparin resistant if the activated clotting time was less than 480 seconds after 400 U/kg heparin. Fifty-two heparin-resistant patients were randomized into 2 cohorts. One cohort received a single bolus (75 U/kg) of recombinant human antithrombin III (n = 28), and the other, the placebo group (n = 24), received a normal saline bolus. If the activated clotting time remained less than 480 seconds, this was defined as treatment failure, and 2 units of fresh frozen plasma were transfused. Patients were monitored for adverse events during hospitalization.ResultsSix (21%) of the patients in the recombinant human antithrombin III group received fresh frozen plasma transfusions compared with 22 (92%) of the placebo-treated patients (P < .001). Two units of fresh frozen plasma did not restore heparin responsiveness. There was no increased incidence of adverse events associated with recombinant human antithrombin III administration. Postoperative 24-hour chest tube bleeding was not different in the 2 groups. Surrogate measures of hemostatic activation suggested that there was less activation of the hemostatic system during cardiopulmonary bypass in the recombinant human antithrombin III group.ConclusionTreatment with recombinant human antithrombin III in a dose of 75 U/kg is effective in restoring heparin responsiveness and promoting therapeutic anticoagulation for cardiopulmonary bypass in the majority of heparin-resistant patients. Two units of fresh frozen plasma were insufficient to restore heparin responsiveness. There was no apparent increase in bleeding associated with recombinant human antithrombin III.

Spontaneous Ca2+-oscillations are a result of periodic increases and decreases of cytosolic Ca2+. In neurons, they are thought to possess integrative properties because amplitude and frequency influence axon outgrowth, neuronal growth cone migration, and long distant wiring within the developing cortex. Ketamine stereoisomers differ in their affinities for the N-methyl-D-aspartic acid receptor and analgesic and anesthetic effects. Using a dual-excitation Ca2+ ratiometric fluorescence technique with the Ca2+-sensitive dye fura-2 AM, we detected spontaneous Ca2+-oscillations in neurons of hippocampal cell cultures. Spontaneous Ca2+-oscillations development is dependent on external Ca2+, and their amplitude and frequency increased in Mg2+-free solution. Ca2+-oscillations are glutamate dependent because blocking of the N-methyl-D-aspartic acid, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic, or kainate receptor resulted in a complete disruption of the oscillations. The ketamine stereoisomers dose-dependently and reversibly suppressed the amplitude and frequency of the spontaneous Ca2+-oscillations. This effect was highly stereoselective with the S+ isomer being nearly four times more potent than the R(-) enantiomer. These results correlate well with the clinical anesthetic and analgesic potency of the stereoisomers and therefore our experimental approach might represent a model system to study mechanisms of anesthetic action on Ca2+-dependent integration of neuronal information.

SUMMARY 1. The aim of the present study was to investigate the potential energy preserving effect of permanent bilateral common carotid artery occlusion (BCCAO) towards additional systemic hypotension of severe duration (30 min). In addition, the role of adenosine A1 receptors in cerebral ischaemic preconditioning was investigated in male Wistar rats. Thus, oligaemic rats were assigned randomly to continuous treatment with the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) or the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT), receiving daily intraperitoneal infusions of 0.1 mg/kg bodyweight CCPA or CPT or placebo (200 µL aqueous 2-hydropropyl-β-cyclodextrin) at a delivery rate of 0.5 µL/h over 14 days. 2. Haemodynamic parameters and arterial blood gases were monitored. Rat cortical energy metabolites ATP, ADP, AMP, phosphocreatine and adenosine were measured using HPLC techniques. Adenosine A1 receptor expression was determined by immunhistochemistry and quantified by western blotting. 3. Two weeks of permanent BCCAO induced an ‘energy saving’ effect in rat cortical ATP concentrations. Under subchronic conditions, significant increases were detected in ADP and AMP concentrations after CCPA compared with placebo. Because similar changes were also seen after CPT, this adenosine A1 receptor-mediated effect does not seems to be specific. Furthermore, no differences in adenosine A1 receptor expression could be detected. 4. Adenosine was not specifically involved in the ‘preconditioning-like’ effect via the modulation of the adenosine A1 receptor in the present oligaemia model. Obviously, adenosine A1 receptor-specific effects after delayed cerebral ischaemic preconditioning do not seem to play an essential role if BCCAO is followed by a prolonged additional severe ischaemic event.

