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Platelet concentrate effects on thromboelastography
P l a t e l e t C o n c e n t r a t e E f f e c t s on T h r o m b o e l a s t o g r a p h y Stephen E. McNulty, DO, Philip Sasso, MD, Joanne Vesci, BS, and Hugh Schieren, PhD Objective: This study evaluated platelet effects on thromboelastography to determine how morphologically abnormal platelets affected native whole blood analysis. Design: Prospective, controlled comparison. Setting: Tertiary care university hospital. Participants: Volunteer cardiac surgery patients. Interventions: Fresh platelets were obtained from volunteers and were either treated normally or cryodisrupted with liquid nitrogen. Fresh platelets, liquid nitrogen-treated platelets, or an equivalent quantity of the patient's blood were added to whole blood samples obtained from cardiac surgery patients before heparinization. Thromboelastographic parameters sensitive to platelet effects were measured in each of the three groups. Measurements and Main Results: Maximum amplitude and s-angle significantly increased in the two groups receiving
added platelets. There were no differences between the fresh platelet and the liquid nitrogen-treated platelet groups (Student's paired t-test). The R-time decreased significantly in both platelet-treated groups compared with the group that did not receive additional platelets. Conclusions: Viscoelastic changes in whole blood coagulation after the addition of platelet concentrates are not dependent on morphologically intact or functionally normal platelets. This in vitro study predicts that transfusion of poorly preserved platelet concentrates as well as fresh platelets would increase clot strength on thromboelastography if the recipient's blood were tested immediately after administration.
HROMBOELASTOGRAPHY has been used to diagnose and manage patients with qualitative and quantitative platelet deficiencies in various clinical situations. L-7 It has been advocated for determining the adequacy of platelet function in patients with active bleeding and for assessing the beneficial effects of transfused components, a,9 Transfusion of platelets may rapidly correct an abnormal thromboelastogram in patients with platelet deficiencies. It is unclear if a thromboelastogram corrected by platelet transfusion signifies the presence of morphologically intact platelets capable of all the complex interactions between the endothelium and platelet membrane.l° The platelet membrane facilitates activation of the coagulation cascade through various platelet-mediated coagulation protein interactions. 11 However, cell-to-cell hemostatic functions, such as adhesion and aggregation, use different pathways that are more dependent on having a morphologically intact platelet.12 It is possible that changes occurring in the thromboelastogram after platelet transfusion are primarily caused by membranecoagulation protein interactions and do not require the presence of a morphologically intact or functionally normal platelet. This study evaluates one aspect of platelet effects on the thromboelastogram using in vitro platelet concentrates. The purpose of this study was to determine how thromboelastographic analysis of whole blood was affected by the addition of platelets treated to irreversibly disrupt morphology.
sample was obtained after separation from citrated whole blood and plasma and before platelet pooling. No additional preservative was added to the ptatelet sample. The platelets were separated into two 1.2-mL cryo tubes (Cybron Corp, Rochester, NY), with 1 mL placed in each tube. One of the sealed cryo tubes was immersed in liquid nitrogen for 30 seconds, followed by a thawing period of 30 minutes. The frozen cryo tube was thawed in a water bath that was heated to 37°C. This freeze-thaw cycle was repeated three times, and the resultant sample of platelets was subsequently used for the liquid nitrogen-treated platelet group. The remaining untreated platelets were maintained at room temperature with gentle agitation. These platelets were subsequently used in the fresh platelet group within 4 hours of collection. A 15-mL blood sample was obtained from cardiac surgery patients through an indwelling radial artery catheter. The blood was withdrawn after the start of surgery, but before heparinization. From this specimen, three 4-mL samples were placed into separate test tubes. Two hundred gL of freshly donated platelets were added to the first test tube. Two hundred gL of liquid nitrogen-treated platelets were added to the second test tube. There were no additions to the third test tube. After gentle mixing of each of the three tubes, 360 IlL were micropipetted into separate disposable thromboelastographic cuvettes. A timer was used to keep the total elapsed time from removal of the blood specimen to the start of the thromboelastogram at 3 minutes. After the pins were lowered into the three cuvettes to start the Thrombelastograph, 2 drops of mineral oil were placed on the surface of the blood. An Eppendorf (Brinkman Instruments Inc, Westbury, NY) micropipette was used for volumetric measurements, using separate disposable Eppendorf pipette tips for each transfer of blood and platelets. Two two-channel Thrombelastograph D (Haemoscope Corp; Morton Grove, 1L) Thrombelastograph Coagulation Analyzers were used to measure the R-time, s-angle, and maximum amplitude (MA) for each specimen. Mechanical and electronic calibration of each channel was checked before each study according to the manufacturer's recommendations. Disposable cups and pins (Haemoscope Corp, Morton Grove, IL) were used in processing the samples. Statistical comparisons were performed among the blood control, fresh platelet, and treated platelet groups using ANOVA. Student's paired t-test was used to compare the fresh platelet and treated platelet groups. Ap < 0.05 was considered to be statistically significant.
