A pancreas-preserving technique for the management of symptomatic pancreatic anastomotic insufficiency refractory to conservative treatment after pancreas head resection.

BACKGROUND AND AIM: Management of symptomatic pancreatic anastomotic insufficiency after pancreas head resection remains controversial. Completion pancreatectomy as one frequently performed option is associated with poor prognosis. PATIENTS AND METHODS: During a 4-year period, a two-step strategy was applied in four consecutive patients suffering from pancreatic anastomotic insufficiency refractory to conservative management after a pancreas head resection. In the first step, sepsis was overbridged by meticulous debridement and resection of the pancreaticojejunostomy, leaving the biliary anastomosis untouched, and selective drainage of the pancreatic duct as well as the peripancreatic area. In the second step, after recovery, the procedure was completed with a novel pancreaticojejunostomy. RESULTS: The surgical procedure was completed in three patients after a mean of 164 (range: 112-213) days. One patient died from cardiac arrest 54 days after the reoperation with resolved abdominal sepsis. No pancreatic anastomotic insufficiency occurred after the new pancreaticojejunostomy had been performed. Three patients are alive and tumor-free with normal exocrine and endocrine pancreatic function after a mean follow-up of 20.3 (3-38) months following the definitive reconstruction. CONCLUSION: The two-step pancreas-preserving strategy can be used as an alternative to completion pancreatectomy for patients suffering from severe pancreatic anastomotic insufficiency.

Treatment with tigecycline of recurrent urosepsis caused by extended-spectrum-beta-lactamase-producing Escherichia coli.

A 25-year-old female was admitted to our intensive care unit with septic shock and multiorgan failure caused by extended-spectrum beta-lactamase-producing Escherichia coli originating from the right renal pelvis. A 16-day course of treatment with meropenem reversed the septic condition, but the infection recurred thereafter. The patient recovered fully after therapy was changed to tigecycline.

Synthetic colloids attenuate leukocyte-endothelial interactions by inhibition of integrin function.

BACKGROUND: It has been suspected that synthetic colloids may interfere with leukocyte adhesion by down-regulation of endothelial cell adhesion molecules. Although inhibition of endothelial inflammation might reduce leukocyte-related tissue injury, the same mechanism may be detrimental for host defense during severe infection. Regarding the widespread use of colloids, the authors performed a laboratory investigation to determine the mechanisms by which synthetic colloids interfere with leukocyte-endothelial interactions. METHODS: Adhesion molecule expression on native and cytokine-activated endothelium from umbilical veins was measured after pretreatment with gelatin and various preparations of dextran or hydroxyethyl starch. Inhibition of neutrophil adhesion to activated endothelium was examined in a flow chamber by perfusion of untreated and colloid-treated neutrophils over colloid-pretreated endothelium at 2 dyn/cm. Comparisons were made between untreated controls, colloid-pretreated endothelium, and colloid-cotreated neutrophils. RESULTS: Intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and P-selectin were not attenuated by any colloid. Accordingly, colloid pretreatment of endothelium alone did not reduce neutrophil adhesion. In contrast, when neutrophils were cotreated by addition of colloids to the perfusate immediately before perfusion, adhesion decreased by 31-51% (P < 0.05) regardless of the colloid type. As indicated by the twofold increased rolling fractions, this reduction was due to an inhibition of neutrophil integrins. CONCLUSIONS: This study shows that synthetic colloids inhibit neutrophil adhesion by a neutrophil-dependent mechanism rather than interfering with endothelial cell activation. This suggests that inhibition of leukocyte sequestration by volume support is a common and transient phenomenon depending on the colloid concentration in plasma.

Effects of fresh versus old stored blood in the priming solution on whole blood lactate levels during paediatric cardiac surgery.

It has been suggested that lactate levels may predict morbidity and mortality in paediatric patients during corrective open-heart surgery. Packed red blood cells (PRBC) are frequently necessary for priming the reservoir used in cardiopulmonary bypass (CPB). The storage of PRBC might cause a significant increase in lactate levels. The purpose of the present study was to quantify the increase in lactate levels in stored red blood cells over time and to compare lactate levels after transfusions of fresh (< or =12 days) versus old blood (>12 days) in 20 patients. We found an increase in lactate levels from 6.0 to 44.7mmol/L (mean 17.0+/-7.8 mmol/L) during storage. Lactate levels were also significantly higher after the onset of CPB in paediatric patients transfused with old blood than in patients transfused with fresh blood (1.43+0.36 versus 3.46+/-0.63, p=0.0006). Our results suggest that the higher lactate levels found after the initiation of CPB should be used with caution when assessing tissue hypoxia and predicting outcome.

Role of cross-allergies to latex in clinical routine of anesthesia.

