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• W2091279052 abstract "Thromboelastography (TEG) analyzes the status of blood coagulation, including abnormalities associated with low platelet count [1]. Using TEG to guide platelet transfusion has thus been advocated by several investigators [2-6]. However, it is not clear whether TEG variables, assessed from the shape of its tracing, are regulated by platelets quantitatively, because these variables are concurrently under the influence of coagulation factors. We examined the modulation of TEG variables by the amount of platelet, which was controlled by the dilution of platelets into the patient's plasma without affecting other factors. We also attempted to evaluate the critical platelet counts in coagulation by using this technique. Methods After approval by the local institutional review board, six volunteers (26-38 yr old; two male, four female) scheduled for elective surgery gave their informed, written consent to participate in our study. No patients received anticoagulant and/or antiplatelet medications. No patient had any abnormality in coagulation, either clinically or by measurements of prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, bleeding time, and platelet count. They received 0.5 mg of atropine and 50 mg of hydroxyzine IM as premedication approximately 1 h before anesthesia. Blood samples were obtained just before the induction of general anesthetic from a 20-gauge plastic cannula inserted in a forearm vein using a two-syringe technique. After the first 6-10 mL of blood was drawn and discarded, the second blood sample was drawn into a polypropylene tube containing 1.2 mL of 3.8% sodium citrate, resulting in 12 mL of citrated blood. Platelet-rich plasma (PRP) was obtained by the centrifugation of citrated blood at 240g for 10 min. A one-half volume of PRP was further centrifuged at 3000g for 5 min to obtain platelet-poor plasma (PPP). PRP and PPP were mixed at preselected ratios (5:0, 4:1, 3:2, 2:3, 1:4, and 0:5 vol/vol) to give a series of plasma containing various amounts of platelet from each patient. The platelet count in each sample was measured by an automated blood cell/platelet counter (MEK-6108; Nihon Kohden, Tokyo, Japan) after mixing PRP and PPP. PT, aPTT, and the concentration of fibrinogen of these samples were measured by the Coagulation Laboratory (ACL 2000; Instrumentation Laboratory, Milano, Italy). There was no significant difference in these values among the samples in each series, which confirmed that the process of mixing PRP and PPP at various ratios did not influence coagulation factors. TEG of citrated plasma was performed by adding Ca2+. In brief, 250 [micro sign]L of the PRP/PPP mixture was pipetted into the prewarmed (37[degree sign]C) cuvette of a thromboelastograph (Hellige, Freiburg, Germany). Coagulation was achieved by adding 50 [micro sign]L of 0.4% CaCl2 to the plasma. CaCl2 was uniformly mixed by lowering and raising the pin of the thromboelastograph three to four times before layering liquid paraffin on the surface of plasma. TEG variables (reaction time [r], coagulation time [k], and maximal amplitude [MA]) were measured from each tracing (Figure 1). All samples were measured within 3 h after the blood sampling.Figure 1: The thromboelastogram measurement was commenced by adding Ca2+ in the citrated plasma. Reaction time (r) was defined as the time from CaCl2 was added in the cuvette until the amplitude of the thromboelastogram tracing reached 2 mm. Coagulation time (k) was defined as the interval when the trace amplitude reached 20 mm after r. Maximal amplitude (MA) was defined as the greatest amplitude on thromboelastogram tracing.Statistical analysis included linear regression and analysis of variance, followed by Bonferroni's test for multiple comparison, as indicated in Results. The statistical significance of the linear regression was confirmed by analysis of variance. A value of P < 0.05 was considered significant. Data are expressed as mean +/- SD. Results We studied the TEG tracings of 36 samples obtained from six individual series of citrated plasma containing various amounts of platelet. Nine samples were omitted because the platelet count was under the detection limit of the particle counter. TEG variables were plotted against the logarithm of platelet count (log (10) [platelet (/[micro sign]L)]). A potent linear relationship between MA and log10 [platelet (/[micro sign]L)] was observed (R2 = 0.739, P < 0.0001) (Figure 2A-1). An inverse linear regression of log10 [platelet (/[micro sign]L)] with k was also seen, although the statistical significance was less potent than with MA (R2 = 0.356, P = 0.001) (Figure 2B-1). We found from each individual plot that log10 [platelet (/[micro sign]L)] was significantly related to MA in every series, whereas two of the six series showed no significant relationship of log10 [platelet (/[micro sign]L)] with k (Figure 2). In contrast, no significant relationship between log10 [platelet (/[micro sign]L)] and r was observed in every series (Table 1).Figure 2: A-1, The relationship of the maximal amplitude (MA) in thromboelastography (TEG) with the logarithm of platelet count (log10 [platelet (/[micro sign]L)]). Six individual series of citrated plasma containing various amounts of platelet were obtained by mixing platelet-rich plasma and platelet-poor plasma from each patient at various ratios (n = 27). The measurement of TEG was commenced by adding Ca2+ in the citrated plasma. A-2 and A-3, Two representative MA-log10 [platelet (/[micro sign]L)] plots obtained from individual series (Patients 1 and 3, respectively). A similar significant linear relationship of log10 [platelet (/[micro sign]L)] with MA was observed in every series. B-1, The relationship of the coagulation