T
METHODS Nine patients scheduled for elective coronary artery bypass gave written consent to participate in this Institutional Review Boardapproved study. Patients receiving intravenous heparin therapy within 6 hours of surgery were excluded from the study. All patients enrolled in the study received aspirin therapy within 36 hours of surgery. On the morning of surgery, a 2-mL specimen of freshly donated, single donor, platelet concentrate was obtained from a healthy volunteer. The platelet
From the Department of Anesthesiologz. Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA. Address reprint requests to Stephen E. McNulty, DO, Thomas Jefferson University Hospital, Department of Anesthesiology, 111 South 11th St, Suite G-6460, Philadelphia, PA 19107-5092. Copyright © 1997 by W.B. Saunders Company 1053-0770/97/1107-000353.00/0 828
Copyright © 1997 by W,B. Saunders Company KEY WORDS: thromboelastography, coagulation, platelets
RESULTS
There were significant changes in the thromboelastogram associated with the addition of the platelet concentrates. Compared with the whole blood control with no platelet additive, addition of either fresh or liquid nitrogen-treated platelets
Journal of Cardiothoracic and Vascular Anesthesia, Vo[ 11, No 7 (December), 1997: pp 828-830
PLATELETS AND TEG
829
resulted in a significant increase in maximum amplitude (p < 0.0005, ANOVA) and c~-angle (p < 0.0001, ANOVA). The corresponding measurements for maximum amplitude (Fig 1) in the whole blood, fresh platelet, and liquid nitrogen-treated platelet groups (mean ± SD) were 56 _+ 10 mm, 71 +_ 6 ram, and 72 ± 7 ram, respectively. The e~-angle (Fig 2) for the whole blood control was 28 ° ± 16 °, whereas the fresh platelet group was 71 ° ± 7 °, and the liquid nitrogen-treated platelet group was 72 ° ± 10°. There was also a significant decrease in R-time (p < 0.0001, ANOVA) compared with control. The R-time for the whole blood control (mean + SD)was 17 + 5 minutes. The R-time for the fresh platelet group was 4 _+ 3 minutes. The R-time for the liquid nitrogen-treated platelet group was 3 ± 3 minutes. There were no significant differences between normal and disrupted platelets for R-time (p = 0.18), c~-angle (p = 0.73), and MA (p = 0.78).
O~ 0~
<¢ 0=
,¢
Fresh
LN Treated
Control
Platelet Type DISCUSSION
The addition of platelet concentrate to a whole blood sample approximates the clinical situation of transfusing platelets, using an in vitro model. However, one of the important distinctions between platelet administration and this in vitro model was that filtration and eventual loss of abnormal platelets did not occur. This was necessary to ensure that one of the blood samples was exposed to a relatively high concentration of abnormal platelets. The dilution volume of 200 gL of platelet additive in 4 mL of whole blood would be equivalent to the administration of 4 to 8 U of platelet concentrate. That estimate is based on an approximate volume of 40 mL/U of platelet concentrate supplied by the blood bank. The in vitro platelet additive is likely equivalent to an even larger volume of administered platelets if the posttransfusion loss of platelets is accounted for. A rapid increase in the quantity of platelet glycoprotein receptors could explain why both groups of 90 8O
E E 70 =_
.....
60
5o
40
3O 20
Fresh
LN Treated
Control
Platelet Type Fig 1. Bar graph representing the differences in maximum amplitude among native whole blood samples (n = 9) given three treatments. Abbreviations: Fresh, single-donor platelets obtained within 4 hours II; LN-treated, platelets treated with liquid nitrogen rapid freeze-thaw processing ~ ; control, native whole blood sample with no platelet additives []. *Fresh and LN-treated platelet additives significantly increased maximum amplitude compared with control (p < 0.0005, ANOVA).
