PubMed · 5577096
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W Helbig. 1971-03-04. [Rationalization for differential cell counts].. https://pubmed.ncbi.nlm.nih.gov/5577096/
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Prestorage leukocyte reduction of platelet concentrates may reduce adverse effects of transfusion while affording better quality control. Platelets and leukocytes may undergo activation during storage, which could affect the performance of leukocyte reduction filters. The purpose of this study was to evaluate the efficiency of leukocyte reduction and concomitant platelet loss with a new apheresis kit with an integral leukocyte reduction filter. Twelve donors underwent plateletpheresis on three occasions using the CS-3000 PLUS Blood Cell Separator with the Access Management System and the Access Closed System Apheresis Kit with Integral Sepacell Leukocyte Reduction Filter and Double Return Line Needle (Baxter-Fenwal Division, Deerfield, IL). Of the three products from each donor, one each was filtered at 4, 24, and 48 hours after completion of the plateletpheresis. Mean prefiltration platelet count was 4.43 x 10(11) and mean postfiltration platelet count was 3.56 x 10(11). Mean platelet recovery at 4, 24, and 48 hours filtration was 75%, 83%, and 84%, respectively. Analysis of variance (ANOVA) demonstrated that platelet recovery with filtration at four hours was significantly less than with filtration at 24 hours (P = 0.0236) and filtration at 48 hours (P = 0.0122). Platelet recovery with filtration at 24 hours did not differ significantly from filtration at 48 hours (P = 0.7684). Mean prefiltration WBC count was 0.93 x 10(6) and mean postfiltration WBC count was 0.12 x 10(6). Efficiency of leukocyte reduction was not significantly related to when filtration was performed. There was no significant variation from donor in platelet recovery or in leukocyte reduction efficiency. This method of prestorage leukocyte reduction demonstrated slightly but statistically significantly better platelet recovery with filtration at 24 or 48 hours after platelet collection compared to four hours. All filtration times provided acceptable platelet yields with very low residual WBC.
The thromboelastogram (TEG) measures functional defects in coagulation, from fibrin formation through platelet aggregation to fibrinolysis. It is comparable with standard laboratory tests of coagulation; however, it provides additional useful qualitative information. This prospective study documents the TEG findings in 103 neonates: 60 were normal and healthy and provided a reference range; 12 surgical babies had established sepsis, 15 had early sepsis, and 16 were non-septic. TEG abnormalities were detected only in those patients with early and established sepsis. Abnormalities were found in all but 1 of this group of 27 patients (96%), whereas only 16 (59%) had thrombocytopenia, 2 (6%) had leukocytosis, and 6 had leukopenia. The TEG had a sensitivity for sepsis of 96% and a specificity of 96%. This exceeds the values for routine full blood-count parameters and other laboratory indicators of sepsis. It was found to be a simple, quick, and sensitive indicator of early sepsis that enabled the clinicians to manage septic newborns earlier.
Leucocyte adhesion molecules are involved in the leucocyte-endothelial interaction and in the activation of coagulation and binding of complement and endotoxin. Thus, they are important in inflammation, systemic acute phase reaction, ischaemia reperfusion injury and resistance against infections. The expression of the adhesion molecules CD11b, CD11c and CD62L on leucocytes and changes in plasma products of neutrophil activation (myeloperoxidase, lactoferrin) and complement activation (C3bc, SC5b-9 (TCC)) were examined in an extracorporeal circulation (ECC) model and the effects of Carmeda bioactive surface (CBAS) heparin coating (n = 7) of the circuits were compared to uncoated control circuits (n = 5). In this model, new 'unactivated' cells mobilized from the bone marrow could not interfere with descriptive measures of cell activation as seen in in vivo studies. In the control group, CD11b and CD11c were upregulated on monocytes and granulocytes during ECC, whereas CD62L was downregulated. Heparin coating reduced the increase in CD11b and CD11c on granulocytes (p < 0.02 at 2 h), but the delayed increase in CD11c on monocytes and the delayed downregulation of CD62L on granulocytes and monocytes did not reach statistical significance. Further, heparin coating also reduced the initial decrease in the absolute cell counts of monocytes and granulocytes (p = 0.01 at 2 h), reflecting reduced adhesion to the oxygenator/tubing. The increases in plasma myeloperoxidase, lactoferrin, C3bc and TCC were lower in the heparin-coated group compared to the control group. The increases in plasma myeloperoxidase and lactoferrin correlated significantly to the increase in CD11b (r = 0.71, p = 0.02 and r = 0.64, p = 0.05, respectively) and CD11c (r = 0.72, p = 0.008 and r = 0.72, p = 0.008, respectively) on granulocytes, suggesting interacting regulatory pathways in the process of neutrophil adhesion, activation and degranulation. Thus, in this in vitro ECC model, heparin coating of oxygenator/tubing sets reduced leucocyte activation and leucocyte adhesion-related phenomena.