time (k) with log10 [platelet (/[micro sign]L)] obtained from the same patients shown in A-1 (n = 27). B-2 and B-3, Two representative k-log10 [platelet (/[micro sign]L)] plots obtained from the corresponding patients shown in A-2 and A-3. A significant linear relationships of log10 [platelet (/[micro sign]L)] with k was observed from four individual series in total six patients.Table 1: Critical Platelet Count Determined from the 2SD Limit of TEG Variables at Normal Platelet Counts (>or=to150 x 103/[micro sign]L)To determine the critical platelet counts in coagulation, we defined the normal limit of TEG as the 2SD limit of each TEG variable from samples containing normal platelet counts (>or=to150 x 103/[micro sign]L) (Table 2). From each individual plot of MA and k against log10 [platelet (/[micro sign]L)], we calculated the platelet counts at which a linear regression line surpasses the lower and longer limits of normal ranges for MA and k, respectively. The platelet count showing the lower limit of normal MA range (46.7 mm) was 58 +/- 29 x 103/[micro sign]L, and the longer limit of k (8.5 min) was 145 +/- 62 x 103/[micro sign]L. The values of individual critical platelet counts are shown in Table 1.Table 2: Changes in TEG VariablesThe samples were also grouped into four levels according to the logarithm of platelet count. A significant decrease in MA and a prolongation in k at platelet counts <66 x 103/[micro sign]L, compared with the corresponding values at normal platelet counts (>or=to150 x 103/[micro sign]L), were observed (Table 2). Discussion Platelet aggregation to form a plug at injured vascular endothelium is the initial step of hemostasis. The following coagulation cascade occurs on the surface of aggregated platelets because phospholipids in the platelet membrane are required for the activation of coagulation factor X and prothrombin [7], which suggests that the amount of platelet influences clot formation. The quantitative abnormality of platelets is thus an important factor in deciding whether the indication of therapeutics (e.g., platelet transfusion, regional anesthesia) is proper during perioperative management. TEG has been advocated as a useful guide of blood transfusion practice in cardiac surgery [2], liver transplantation [3-5], and intensive care medicine [6]. The diagnostic use of TEG for patients at risk of coagulopathy, in whom epidural anesthesia is indicated, has also been attempted by several investigators [8,9]. It has been reported that several TEG variables are associated with platelet dysfunction [8-10], whereas the resultant changes in TEG are also influenced by coagulation factors, causing the evaluation complex. We measured TEG of citrated plasma after recalcification. Our method made it possible to analyze the modulation of TEG merely by the amount of platelet because we could obtain a series of plasma with various platelet counts from one patient at a time without affecting the concentration of coagulation factors. Using this method, a potent linear relationship of log10 [platelet (/[micro sign]L)] with MA was demonstrated. We then attempted to determine the critical level of platelet count in coagulation by two approaches. First, from an individual linear regression line of MA against log10 [platelet (/[micro sign]L)], we determined the critical platelet count at which MA value is less than the normal limit, i.e., mean - 2SD of MA from samples in normal platelet counts (>or=to150 x 103/[micro sign]L). Because MA reflects clot strengthening [1], it has been suggested that the abnormality in hemostasis occurs under the calculated value (58 +/- 29 x 103/[micro sign]L). However, the wide-spread variance of these individual critical platelet counts indicated that the significance of platelet count regarding the strength of clot varied among individuals, possibly due to the complex interaction of platelet function with other factors relating to blood coagulation. We also studied the individual plot of k as a function of platelet count. The k time is thought to be affected by the amount of platelet, as well as the concentration of coagulation factors, because it represents the velocity to form a clot as a result of fibrin cross-linkage at the surface of platelets [1]. However, a linear-relationship of log10 [platelet (/[micro sign]L)] with k was observed only in two thirds of the six individual series of platelet-containing plasma, in contrast to that of MA, which was observed in every series. This indicates that the amount of platelet is not the principal factor of the clot-forming rate and suggests that the calculated critical platelet count for k (69 +/- 46 x 103/[micro sign]L) has further limiting value, compared with that for MA. The second approach to determining the critical platelet count was to evaluate the change in MA among the groups classified by the logarithm of platelet count. We found that the MA of the group at platelet counts <66 x 103/[micro sign]L was significantly smaller than that of the group at normal platelet counts (>or=to150 x 103/[micro sign]L). The k time of the group at <66 x 103/[micro sign]L platelet counts was also significantly prolonged compared with that of the group at normal platelet counts, the same as shown for the change in MA. In summary, two variables of TEG, MA and k, were linearly related with log10 [platelet (/[micro sign]L)]. We propose that the platelet count <66 x 103/[micro sign]L is implicated in the risk of dysfunction to form a clot, whereas the critical platelet count evaluated by using TEG varied among individuals." @default.
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• W2091279052 title "Quantitative Measurement of Thromboelastography as a Function of Platelet Count" @default.
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