Fig 2. Bar graph representing the differences in ~-angle between native whole blood samples (n = 9) given three treatments. Abbreviations: Fresh, single-donor platelets obtained within 4 hours II; IN-treated, platelets treated with liquid nitrogen rapid freeze-thaw processing D; control, native whole blood sample with no p|atelet additives I~. *Fresh and LN-treated platelet additives significantly increased ~-angle compared with control (p < 0.0001, ANOVA).
platelet-treated blood samples were relatively hypercoagulable. This study demonstrated that both denatured and fresh platelet additives to whole blood significantly affected the thromboelastogram in a similar manner consistent with previous reports.13.~4 Several other issues regarding methodology should be addressed. This study used defective platelets that were subjected to repeated, rapid freeze-thaw processing. The rapid freezethaw process reliably causes disruption of cell membranes. 15 These morphologically disrupted platelets would be incapable of any additional cell-to-cell interactions such as adhesion or aggregation. However, because nothing was removed during processing, the liquid nitrogen-treated platelet sample should have fully retained capability for interactions with coagulation proteins. The samples were not filtered before mixing with the whole blood so that membrane components and granule contents released during freeze-thaw processing were preserved. 16 Similarities in the thromboelastographic changes produced by the fresh platelet group compared with the liquid nitrogentreated group indicates that the thromboelastogram was unable to discriminate the impaired platelets under the conditions of this study. It would seem that interaction between coagulation proteins from the whole blood and platelet glycoprotein receptors was sufficient to mask the deficiencies in the liquid nitrogen-treated platelets. These findings may be consistent with other studies in which the thromboelastogram was unable to detect aspirin-induced platelet abnormalities.7,~7 However, the liquid nitrogen-treated platelets were not independently tested to establish the exact functional defects that occurred during processing. Testing was not performed to quantitate the level of platelet function in the fresh platelet group. It is possible that the fresh platelets may have had some degree of impairment.~8 However, fresh platelets treated similarly were shown to have 90%
830
McNULTY ET AL
preservation of morphology, 76% preservation of aggregation, and effective correction of prolonged bleeding times. 19 The adhesive and aggregating functions of these platelets were, therefore, likely to be significantly better than the platelets subjected to repeated, rapid freezing and thawing. 2°,21 The results of this study support the responsiveness of the thromboelastogram to platelets in the coagulation process. However, the authors question the validity of using thromboelastographic analysis as a test that confirms the presence of normal platelets. This study supports that changes observed in the thromboelastogram after platelet transfusion do not require an intact platelet. It predicts that transfusion of poorly preserved platelet concentrates as well as fresh platelets would correct the
thromboelastograrn if the recipient's blood were tested immediately after administration, before the abnormal platelets were eliminated from the circulation. It should be emphasized that the liquid nitrogen processing used in this study was meant for in vitro use only. The results should not be construed as evidence for suitability to transfuse platelets treated in this manner to patients. These findings do not preclude the usefulness of thromboelastography as a clinical guide to assessing the adequacy of platelet component therapy, or in managing patients with known or suspected platelet deficiencies. However, further study is warranted to better define the role of the thromboelastogram in assessing the full range of platelet activities.
REFERENCES
1. Tuman KJ, Spiess BD, McCarthy RJ, Ivankovich AD: Effects of progressive blood loss on coagulation as measured by thromboelastography. Anesth Analg 66:856-863, 1987 2. Spiess BD, Tuman KJ, McCarthy RJ, et al: Thromboelastography as an indicator of post-cardiopulmonary bypass coagulopathies. J Clin Monit 3:25-30, 1987 3. Mongan PD, Hosking MP: The role of desmopressin acetate in patients undergoing coronary artery bypass surgery: A controlled clinical trial with thromboelastographic risk stratification. Anesthesiology 77:38-46, 1992 4. Essell JH, Martin TJ, Salinas J, et al: Comparison of thromboelastography to bleeding time and standard coagulation tests in patients after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 7:410-415, 1993 5. Pivalizza EG: Heparinase and thromboelastography in liver transplantation for a patient with yon Willebrand's disease. Anesthesiology 84:1236-1239, 1996 6. Tuman KJ, Spiess BD, Schoen RE, Ivankovich AD: Use of thromboelastography in the management of yon Willebrand's disease during cardiopulmonary bypass. J Cardiothorac Anestb 1:321-324, 1987 7. Orlikowski CEP, Payne AJ, Moodley J, Rocke DA: Thromboelastography after aspirin ingestion in pregnant and non-pregnant subjects. Br J Anaesth 69:159-161, 1992 8. Kang YG, Martin DJ, Marquez J, et al: Intraoperative changes in blood coagulation and thromboelastographic monitoring in liver transplantation. Anesth Analg 64:888-896, 1985 9. Pivalizza EG, Abramson DC: Thromboelastography as a guide to platelet transfusion. Anesthesiology 82:1086, 1995 i0. Body SC: Platelet activation and interactions with the microvasculature. J Cardiovasc Pharmaco127:S13-$25, 1996 1I. Walsh PN, Schmaier AH: Platelet-coagulant protein interactions.
