Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure

Abstract

Influence of hematocrit on hemostasis in continuous venoven-treatment modality for patients with acute renal failure ous hemofiltration during acute renal failure.[1]. Since then, various other regimens for continuous Background. Hematocrit plays a major role in primary herenal replacement therapy, for example, continuous vemostasis by influencing blood viscosity and platelet adhesion.novenous hemofiltration (CVVH), have been developed. During continuous venovenous hemofiltration (CVVH), it isCVVH is especially suitable in patients with water and suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses electrolyte imbalances that are hemodynamically unstain the extracorporeal system. In order to examine this hypotheble [2]. The latter advantage and its ability to treat uremia sis, we studied the influence of hematocrit on hemostasis during effectively, even in cases of hypercatabolism, have led CVVH.to the rapid spread of this modality in recent years [3].Methods. Fourteen patients (8 men and 6 women, mean age Bleeding represents an important morbidity and mor-65 Ϯ 10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fretality factor in acute renal failure (ARF), and therefore, senius, Oberursel, Germany) were used in all of the patients; changes in hemostasis during CVVH may influence the blood flow rates were adjusted to 120 ml/min. No blood prodprognosis of ARF [4, 5]. The continuous contact between ucts and coagulation-related medication, except unfractionated blood and thrombogeneic foreign materials (hemofilter, heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemosta-extracorporeal circulation system), inherent in CVVH,

Coagulation, Fibrinolysis and Inhibitors in Failing Filters during Continuous Venovenous Hemofiltration in Critically Ill Patients with Acute Kidney Injury: Effect of Anticoagulation Modalities

“…Concentrations of TAT were low as compared to concentrations reported by others in critically ill patients, but higher in nonsurvivors than in survivors indicative of the harmful effects of coagulation activation in critically ill patients, many of them having sepsis, activating coagulation [9,13,16,19] . In case of early filter failure, concentrations of TAT were higher over time than when the filter lasted >24 h, suggesting that thrombin generation in the patient affected filter survival.…”

“…Indeed, heparin has been suggested to only partly determine filter survival in previous studies. A poor relation with aPTT is suggested, as found in this study also, possibly following dosing problems or heparin resistance, for instance by low antithrombin levels [9,10,17,23] . We did not observe a difference in filter survival between heparin and citrate as suggested by others [3,[5][6][7] , possibly due to the relatively small number of patients.…”

“…In critically ill patients, in whom sepsis is common, the coagulation/fibrinolysis balance is often deranged at initiation of CVVH and this may affect circuit survival, even when anticoagulation is used [9][10][11][12][13][14][15][16][17][18][19] . Simultaneous pro-and anticoagulant and pro-and antifibrinolytic processes may occur, which can be unravelled by using the following specific indicators.…”

“…Data on the activation of coagulation during CVVH are, however, conflicting. Some studies report the evidence for thrombin generation during CVVH [10,12,15,17] , whereas others do not [9,16,18] . Circulating zymogen protein C is activated by thrombomodulin, which is expressed on the surface of endothelial cells and on monocytes, once activated by thrombin.…”

“…Some prior studies on coagulation and fibrinolysis activation and inhibition did not differentiate between events in the patient and in the extracorporeal circuit, by only evaluating plasma levels of indicators [9][10][11][12][13] . In the few studies that studied specific indicators of coagulation and fibrinolysis activation and inhibition directly before and after the hemofilter, the mechanism of filter clotting and premature failure remained incompletely understood [15][16][17][18] .…”