Peri-operative myocardial ischaemia is the single most important risk factor for an adverse cardiac outcome after non-cardiac surgery. The present study examines whether intermittent 12-lead ECG recordings can be used as an early warning tool to identify patients suffering from peri-operative myocardial ischaemia and subsequent myocardial cell damage. Fifty-five vascular surgery patients at risk for or with a history of coronary artery disease were monitored for peri-operative myocardial ischaemia using intermittent 12-lead ECG recordings taken pre-operatively and at 15 min, 20 h, 48 h, 72 h and 84 h postoperatively. The effectiveness of the 12-lead ECG was gauged by examining concordance with continuous 3-channel Holter monitoring and capturing peri-operative myocardial ischaemia by serial analyses of creatine kinase myocardial band isoenzyme and cardiac troponin T and I. The incidence of peri-operative myocardial ischaemia detected by 12-lead ECG was 44% and was identifiable in most patients (88%) 15 min after surgery. The incidence of peri-operative myocardial ischaemia detected by continuous monitoring was 53%, with the most severe episodes occurring intra-operatively and during emergence from anaesthesia. The concordance of the 12-lead method with continuous monitoring was 72%. The concordance of creatine kinase myocardial band isoenzyme activity with the 12-lead method was 71% and with Holter monitoring 57%. The concordance of mass concentration of creatine kinase myocardial band with 12-lead ECG recordings was 75%, and the corresponding value for Holter monitoring was 68%. The concordance of cardiac troponin T and I levels with the 12-lead method was 85% and 87%, respectively, and concordance with Holter monitoring was 72% and 66%, respectively. The postoperative 12-lead ECG identified peri-operative myocardial ischaemia associated with subsequent myocardial cell damage in most patients undergoing vascular surgery.

In 25 cardiac surgical patients, right ventricular ejection fraction was continuously measured with a new pulmonary artery catheter and transoesophageal echocardiography, scanning the 'fractional area change' in a standardised transatrial cross section area. Measurements were recorded at three predefined time points (pre-, intra-, and postoperatively). Both methods were compared using the Bland-Altman analysis. Comparing right ventricular ejection fraction values obtained from the pulmonary artery catheter with those assessed by transoesophageal echocardiography, bias was -3.7%, with a precision of 30.9%. Bias and precision significantly improved when the heart rate was less than 100 beats.min(-1), pulmonary artery pressures were low and cardiac performance adequate. In conclusion, the new continuous pulmonary artery catheter system appears to be a valid and useful bedside monitoring device in the haemodynamic management of critically ill patients.

To study the relationship between the metabolism of amyloid precursor protein (APP) and cellular energy failure, HEK 293 cells stably transfected with betaAPP 695 underwent graded energy failure induced either by i) hypoxia (pO(2) 25 mm Hg), ii) inhibition of the respiratory chain by sodium azide (NaN(3)), or iii) by combined glucose deprivation/hypoxia of different duration and severity. Secreted APP (APPs) and the derivative betaA4 were quantified autoradiographically by immunoprecipitation, and [(35)S] methionine labeling. APP holoprotein (APPh) was determined by Western blot analysis. The concentrations of the energy-rich metabolites ATP, ADP, creatine phosphate (CrP), and adenosine were measured by high performance liquid chromatography. Mild to moderate energy failure after NaN(3) treatment (2h, 4h) and hypoxia (2h, 8h) was characterized by normal ATP concentration but also by a high reduction in CrP. A stress condition indicated by an increased ATP turnover and adenosine increase was obtained. Intracellular APPh increased but its metabolites APPs and betaA4 as measured in the extracellular compartment decreased. These changes may point to a compensatory response of APP but also to a initial disturbance in intracellular APP metabolism. Severe abnormalities in both energy formation and utilization after 8h NaN(3) and hypoxia glucose deprivation were found to be accompanied by a drastic fall in intracellular APPh concentration by at least 50%, paralleled by an accelerating reduction in the extracellular concentrations of both APPs and betaA4.A significant linear correlation between APPh and ATP and between CrP and betaA4 became obvious. The data of the present study indicate that abnormalities in APP metabolism were generated in an energy-dependent manner. The obvious similarities to sporadic Alzheimer s disease are discussed.

Although several clinical studies have shown that increased serum concentrations of protein S100B predict ischaemic brain damage after cardiac surgery, S100B may also be released from the heart or other injured tissue. We therefore investigated the correlation between serum S100B levels and those of the specific cardiac marker troponin I in order to assess the cerebral vs. extracerebral origin of S100B. In 64 cardiac surgical patients, serial blood samples were drawn for the measurement of S100B and troponin I before surgery and for seven days after surgery. Neurological function was assessed before with the National Institutes of Health Stroke Scale and the Folstein Mini Mental Test. The data show that a sustained increase in serum S100B levels is associated with neurological dysfunction, as witnessed by a positive correlation between S100B values and the results of the neuropsychological tests. In contrast, the early postoperative increased levels of protein S100B derive from cardiac tissue, as shown by the positive correlation between S100B and cardiac troponin I levels.