in, Colman RW, Hirsch J, Marder VJ, Salzman EW, (eds): Hemostasis and Thrombosis: Basic Principles and Clinical Practice, (2nd ed). Philadelphia, PA: Lippincott, 1987, pp 689-709 12. Campbell FW, Edmunds LH: Platelet function and cardiopulmonary bypass, in, Gravlee GR Davis RF, Utley JR, (eds): Cardiopulmonary Bypass: Principles and Practice. Baltimore, MD: Williams and Wilkins, 1993, pp 407-435 13. deGaetano G, Bottecchia D, Verrnylen J: Effect of platelets on clot structuration, a thromboelastographic study. Thromb Res 3:425435, 1973 14. Clayton DG, Miro AM, Kramer DJ, et al: Quantification of thromboelastographic changes after blood component transfusion in patients with liver disease in the intensive care unit. Anesth Analg 81:272-278, 1995 15. McGann LE, Yang H, Walterson M: Manifestations of cell damage after freezing and thawing. Cryobiology 25:178-185, 1988 16. Aiken M, Ciaglowski RE, Walz DA: Isolation and identification of a 23,000-dalton heparin binding fragment from the amino terminus of bovine thrombospondin. Arch Biochem Biophys 250:257-262, 1986 17. Trentalange MJ, Walts LF: A comparison of thromboelastogram and template bleeding time in the evaluation of platelet function after aspirin ingestion. J Clin Anesth 3:377-381, 1991 18. Bode AP: Platelet activation may explain storage lesion in platelet concentrates. Blood Cells 16:109-126, 1990 19. Lazarus HM, Kaniecki-Green EA, Warm SE, et al: Therapeutic effectiveness of frozen platelet concentrates for transfusion. Blood 57:243-249, 1981 20. Owens M, Cimino C, Donnelly J: Cryopreserved platelets have decreased adhesive capacity. Transfusion 31:160-163, 1991 21. Slichter SJ: Platelet transfusion therapy. Hematol Oncol Clin North Am 4:291-311, 1990
added platelets. There were no differences between the fresh platelet and the liquid nitrogen-treated platelet groups (Student's paired t-test). The R-time decreased significantly in both platelet-treated groups compared with the group that did not receive additional platelets. Conclusions: Viscoelastic changes in whole blood coagulation after the addition of platelet concentrates are not dependent on morphologically intact or functionally normal platelets. This in vitro study predicts that transfusion of poorly preserved platelet concentrates as well as fresh platelets would increase clot strength on thromboelastography if the recipient's blood were tested immediately after administration.
HROMBOELASTOGRAPHY has been used to diagnose and manage patients with qualitative and quantitative platelet deficiencies in various clinical situations. L-7 It has been advocated for determining the adequacy of platelet function in patients with active bleeding and for assessing the beneficial effects of transfused components, a,9 Transfusion of platelets may rapidly correct an abnormal thromboelastogram in patients with platelet deficiencies. It is unclear if a thromboelastogram corrected by platelet transfusion signifies the presence of morphologically intact platelets capable of all the complex interactions between the endothelium and platelet membrane.l° The platelet membrane facilitates activation of the coagulation cascade through various platelet-mediated coagulation protein interactions. 11 However, cell-to-cell hemostatic functions, such as adhesion and aggregation, use different pathways that are more dependent on having a morphologically intact platelet.12 It is possible that changes occurring in the thromboelastogram after platelet transfusion are primarily caused by membranecoagulation protein interactions and do not require the presence of a morphologically intact or functionally normal platelet. This study evaluates one aspect of platelet effects on the thromboelastogram using in vitro platelet concentrates. The purpose of this study was to determine how thromboelastographic analysis of whole blood was affected by the addition of platelets treated to irreversibly disrupt morphology.
