Thoracic epidural anaesthesia (TEA) reduces cardiac and splanchnic sympathetic activity and thereby influences perioperative function of vital organ systems. A recent meta-analysis suggested that TEA decreased postoperative cardiac morbidity and mortality. TEA appears to ameliorate gut injury in major surgery as long as the systemic haemodynamic effects of TEA are adequately controlled. The functional benefit in fast-track and laparoscopic surgery needs to be clarified. Better pain control with TEA is established in a wide range of surgical procedures. In a setting of advanced surgical techniques, fast-track regimens and a low overall event rate, the number needed to treat to prevent one death by TEA is high. The risk of harm by TEA is even lower, and other methods used to control perioperative pain and stress response also carry specific risks. To optimize the risk-benefit balance of TEA, safe time intervals regarding the use of concomitant anticoagulants and consideration of reduced renal function impairing their elimination must be observed. Infection is a rare complication and is associated with better prognosis. Close monitoring and a predefined algorithm for the diagnosis and treatment of spinal compression or infection are crucial to ensure patient safety with TEA. The risk-benefit balance of analgesia by TEA is favourable and should foster clinical use.

In the Intraoperative Hypothermia for Aneurysm Surgery Trial, neither systemic hypothermia nor supplemental protective drug affected short- or long-term neurologic outcomes of patients undergoing temporary clipping.

Purpose:To describe the epidemiology of the acute respiratory distress syndrome (ARDS) in a Brazilian ICU.Methods: This prospective observational, non-interventional study, included all consecutive patients with ARDS criteria [1] admitted in the ICU of a Brazilian tertiary hospital, between January 1997 and September 2001. Were collected in a prospective fashion the following variables: age, gender, APACHE II score at ICU admission and at ARDS diagnosis, cause of ARDS, presence of AIDS, cancer and immunosuppression, occurrence of barotrauma, performance of traqueostomy, mortality, duration of mechanical ventilation (MV), length of stay (LOS) in ICU and in hospital. The lung injury score (LIS) [2] was used to quantify the degree of pulmonary injury in the first week of ARDS. Results:There was 2182 patients (P) admitted in ICU during the study period, of whom 141 (6.46%) had ARDS criteria. Seventy-six (54%) were men, the mean age was 46 ± 18 years, APACHE II 18 ± 7 and 19 ± 7 at admission and at ARDS diagnosis, respectively. Septic shock accounted for 42% (60 P) of the ARDS causes, sepsis 22% (31 P), diffuse pulmonary infection 16% (23 P), aspiration pneumonia 11% (15 P), non-septic shock 5% (7 P) and others 4% (5 P). Ten percent (14 P) had AIDS, 30% (43 P) cancer and 25% (36 P) immunosuppression. All patients were mechanically ventilated with Tidal Volume between 4 and 8 ml/kg. Only 3.5% (5 P) had barotrauma and 10% (14 P) performed traqueostomy. Mortality rate was 79% in the ICU. The patients required 12 ± 10 days on MV, ranging from 1 to 55 days. The LOS in ICU and hospital was 14 ± 13 (1-69) days and 28 ± 32 (1-325) days, respectively. There was a time delay of 3.7 ± 4.5 days between admission in ICU and the onset of ARDS. The Murray score (mean ± SD) was 3.2 ± 0.4, 3 ± 0.5, 3 ± 0.5, 2.9 ± 0.6, 2.8 ± 0.7, 2.7 ± 0.7 and 2.6 ± 0.8 in the first 7 days, respectively.Conclusions: ARDS in our hospital has a similar incidence of reports in the USA and Europe. There was a higher mortality, which could be explained by a high incidence of infection causes of ARDS, mainly septic shock, and elevated combined occurrence of AIDS, cancer and immunosuppression, along the degree of LIS. The incidence of barotrauma was low, as a consequence of the current mechanical ventilation strategies. References:1. Bernard GR, Artigas A, Brigham KL, et al.: Am Respir Crit Care Med 1994 P2Role of multiple organ dysfunction syndrome in ARDS mortality FS Dias, N Almeida, IC Wawrzeniack, PB Nery Hospital São Lucas da PUCRS, Av. Ipiranga 6690, RS, Brazil Purpose: To correlate the occurrence and level of organ dysfunction in ARDS with mortality. Methods:This cohort study includes all consecutive patients with ARDS criteria [1] admitted in the ICU between January 1997 and September 2001. Were collected in a prospective fashion the following variables: age, gender, APACHE II score at the ARDS diagnosis, the occurrence of organ dysfunction determined by the multiple organ dysfunction syndrome (MODS) [2] in the first week, and mortality in ...

