I Stefanidis, B Heintz, D Frank, P R Mertens, H P Kierdorf
{"title":"Influence of hematocrit on hemostasis in continuous venovenous hemofiltration during acute renal failure.","authors":"I Stefanidis, B Heintz, D Frank, P R Mertens, H P Kierdorf","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH.</p><p><strong>Methods: </strong>Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment.</p><p><strong>Results: </strong>The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8).</p><p><strong>Conclusion: </strong>Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.</p>","PeriodicalId":17704,"journal":{"name":"Kidney international. Supplement","volume":" 72","pages":"S51-5"},"PeriodicalIF":0.0000,"publicationDate":"1999-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kidney international. Supplement","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Hematocrit plays a major role in primary hemostasis by influencing blood viscosity and platelet adhesion. During continuous venovenous hemofiltration (CVVH), it is suspected that an increased hematocrit is accompanied by an activation of hemostasis and frequently leads to thromboses in the extracorporeal system. In order to examine this hypothesis, we studied the influence of hematocrit on hemostasis during CVVH.
Methods: Fourteen patients (8 men and 6 women, mean age 65+/-10 years) with acute renal failure undergoing CVVH were prospectively enrolled. Polysulfone hemofilters (AV 600; Fresenius, Oberursel, Germany) were used in all of the patients; blood flow rates were adjusted to 120 ml/min. No blood products and coagulation-related medication, except unfractionated heparin, were applied. Study exclusion criteria included a history of thromboembolism and artificial heart valves. Hemostasis activation markers (fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin, platelet retention) and hematocrit values were determined before and at three-day intervals during the course of CVVH treatment.
Results: The mean hematocrit value (mean +/- SEM) was 29+/-1% (range, 22 to 35%). Patients with hematocrit values of less than 30% (N = 7) were compared with patients with higher hematocrit values (>30%, N = 7). The patients with a lower hematocrit (<30%) showed a stronger activation of hemostasis during CVVH when compared with those with a higher hematocrit (>30%), as indicated by a tendency toward higher values for fibrinopeptide A (25+/-8 vs. 14+/-5 ng/ml, P = 0.35), thrombin-antithrombin III complex (15+/-4 vs. 10+/-2 ng/ml, P = 0.66), and a higher beta-thromboglobulin/creatinine ratio (0.62+/-0.17 vs. 0.48+/-0.12, P = 0.8).
Conclusion: Contrary to our hypothesis, hematocrit values of more than 30% are not accompanied by an increased hemostasis activation during CVVH. Concerning hemostasis activation, hematocrit values between 30 and 35% may be suitable for patients on CVVH.