sample was obtained after separation from citrated whole blood and plasma and before platelet pooling. No additional preservative was added to the ptatelet sample. The platelets were separated into two 1.2-mL cryo tubes (Cybron Corp, Rochester, NY), with 1 mL placed in each tube. One of the sealed cryo tubes was immersed in liquid nitrogen for 30 seconds, followed by a thawing period of 30 minutes. The frozen cryo tube was thawed in a water bath that was heated to 37°C. This freeze-thaw cycle was repeated three times, and the resultant sample of platelets was subsequently used for the liquid nitrogen-treated platelet group. The remaining untreated platelets were maintained at room temperature with gentle agitation. These platelets were subsequently used in the fresh platelet group within 4 hours of collection. A 15-mL blood sample was obtained from cardiac surgery patients through an indwelling radial artery catheter. The blood was withdrawn after the start of surgery, but before heparinization. From this specimen, three 4-mL samples were placed into separate test tubes. Two hundred gL of freshly donated platelets were added to the first test tube. Two hundred gL of liquid nitrogen-treated platelets were added to the second test tube. There were no additions to the third test tube. After gentle mixing of each of the three tubes, 360 IlL were micropipetted into separate disposable thromboelastographic cuvettes. A timer was used to keep the total elapsed time from removal of the blood specimen to the start of the thromboelastogram at 3 minutes. After the pins were lowered into the three cuvettes to start the Thrombelastograph, 2 drops of mineral oil were placed on the surface of the blood. An Eppendorf (Brinkman Instruments Inc, Westbury, NY) micropipette was used for volumetric measurements, using separate disposable Eppendorf pipette tips for each transfer of blood and platelets. Two two-channel Thrombelastograph D (Haemoscope Corp; Morton Grove, 1L) Thrombelastograph Coagulation Analyzers were used to measure the R-time, s-angle, and maximum amplitude (MA) for each specimen. Mechanical and electronic calibration of each channel was checked before each study according to the manufacturer's recommendations. Disposable cups and pins (Haemoscope Corp, Morton Grove, IL) were used in processing the samples. Statistical comparisons were performed among the blood control, fresh platelet, and treated platelet groups using ANOVA. Student's paired t-test was used to compare the fresh platelet and treated platelet groups. Ap < 0.05 was considered to be statistically significant.
T
METHODS Nine patients scheduled for elective coronary artery bypass gave written consent to participate in this Institutional Review Boardapproved study. Patients receiving intravenous heparin therapy within 6 hours of surgery were excluded from the study. All patients enrolled in the study received aspirin therapy within 36 hours of surgery. On the morning of surgery, a 2-mL specimen of freshly donated, single donor, platelet concentrate was obtained from a healthy volunteer. The platelet
From the Department of Anesthesiologz. Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA. Address reprint requests to Stephen E. McNulty, DO, Thomas Jefferson University Hospital, Department of Anesthesiology, 111 South 11th St, Suite G-6460, Philadelphia, PA 19107-5092. Copyright © 1997 by W.B. Saunders Company 1053-0770/97/1107-000353.00/0 828
Copyright © 1997 by W,B. Saunders Company KEY WORDS: thromboelastography, coagulation, platelets
RESULTS
There were significant changes in the thromboelastogram associated with the addition of the platelet concentrates. Compared with the whole blood control with no platelet additive, addition of either fresh or liquid nitrogen-treated platelets
Journal of Cardiothoracic and Vascular Anesthesia, Vo[ 11, No 7 (December), 1997: pp 828-830
PLATELETS AND TEG
829
resulted in a significant increase in maximum amplitude (p < 0.0005, ANOVA) and c~-angle (p < 0.0001, ANOVA). The corresponding measurements for maximum amplitude (Fig 1) in the whole blood, fresh platelet, and liquid nitrogen-treated platelet groups (mean ± SD) were 56 _+ 10 mm, 71 +_ 6 ram, and 72 ± 7 ram, respectively. The e~-angle (Fig 2) for the whole blood control was 28 ° ± 16 °, whereas the fresh platelet group was 71 ° ± 7 °, and the liquid nitrogen-treated platelet group was 72 ° ± 10°. There was also a significant decrease in R-time (p < 0.0001, ANOVA) compared with control. The R-time for the whole blood control (mean + SD)was 17 + 5 minutes. The R-time for the fresh platelet group was 4 _+ 3 minutes. The R-time for the liquid nitrogen-treated platelet group was 3 ± 3 minutes. There were no significant differences between normal and disrupted platelets for R-time (p = 0.18), c~-angle (p = 0.73), and MA (p = 0.78).
