18 research outputs found
Citrate confers less filter-induced complement activation and neutrophil degranulation than heparin when used for anticoagulation during continuous venovenous haemofiltration in critically ill patients
Background: During continuous venovenous haemofiltration (CVVH), regional anticoagulation with citrate may be superior to heparin in terms of biocompatibility, since heparin as opposed to citrate may activate complement (reflected by circulating C5a) and induce neutrophil degranulation in the filter and myeloperoxidase (MPO) release from endothelium. Methods. No anticoagulation (n = 13), unfractionated heparin (n = 8) and trisodium citrate (n = 17) regimens during CVVH were compared. Blood samples were collected pre- and postfilter; C5a, elastase and MPO were determined by ELISA. Additionally, C5a was also measured in the ultrafiltrate. Results: In the heparin group, there was C5a production across the filter which most decreased over time as compared to other groups (P = 0.007). There was also net production of elastase and MPO across the filter during heparin anticoagulation (P = 0.049 or lower), while production was minimal and absent in the no anticoagulation and citrate group, respectively. During heparin anticoagulation, plasma concentrations of MPO at the inlet increased in the first 10 minutes of CVVH (P = 0.024). Conclusion: Citrate confers less filter-induced, potentially harmful complement activation and neutrophil degranulation and less endothelial activation than heparin when used for anticoagulation during continuous venovenous haemofiltration in critically ill patients
Identification of microorganisms grown in blood culture flasks using liquid chromatography-tandem mass spectrometry
Aim: Bloodstream infections are a common cause of disease and a fast and accurate identification of the causative agent or agents of bloodstream infections would aid the start of adequate treatment. Materials & methods: A liquid chromatography-tandem mass spectrometry (LC-MS/MS) shotgun proteomics method was developed for the identification of bacterial species directly from blood cultures that were simulated by inoculating blood culture bottles with single or multiple Clinically relevant microorganisms. Results: Using LC-MS/MS, the single species were correctly identified in 100% of the blood cultures, whereas for polymicrobial infections, 78% of both species were correctly identified in blood cultures. Conclusion: The LC-MS/MS method allows for the identification of the causative agent of positive blood cultures. © 2017 2017 Netherlands Organization for Applied Scientific Research TNO
Stability Design of the Filter with Head Loss
The optimum design of the filter with head loss is performed using S_ as a parameter of stability, where S_ is an area of distribution of the residual vertical effective normal stress Ï_. in a critical state. The following three types of distributions of coefficient of permeability k are investigated precisely here : (1) Two-layer varying type, (2) locally linearly varying type, (3) locally bi-hyperbolically varying type and (4) locally hyperbolically varying type, which are considered to be able to represent almost all distributions of k of a filter. The filter is approximated to a 1000-layered system systematically and S_ of the filter is analysed using the computer program CRIT1 (Critical State Calculation Program for Seepage Failure of a Multi-Layered Ground). In this paper, the various cases of k_r (>1.0) are investigated systematically, where k_r is the ratio of coefficients of permeability at the top and the bottom of a filter. The following results are then obtained : (1) For a given value of k_r, the two-layered system : [numerical formula] is the most stable against seepage failure, where [numerical formula] is the ratio of lengths of the upper and the lower strata of the two-layered system. The superscript * represents the value of the most stable filter. (2) l_r^* increases from 1.0+0 to infinity (l_1^* decreases from 1/2L-0 to 0.0+0), as k_r increases from 1.0+0 to infinity, where L is the total length of the most stable filter. That is to say, the two layer varying point of the most stable filter is descending from the middle to the bottom of the filter, as k_r increases from 1.0+0 to infinity. (3) [numerical formula] is increasing from 0.0+0 to 1.0-0,as k_r increases from 1.0+0 to infinity, where S_ is the value of S_ of the most stable filter. S_ is represented as : [numerical formula] (4) k_^* is increasing from 1.0+0 to infinity, as k_r increases from 1.0+0 to infinity, where k_^* is the average coefficient of permeability of the most stable filter and k_l is the coefficient of permeability at the bottom of the filter. k_^* is represented as : [numerical formula]
Coagulation, Fibrinolysis and Inhibitors in Failing Filters during Continuous Venovenous Hemofiltration in Critically Ill Patients with Acute Kidney Injury: Effect of Anticoagulation Modalities
Introduction: The mechanisms of early filter failure and clotting with different anticoagulation modalities during continuous venovenous hemofiltration (CVVH) are largely unknown. Methods: Citrate, heparin and no anticoagulation were compared. Blood was drawn pre- and post filter up to 720 min. Concentrations of the thrombin-antithrombin (TAT), activated protein C-protein C inhibitor (APC-PCI), and type I plasminogen activator inhibitor (PAI-1) were determined. Results: In case of early filter failure (<24 h), inlet concentrations of TAT and APC-PCI were higher over time, irrespective of anticoagulation. There was more production of APC-PCI and platelet-derived PAI-1 in the filter after 10 min in the heparin group than in other groups. In clotting filters, production of APC-PCI and PAI was also higher with heparin than citrate. Conclusion: Coagulation activation in plasma and inhibition of anticoagulation in plasma and filter may partly determine early CVVH filter failure due to clotting, particularly when heparin is used. Regional anticoagulation by citrate circumvents the inhibition of anticoagulation and fibrinolysis by platelet activation following heparin. (C) 2015 S. Karger AG, Base