STUDY OBJECTIVE: To determine the applicability and reliability of a screening questionnaire to detect patients at high-risk of latex allergy; to assess the importance of other allergies such as profilin allergies (pollinosis) for presence of latex sensitization; and to determine the clinical effectiveness of preemptive avoidance of latex exposure in high-risk patients. DESIGN: Prospective, clinical trial. SETTING: Operative theater of a university hospital. PATIENTS: 95 adult patients. INTERVENTIONS: Patients were preoperatively screened and classified for present latex allergy (high-risk and low-risk group) according to a specially designed screening questionnaire. Anesthesia and surgery in the high-risk group were performed strictly avoiding latex-containing materials. The low-risk group (other allergies including pollinosis) received routine treatment, without latex-avoidance. Effects of latex avoidance or exposure were evaluated by measuring specific IgE titers perioperatively. MEASUREMENTS AND MAIN RESULTS: According to the questionnaire, 45 patients at high risk were defined. Validity of classification of high-risk patients is supported by significantly higher total IgE and latex and grass profilin specific IgE compared to the low-risk group. There were no significant differences in other profilin-specific IgEs. In one case of severe anaphylactic reaction a drop of latex-specific IgE during surgery could be observed. CONCLUSION: The questionnaire allowed the identification of most patients at high risk for latex allergy. In isolated pollinosis no changes in any specific IgE levels were detectable. Strict avoidance of perioperative latex exposure in high-risk patients increases safety during anesthesia and surgery.

Correlation of meropenem plasma levels with pharmacodynamic requirements in critically ill patients receiving continuous veno-venous hemofiltration.

BACKGROUND: In patients with acute renal failure, the pharmacokinetics of meropenem depend on the operational characteristics of the renal replacement therapy. Dosage recommendations are based on the correlation of plasma levels with pharmacodynamic requirements. METHODS: Eight critically ill patients with acute renal failure were treated by continuous veno-venous hemofiltration with a filtrate flow of 1,600 ml/h and received 500 mg of meropenem every 12 h. Plasma and hemofiltrate concentrations of meropenem at steady state were determined by HPLC. RESULTS: Peak levels in plasma amounted to 39.5 +/- 10.5 mg/l (mean +/- SD) and trough levels were 2.4 +/- 1.5 mg/l. The minimal inhibitory concentration (MIC) for susceptible bacteria (4 mg/l) was covered for 40% of the dosing interval or longer in all patients. The MIC for intermediately susceptible organisms (8 mg/l) was covered for 33% in 6 of the 8 patients. The elimination half-life was prolonged to 3.63 +/- 0.77 h. The sieving coefficient of meropenem was 0.91 +/- 0.10 and the recovery in hemofiltrate amounted to 30.9 +/- 11.5% of the dose. CONCLUSIONS: A dosage of 500 mg twice daily provides appropriate serum levels for the treatment of infections caused by susceptible bacteria. A higher dosage is adequate for infections by intermediately susceptible bacteria or for renal replacement therapies with markedly higher filtrate flow rates.

Pseudomonas aeruginosa activates Cl- channels in host epithelial cells.

Exposure to Pseudomonas aeruginosa triggers the apoptotic cell death of Chang epithelial cells, and this depends on the expression of both the CD95 receptor and CD95 ligand. In lymphocytes CD95-mediated apoptosis is paralleled by the activation of outwardly rectifying Cl- channels. The present study was performed to explore whether P. aeruginosa-induced apoptosis of Chang epithelial cells is paralleled by activation of Cl- channels. According to whole-cell patch-clamp recordings, exposure of Chang epithelial cells to P. aeruginosa does lead to rapid activation of an outwardly rectifying Cl- -selective current. The current is inhibited by the Cl- channel blocker NPPB. Exposure of Chang epithelial cells to P. aeruginosa led to a significant decrease of cell membrane capacitance by 6%, pointing to a decrease in cell volume by 7%. Exposure to P. aeruginosa depolarized the mitochondrial membrane potential indicating apoptotic cell death. The decline of mitochondrial membrane potential was not significantly affected by NPPB. In conclusion, P. aeruginosa-induced apoptosis of Chang epithelial cells is paralleled by activation of Cl- channels. Activation of the channels participates in the alteration of cell volume but is not a prerequisite for P. aeruginosa-induced apoptosis.

The effects of fresh frozen plasma on neutrophil-endothelial interactions.

