plasma exchange (pe) and immunoadsorption (iA) are standard therapeutic options of immunemediated neurological disorders. This study evaluates the relation of the relative quantity of applied dose of PE and/ or IA and its achieved therapeutic effectiveness within the treated underlying neurological disorders. In a retrospective study, we evaluated data from PE and IA carried out 09/2009-06/2014 in neurological patients at the University-Hospital of Saarland, Germany. Apheresis dose was defined as the ratio of the extracorporeal treated plasma volume to the patient's plasma volume. Effectiveness was assessed through disease-specific tests and scores by the attending neurologist(s); results were classified into response or no response. 1101 apheresis (PE:238, IA:863), in 153 hospitalstays were carried out, averaged, 7.0 treatments per patients, 82% responded, 18% not. Mean applied apheresis dose per treatment was 0.91 with mean doses of 1.16 for PE and 0.81 for IA. The totally applied mean dose per stay was 5.6 (PE:5.01, IA:5.81). No correlation was seen between apheresis dosing and treatment effectiveness (PE:R2 = 0.074, IA:R2 = 0.0023). PE and IA in therapy-refractory immune-mediated neurological disorders majorly achieved a measurable severity improvementwithout correlation to the applied dose. Moreover, our data rather suggest, that effectiveness may be given with volumes below currently recommended volumes. Apheresis is an established method of removing proteins and antibodies from the blood, here of interest plasmapheresis (PE) and immunoadsorption (IA), two methods with different targeted blood components. In PE, the patient's plasma is withdrawn and replaced by fresh frozen plasma or by protein-contending solutions. In IA, the patient's plasma is passed through an adsorber, eliminating the target components. PE and/ or IA are, at least in therapy-refractory cases 1 , the standard therapeutic option for immune-mediated neurological diseases, here chronic inflammatory demyelinating polyneuropathy (CIDP) Guillain-Barré syndrome (GBS), myasthenia gravis, or multiple sclerosis. Central pathogenic elements of these immune-mediated diseases are B-lymphocytes and antibodies as directed to structures of the nervous system and are involved in the process of neuroinflammation, leading to neurological symptoms e.g the ascending paralysis or sensory deficits. So far, recommendations for relative plasma volume per patient and treatment are few and inconsistent. In our study, we exactly ask the question of a direct proportional effectiveness of PE and IA regarding response/ no response correlated to the applied apheresis dose, meaning the relative quantity of treated plasma volume. Methods Study population. All patients with study relevant immune-mediated nlogeuroical disorders and treated in the Department of Neurology at the Saarland University Medical Centre (UKS) between Sept 2009 and June 2014, were per se eligible for this study. Thereof, the therapeutic option of apheresis was considered in case of therapy failure ...

Objectives: After elective cardiac surgery a postoperative anticoagulation is obligatory. With critically ill patients the conventional anticoagulation standard heparin is sometimes impossible, e.g. based on HIT II. Then, argatroban is currently a possible alternative, however, due to its impaired metabolism in critically ill patients, anticoagulation effect is harder to anticipate, thus resulting in higher bleeding risk. Furthermore, to date no antidote is available. Hence, severe postoperative bleeding incidents under anticoagulation are commonly mono-causal attributed to the anticoagulation itself. This study concentrates on the number of well-defined postoperative bleeding incidents before any anticoagulation started, then actually under argatroban as well as compared to those under heparin (or switched from heparin to argatroban). Material and methods: Retrospective study including 215 patients undergoing elective cardiac surgery with a postoperative stay in ICU ≥48 h. Postoperative bleeding complications before and after start of anticoagulation were evaluated. Definition of bleeding complications were: decrease of hemoglobin by more than 2 g/dl without dilution (mean value of volume balance plus one standard deviation) and/or increased need of red blood cell transfusion/day (average transfusion rate + 2 standard deviations). Results: Within the study group of 215 patients, 143 were treated with heparin, 43 with argatroban, 29 switched from heparin to argatroban. Overall, 26.5% (57/215) postoperative bleeding complications occurred. In 54.4% (31/57) bleeding complications occurred before start of anticoagulation; in 43.6% (26/57) after. Of these, 14 bleeding incidents occurred under heparin 9.8% (14/143), 6 under argatroban 14% (6/43) and 6 switched 20.7% (6/29). Higher bleeding complications before start of anticoagulation was related to concomitant factors influencing the overall bleeding risk; e.g. score of severity of illness. These observations further correlate with postoperative, but not anticoagulation induced mortality rate of 2.8% of then given heparin, 20.9% then argatroban, 20.7% then switched. Conclusions: Postoperative bleeding complications cannot simply be attributed to anticoagulation since occurring often before anticoagulation was started. The risk for bleeding complications after start of anticoagulation was quite comparable for argatroban and heparin. Accordingly, the influence of argatroban on bleeding complications in the postoperative period may be less significant than previously thought.

Acute kidney injury (AKI) is a common complication in critically ill patients with an incidence of up to 50% in intensive care patients. The mortality of patients with AKI requiring dialysis in the intensive care unit is up to 50%, especially in the context of sepsis. Different approaches have been undertaken to reduce this high mortality by changing modalities and techniques of renal replacement therapy: an early versus a late start of dialysis, high versus low dialysate flows, intermittent versus continuous dialysis, anticoagulation with citrate or heparin, the use of adsorber or special filters in case of sepsis. Although in smaller studies some of these approaches seemed to have a positive impact on the reduction of mortality, in larger studies these effects could not been reproduced. This raises the question of whether there exists any impact of renal replacement therapy on mortality in critically ill patients—beyond an undeniable impact on uremia, hyperkalemia and/or hypervolemia. Indeed, this is one of the essential challenges of a nephrologist within an interdisciplinary intensive care team: according to the individual situation of a critically ill patient the main indication of dialysis has to be identified and all parameters of dialysis have to be individually chosen with respect to the patient’s situation and targeting the main dialysis indication. Such an interdisciplinary and individual approach would probably be able to reduce mortality in critically ill patients with dialysis requiring AKI.

Peritonitis is a common complication of peritoneal dialysis (PD). Our root cause analysis allowed to attribute some cases to leakage of the PD catheter. Accordingly, a clinically based stress test study on potential material damage issues of PD catheters was performed, focusing on material damage caused by cleaning, de- and attachment procedures during dialysate changes and on the individual storage methods of PD catheters between dialysate changes. PD catheters were exposed to both chemical stress by repeating dialysate-flow and physical stress simulating de- and connecting, fixation, pressure, flexing, folding etc.—simulating standard clinical daily routine of 8–10 years PD catheter usage. Potentially by normal usage caused damages should be then detected by intraluminal pressure, light- and electron microscopy. The multi-step visual control showed no obvious damages on PD catheters nor any leakage or barrier indulgence. Our tests simulating daily routine usage of PD catheters for several years could not detect any material defects under chemical or physical stress. Hence, we presume that most PD catheter damages, as identified cause for peritonitis in some of our patients, may be due to accidental, unnoticed external damage (e.g. through scissors, while changing dressings) or neglecting PD catheter handling specifications.