This randomised, placebo-controlled, patient and observer blinded trial was conducted to determine whether acupuncture at the acupuncture point P6 is effective in preventing postoperative nausea and vomiting (PONV) compared to placebo acupuncture. Female patients (n = 220) scheduled for gynaecological or breast surgery were randomly assigned to two groups receiving either acupuncture (n = 109) or placebo acupuncture (n = 111). Each group was stratified for type of surgery and included two subgroups receiving intervention either before or after induction of anaesthesia. The incidence of PONV and/or antiemetic rescue medication within 24 h after surgery was the main outcome measure which showed no statistically significant difference between groups (43.7% acupuncture, 50.9% placebo, p = 0.27). The differences were more pronounced for patients having gynaecological surgery (48.9% acupuncture, 67.6% placebo, p = 0.07) than for those having breast surgery (38.7% acupuncture, 40.3% placebo, p = 0.86). The secondary outcome, vomiting, was significantly reduced by acupuncture from 39.6% to 24.8% (p = 0.03). Subgroup analysis showed no difference between applications of acupuncture before compared to after induction of anaesthesia.

Background and objective The use of propofol compared with isoflurane is associated with improved patient comfort and decreased costs. However, as the cost saving, the quicker recovery time and patient comfort may not be evident if sevoflurane is substituted for isoflurane; these two anaesthetic agents were analysed in elderly patients. Methods In a prospective randomized study, 96 patients undergoing elective ophthalmic surgery received either total intravenous anaesthesia with propofol (Group P), propofol for induction and sevoflurane for maintenance (Group P/S) or sevoflurane for inhalation induction and maintenance (Group S). Analyses focussed on haemodynamics, the quality of recovery, and the costs for the anaesthetic and the entire procedure. Results Bradycardia or hypotension, mainly registered in Groups P and P/S, did not influence patients' recovery. In Group S, postoperative nausea and vomiting occurred frequently, and 50% of patients complained of discomfort during induction. In Group P/S, the costs for anaesthetics and total costs were lower than those in Groups P and S. Conclusions Propofol- and sevoflurane-based maintenance of anaesthesia were similar with regard to patient comfort and recovery in the elderly. Cost analysis revealed that it was less expensive to use propofol for induction and sevoflurane for maintenance than to use either propofol or sevoflurane as sole agents for anaesthesia.

Endothelial damage during early endotoxemia has been shown to be leukocyte-independent. Platelet-activating factor (PAF) and serotonin-receptor antagonism are known to reduce leukocyte-independent macromolecular leakage significantly, thereby focusing the field of interest to the platelets. We hypothesized that inhibition of the GP IIb/IIIa receptor, using the unspecific GP IIb/IIIa inhibitor abciximab, would reduce leukocyte-independent endothelial damage during early endotoxemia, and furthermore, that inhibition of the GP IIb/IIIa receptor with abciximab might improve microcirculatory disturbances, seen in a leukocyte-dependent animal model during endotoxemia.In male Wistar rats, venular wall shear rate, macromolecular efflux, and leukocyte-endothelial interaction were determined in mesenteric postcapillary venules using intravital microscopy at baseline, 60, and 120 min after the start of the experiment. The experiment was divided into two parts. In the first part, we investigated the effects of the GP IIb/IIIa inhibitor abciximab on leukocyte-independent endothelial permeability during endotoxemia. In the second part of the experiment, we focused on the effects of the GP IIb/IIIa inhibitor abciximab on microcirculatory disturbances during endotoxemic states, without a modification of the leukocyte-endothelial interaction, putting the main emphasis again on endothelial permeability.GP IIb/IIIa inhibition with abciximab resulted in a significant reduction of macromolecular efflux during leukocyte-independent endotoxemia. Both pretreatment with abciximab and post-treatment with abciximab reduced macromolecular leakage during leukocyte-dependent endotoxemia to values comparable to control values, and prevented an increase in leukocyte adherence, that has been reduced to values comparable to control values, too.GP IIb/IIIa inhibition, using abciximab, protects against endothelial dysfunction and an increase in leukocyte adherence to the vascular wall during experimental endotoxemia. The protective properties of abciximab on microcirculation seemed to be leukocyte-independent.