O~ 0~
<¢ 0=
,¢
Fresh
LN Treated
Control
Platelet Type DISCUSSION
The addition of platelet concentrate to a whole blood sample approximates the clinical situation of transfusing platelets, using an in vitro model. However, one of the important distinctions between platelet administration and this in vitro model was that filtration and eventual loss of abnormal platelets did not occur. This was necessary to ensure that one of the blood samples was exposed to a relatively high concentration of abnormal platelets. The dilution volume of 200 gL of platelet additive in 4 mL of whole blood would be equivalent to the administration of 4 to 8 U of platelet concentrate. That estimate is based on an approximate volume of 40 mL/U of platelet concentrate supplied by the blood bank. The in vitro platelet additive is likely equivalent to an even larger volume of administered platelets if the posttransfusion loss of platelets is accounted for. A rapid increase in the quantity of platelet glycoprotein receptors could explain why both groups of 90 8O
E E 70 =_
.....
60
5o
40
3O 20
Fresh
LN Treated
Control
Platelet Type Fig 1. Bar graph representing the differences in maximum amplitude among native whole blood samples (n = 9) given three treatments. Abbreviations: Fresh, single-donor platelets obtained within 4 hours II; LN-treated, platelets treated with liquid nitrogen rapid freeze-thaw processing ~ ; control, native whole blood sample with no platelet additives []. *Fresh and LN-treated platelet additives significantly increased maximum amplitude compared with control (p < 0.0005, ANOVA).
Fig 2. Bar graph representing the differences in ~-angle between native whole blood samples (n = 9) given three treatments. Abbreviations: Fresh, single-donor platelets obtained within 4 hours II; IN-treated, platelets treated with liquid nitrogen rapid freeze-thaw processing D; control, native whole blood sample with no p|atelet additives I~. *Fresh and LN-treated platelet additives significantly increased ~-angle compared with control (p < 0.0001, ANOVA).
platelet-treated blood samples were relatively hypercoagulable. This study demonstrated that both denatured and fresh platelet additives to whole blood significantly affected the thromboelastogram in a similar manner consistent with previous reports.13.~4 Several other issues regarding methodology should be addressed. This study used defective platelets that were subjected to repeated, rapid freeze-thaw processing. The rapid freezethaw process reliably causes disruption of cell membranes. 15 These morphologically disrupted platelets would be incapable of any additional cell-to-cell interactions such as adhesion or aggregation. However, because nothing was removed during processing, the liquid nitrogen-treated platelet sample should have fully retained capability for interactions with coagulation proteins. The samples were not filtered before mixing with the whole blood so that membrane components and granule contents released during freeze-thaw processing were preserved. 16 Similarities in the thromboelastographic changes produced by the fresh platelet group compared with the liquid nitrogentreated group indicates that the thromboelastogram was unable to discriminate the impaired platelets under the conditions of this study. It would seem that interaction between coagulation proteins from the whole blood and platelet glycoprotein receptors was sufficient to mask the deficiencies in the liquid nitrogen-treated platelets. These findings may be consistent with other studies in which the thromboelastogram was unable to detect aspirin-induced platelet abnormalities.7,~7 However, the liquid nitrogen-treated platelets were not independently tested to establish the exact functional defects that occurred during processing. Testing was not performed to quantitate the level of platelet function in the fresh platelet group. It is possible that the fresh platelets may have had some degree of impairment.~8 However, fresh platelets treated similarly were shown to have 90%
830
McNULTY ET AL
preservation of morphology, 76% preservation of aggregation, and effective correction of prolonged bleeding times. 19 The adhesive and aggregating functions of these platelets were, therefore, likely to be significantly better than the platelets subjected to repeated, rapid freezing and thawing. 2°,21 The results of this study support the responsiveness of the thromboelastogram to platelets in the coagulation process. However, the authors question the validity of using thromboelastographic analysis as a test that confirms the presence of normal platelets. This study supports that changes observed in the thromboelastogram after platelet transfusion do not require an intact platelet. It predicts that transfusion of poorly preserved platelet concentrates as well as fresh platelets would correct the
thromboelastograrn if the recipient's blood were tested immediately after administration, before the abnormal platelets were eliminated from the circulation. It should be emphasized that the liquid nitrogen processing used in this study was meant for in vitro use only. The results should not be construed as evidence for suitability to transfuse platelets treated in this manner to patients. These findings do not preclude the usefulness of thromboelastography as a clinical guide to assessing the adequacy of platelet component therapy, or in managing patients with known or suspected platelet deficiencies. However, further study is warranted to better define the role of the thromboelastogram in assessing the full range of platelet activities.