OBJECTIVETight glycemic control (TGC) in critically ill patients is associated with an increased risk of hypoglycemia. Whether those short episodes of hypoglycemia are associated with adverse morbidity and mortality is a matter of discussion. Using a case-control study design, we investigated whether hypoglycemia under TGC causes permanent neurocognitive dysfunction in patients surviving critical illness.RESEARCH DESIGN AND METHODSFrom our patient data management system, we identified adult survivors treated for >72 h in our surgical intensive care unit (ICU) between 2004 and 2007 (n = 4,635) without a history of neurocognitive dysfunction or structural brain abnormalities who experienced at least one episode of hypoglycemia during treatment (hypo group) (n = 37). For each hypo group patient, one patient stringently matched for demographic- and disease-related data were identified as a control subject. We performed a battery of neuropsychological tests investigating five areas of cognitive functioning in both groups at least 1 year after ICU discharge. Test results were compared with data from healthy control subjects and between groups.RESULTSCritical illness caused neurocognitive dysfunction in all tested domains in both groups. The dysfunction was aggravated in hypo group patients in one domain, namely that of visuospatial skills (P < 0.01). Besides hypoglycemia, both hyperglycemia (r = −0.322; P = 0.005) and fluctuations of blood glucose (r = −0.309; P = 0.008) were associated with worse test results in this domain.CONCLUSIONSHypoglycemia was found to aggravate critical illness–induced neurocognitive dysfunction to a limited, but significant, extent; however, an impact of hyperglycemia and fluctuations of blood glucose on neurocognitive function cannot be excluded.

Knowledge of sepsis is growing rapidly and new pathogenetic concepts and therapeutic strategies evolve. The animal models of sepsis catalyze this development. Any model of this complex disease is inevitably a compromise between clinical realism and experimental simplification. Against the background of current pathogenetic concepts this review tries to analyze the validity and clinical relevance of each model. Endotoxemia and bacteremia represent models without an infectious focus. They reproduce many characteristics of sepsis and are highly controlled and standardized. However, they reflect a primarily systemic challenge and create neither an infectious focus nor the protracted immune reaction that characterizes sepsis. In this respect, any model with an infectious focus is decisively closer to clinical reality. In these models the peritoneal cavity is contaminated either by bacteria or inoculated feces or perforation of the bowel wall. Both the bolus injection and the implantation of carriers loaded with bacteria or feces are used. In fecal spesis and perforation models the complete spectrum of enteric pathogens is present in the septic focus and infective selection is undisturbed. Here the pathophysiologic and immunologic features of clinical sepsis are successfully reproduced. However, presumably due to inadequate control of the bacterial challenge, only poor interlaboratory standardization is possible. As to optimize models for the clinical reality the choice of an appropriate class of models is crucial. Moreover the incorporation of clinical therapy such as volume resuscitation, antibiotic therapy and surgical treatment of the septic focus is indispensable. Finally, the importance of simulation of comorbidities cannot be overemphasized.

TEA with 10 ml bupivacaine, 0.25%, induced thoracic and lumbar sympathetic block that precedes and exceeds sensory block. Caudal limit of sympathetic block could not be demonstrated in this study.

Thoracic epidural analgesia attenuated systemic response and improved survival in severe acute pancreatitis. These effects might be explained by improved mucosal perfusion.

Microcirculatory dysfunction contributes significantly to tissue hypoxia and multiple organ failure in sepsis. Ischemia of the gut and intestinal hypoxia are especially relevant for the evolution of sepsis because the mucosal barrier function may be impaired, leading to translocation of bacteria and toxins. Because sympathetic blockade enhances intestinal perfusion under physiologic conditions, we hypothesized that thoracic epidural anesthesia (TEA) may attenuate microcirculatory perturbations during sepsis. The present study was designed as a prospective and controlled laboratory experiment to assess the effects of continuous TEA on the mucosal microcirculation in a cecal ligation and perforation model of sepsis in rats. Anesthetized Sprague-Dawley rats underwent laparotomy and cecal ligation and perforation to induce sepsis. Subsequently, either bupivacaine 0.125% (n = 10) or isotonic sodium chloride solution (n = 9) was continuously infused via the thoracic epidural catheter for 24 h. In addition, a sham laparotomy was carried out in eight animals. Intravital videomicroscopy was then performed on six to ten villi of ileum mucosa. The capillary density was measured as areas encircled by perfused capillaries, that is, intercapillary areas. The TEA accomplished recruitment of microcirculatory units in the intestinal mucosa by decreasing total intercapillary areas (1,317 +/- 403 vs. 1,001 +/- 236 microm2) and continuously perfused intercapillary areas (1,937 +/- 512 vs. 1,311 +/- 678 microm2, each P < 0.05). Notably, TEA did not impair systemic hemodynamic variables beyond the changes caused by sepsis itself. Therefore, sympathetic blockade may represent a therapeutic option to treat impaired microcirculation in the gut mucosa resulting from sepsis. Additional studies are warranted to assess the microcirculatory effects of sympathetic blockade on other splanchnic organs in systemic inflammation.