UNLABELLED: Leukocyte adhesion to endothelial cells contributes to microcirculatory disturbances during severe shock syndromes. Whereas certain plasma expanders inhibit leukocyte adhesion, contaminants of plasma protein solutions upregulate endothelial cell adhesion molecules in certain cases. We performed this study to determine whether fresh frozen plasma (FFP) affects neutrophil-endothelial interactions in cocultures of neutrophils and human umbilical vein endothelial cells (HUVEC) in vitro. HUVEC (n = 9) were incubated with either 20% FFP or 20% serum in medium for 6 h. Expression of E-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule-1 was induced by tumor necrosis factor alpha (0.5 ng/mL for 4 h) and measured by flow cytometry. Neutrophil adhesion was examined in a parallel plate flow chamber in which isolated neutrophils were perfused over pretreated HUVEC under postcapillary flow conditions. Incubation with FFP decreased E-selectin and intercellular adhesion molecule 1 on activated HUVEC by 28% and 22%, respectively (P < or = 0.01; analysis of covariance). Consequently, neutrophil adhesion decreased by 20%-41% in FFP-treated cocultures (n = 4; P < or = 0.01; paired Student's t-test). We conclude that FFP attenuates the inflammatory response of endothelial cells with regard to neutrophil-endothelial interactions. Because the composition of patients' plasma is affected not only by transfusion, but more frequently by shock treatment with IV fluids, plasma dilution in critically ill patients could be important. IMPLICATIONS: During shock, fluid administration leads to a massive dilution of plasma. Apart from maintaining hemodynamics, this might affect tissue damage by influencing leukocyte accumulation in the microvasculature. Using endothelial cells, isolated neutrophils, and a parallel plate flow chamber, we studied the effects of fresh frozen plasma on neutrophil-endothelial interactions.

CFTR is a pattern recognition molecule that extracts Pseudomonas aeruginosa LPS from the outer membrane into epithelial cells and activates NF-kappa B translocation.

Immune cells are activated during cellular responses to antigen by two described mechanisms: (i) direct uptake of antigen and (ii) extraction and internalization of membrane components from antigen-presenting cells. Although endocytosis of microbial antigens by pattern recognition molecules (PRM) also activates innate immunity, it is not known whether this involves extraction and internalization of microbial surface components. Epithelial cells on mucosal surfaces use a variety of receptors that are distinct from the classical endocytic PRM to bind and internalize intact microorganisms. Nonclassical receptor molecules theoretically could act as a type of endocytic PRM if these molecules could recognize, bind, extract, and internalize a pathogen-associated molecule and initiate cell signaling. We report here that the interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) and the outer core oligosaccharide of the lipopolysaccharide (LPS) in the outer membrane of Pseudomonas aeruginosa satisfies all of these conditions. P. aeruginosa LPS was specifically recognized and bound by CFTR, extracted from the organism's surface, and endocytosed by epithelial cells, leading to a rapid (5- to 15-min) and dynamic translocation of nuclear transcription factor NF-kappa B. Inhibition of epithelial cell internalization of P. aeruginosa LPS prevented NF-kappa B activation. Cellular activation depended on expression of wild-type CFTR, because both cultured Delta F508 CFTR human airway epithelial cells and lung epithelial cells of transgenic-CF mice failed to endocytose LPS and translocate NF-kappa B. CFTR serves as a critical endocytic PRM in the lung epithelium, coordinating the effective innate immune response to P. aeruginosa infection.

The effect of remifentanil or fentanyl on postoperative vomiting and pain in children undergoing strabismus surgery.

UNLABELLED: Postoperative vomiting (POV) after strabismus surgery in children results in discomfort and prolonged hospital stays. Opioids increase the incidence of POV. Remifentanil has a context-sensitive half-life of 3 to 4 min, and how this short half-life influences POV in those patients is unknown. We conducted a prospective, double-blinded study in 81 ASA status I or II children from 2 to 12 yr of age undergoing elective strabismus surgery under general anesthesia. Patients were randomized to receive either remifentanil (bolus 1 microg/kg; infusion 0.1-0.2 microg x kg(-1) x min(-1)) or fentanyl (2 microg/kg, and 1 microg/kg every 45 min). POV episodes were recorded for 25 h. Pain scores were obtained by using an objective pain scale for 60 min during recovery. The number of patients who experienced POV did not differ significantly between groups (49% vs 48%). However, in the Remifentanil group, POV episodes were significantly less frequent (0.95 vs 2.2 episodes). In contrast, fentanyl was associated with lower pain scores during the first 30 min of recovery. We conclude that children undergoing strabismus surgery under balanced anesthesia with remifentanil, compared with fentanyl, showed less frequent POV. However, early postoperative analgesia was better with fentanyl. IMPLICATIONS: Opioids increase the incidence of postoperative vomiting (POV). Remifentanil is characterized by the shortest half-life of all opioids used in anesthetic practice. Therefore, we studied the effect of remifentanil on POV compared with the longer-acting opioid fentanyl in children undergoing strabismus surgery.