Vascular access failure-cause or complication of central venous catheterization: Case report

© 2020, University of Kragujevac, Faculty of Science. All rights reserved. The quality of life and patient survival rate in terminal chronic renal insufficiency depends on the duration of vascular approaches. Dialysis catheters are used to establish an adequate vascular approach when emergency hemodialysis is indicated and when all approaches are exhausted. Complications of CVC can be classified into three categories: mechanical (hematoma, arterial puncture, pneumothorax, hemothorax, catheter misplacement, and stenosis), infectious (insertion site infection, CVC colonization, and bloodstream infection) and thrombotic (deep vein thrombosis). Despite the increasing prevalence of haemodialysis patients with complex access issues, there remains no consensus on the definition of vascular access failure or end-stage vascular access. The dilema in these cases remains whether the generalized vascular insufficiency is the cause or a complication of exhausted vascular accesses. This case report is one of the examples of combined complications with generalized vascular access insufficiency. During the year and a half of the chronic dialysis program, the patient had several changes of vascular approaches, and each approach became dysfunctional in certain time due to various causes. After six months of successful hemodialysis, the patient was admitted with signs of infection and during hospitalization was again subjected to multiple changes of the vascular approach due to infection, thrombosis, and vascular access failure

New Therapeutic Concepts in Post-Resuscitation Care

After the return of spontaneous circulation (ROSC), as a result of global ischaemia due to cardiac arrest followed by reperfusion, a condition develops called post-cardiac arrest syndrome. It manifests, alongside the pathology that caused the cardiac arrest, as a systemic inflammatory response, including severe cardio-circulatory and neurological dysfunction, leading to a fatal outcome. Th e aim of post-resuscitation care is to reduce the consequences of circulatory arrest, reperfusion, and the inflammatory response of the body on vital organ functions. The basis of post-resuscitation care comprises application of therapeutic hypothermia and early coronary angiography with PCI. However, after the initial enthusiasm, the validity of applying these aggressive methods in all comatose post-cardiac arrest patients was questioned. Currently, instead of therapeutic hypothermia, a strategy of maintaining a targeted body temperature, usually 36 °C, is being applied because there is no clear evidence of benefit for maintaining a lower body temperature in relation to the outcome. Additionally, patients with an obvious cardiac aetiology of cardiac arrest do not undergo early coronarography unless there is a clear indication of coronary artery occlusion. In the post-resuscitation period, the maintenance of adequate ventilation, maintaining levels of oxygen and carbon dioxide in the normal range, haemodynamic stability, control of blood glucose and electrolytes, and epileptic attack prevention are all strongly recommended measures. Th ere is no evidence to suggest that the application of the so-called neuroprotective agents affects the outcome of cardiac arrest

Vascular Access Failure - Cause or Complication of Central Venous Catheterization: Case Report

The quality of life and patient survival rate in terminal chronic renal insufficiency depends on the duration of vascular approaches. Dialysis catheters are used to establish an adequate vascular approach when emergency hemodialysis is indicated and when all approaches are exhausted. Complications of CVC can be classified into three categories: mechanical (hematoma, arterial puncture, pneumothorax, hemothorax, catheter misplacement, and stenosis), infectious (insertion site infection, CVC colonization, and bloodstream infection) and thrombotic (deep vein thrombosis). Despite the increasing prevalence of haemodialysis patients with complex access issues, there remains no consensus on the definition of vascular access failure or end-stage vascular access. The dilema in these cases remains whether the generalized vascular insufficiency is the cause or a complication of exhausted vascular accesses. This case report is one of the examples of combined complications with generalized vascular access insufficiency. During the year and a half of the chronic dialysis program, the patient had several changes of vascular approaches, and each approach became dysfunctional in certain time due to various causes. After six months of successful hemodialysis, the patient was admitted with signs of infection and during hospitalization was again subjected to multiple changes of the vascular approach due to infection, thrombosis, and vascular access failure

IL-33 receptor (ST2) deficiency downregulates myeloid precursors, inflammatory NK and dendritic cells in early phase of sepsis

Abstract Background Sepsis is a life-threatening disease mediated by profound disturbances in systemic inflammatory response to infection. IL-33 is multifunctional regulator of numerous aspects of innate and adaptive immune response. The aim of this article was to further evaluate the role of IL-33 receptor (ST2) in different pathways of innate immunity during early polymicrobial sepsis. Methods Polymicrobial sepsis was induced using cecal ligation and puncture (CLP) model in ST2 deficient (ST2−/−) and wild type BALB/c mice. Peritoneal and spleen cells were isolated for further phenotyping. Apoptosis was determined by immunohistochemistry and flow cytometry. Results Deletion of ST2 leads to increased susceptibility to early manifestations of sepsis as evaluated by clinical signs and survival. These are accompanied by decrease in the total number of neutrophils, eosinophils and mast cells in peritoneal cavity 12 h after CLP. In early sepsis there was also low number of precursors of myeloid cells in particular CD11b+Ly6G+Ly6Clow cells in spleen of ST2−/− mice. Although the number of NK cells in the spleen was similar, there were significant differences in the presence of inflammatory IFN-γ and IL-17 producing NK cells. Further, ST2 deletion affects the phenotype and maturation of dendritic cell in sepsis. The total number of dendritic cells in the spleen was lower as well as IL-12 expressing dendritic cells. Finally, there was higher frequency of active caspase-3 positive and early apoptotic cells, in particular CD11c positive cells, in spleen of septic ST2−/− mice. Conclusion Taken together, our data provide the evidence that ST2 deficiency in early phase of sepsis downregulates myeloid precursors, inflammatory NK and dendritic cells