REFERENCES
1. Tuman KJ, Spiess BD, McCarthy RJ, Ivankovich AD: Effects of progressive blood loss on coagulation as measured by thromboelastography. Anesth Analg 66:856-863, 1987 2. Spiess BD, Tuman KJ, McCarthy RJ, et al: Thromboelastography as an indicator of post-cardiopulmonary bypass coagulopathies. J Clin Monit 3:25-30, 1987 3. Mongan PD, Hosking MP: The role of desmopressin acetate in patients undergoing coronary artery bypass surgery: A controlled clinical trial with thromboelastographic risk stratification. Anesthesiology 77:38-46, 1992 4. Essell JH, Martin TJ, Salinas J, et al: Comparison of thromboelastography to bleeding time and standard coagulation tests in patients after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 7:410-415, 1993 5. Pivalizza EG: Heparinase and thromboelastography in liver transplantation for a patient with yon Willebrand's disease. Anesthesiology 84:1236-1239, 1996 6. Tuman KJ, Spiess BD, Schoen RE, Ivankovich AD: Use of thromboelastography in the management of yon Willebrand's disease during cardiopulmonary bypass. J Cardiothorac Anestb 1:321-324, 1987 7. Orlikowski CEP, Payne AJ, Moodley J, Rocke DA: Thromboelastography after aspirin ingestion in pregnant and non-pregnant subjects. Br J Anaesth 69:159-161, 1992 8. Kang YG, Martin DJ, Marquez J, et al: Intraoperative changes in blood coagulation and thromboelastographic monitoring in liver transplantation. Anesth Analg 64:888-896, 1985 9. Pivalizza EG, Abramson DC: Thromboelastography as a guide to platelet transfusion. Anesthesiology 82:1086, 1995 i0. Body SC: Platelet activation and interactions with the microvasculature. J Cardiovasc Pharmaco127:S13-$25, 1996 1I. Walsh PN, Schmaier AH: Platelet-coagulant protein interactions.
in, Colman RW, Hirsch J, Marder VJ, Salzman EW, (eds): Hemostasis and Thrombosis: Basic Principles and Clinical Practice, (2nd ed). Philadelphia, PA: Lippincott, 1987, pp 689-709 12. Campbell FW, Edmunds LH: Platelet function and cardiopulmonary bypass, in, Gravlee GR Davis RF, Utley JR, (eds): Cardiopulmonary Bypass: Principles and Practice. Baltimore, MD: Williams and Wilkins, 1993, pp 407-435 13. deGaetano G, Bottecchia D, Verrnylen J: Effect of platelets on clot structuration, a thromboelastographic study. Thromb Res 3:425435, 1973 14. Clayton DG, Miro AM, Kramer DJ, et al: Quantification of thromboelastographic changes after blood component transfusion in patients with liver disease in the intensive care unit. Anesth Analg 81:272-278, 1995 15. McGann LE, Yang H, Walterson M: Manifestations of cell damage after freezing and thawing. Cryobiology 25:178-185, 1988 16. Aiken M, Ciaglowski RE, Walz DA: Isolation and identification of a 23,000-dalton heparin binding fragment from the amino terminus of bovine thrombospondin. Arch Biochem Biophys 250:257-262, 1986 17. Trentalange MJ, Walts LF: A comparison of thromboelastogram and template bleeding time in the evaluation of platelet function after aspirin ingestion. J Clin Anesth 3:377-381, 1991 18. Bode AP: Platelet activation may explain storage lesion in platelet concentrates. Blood Cells 16:109-126, 1990 19. Lazarus HM, Kaniecki-Green EA, Warm SE, et al: Therapeutic effectiveness of frozen platelet concentrates for transfusion. Blood 57:243-249, 1981 20. Owens M, Cimino C, Donnelly J: Cryopreserved platelets have decreased adhesive capacity. Transfusion 31:160-163, 1991 21. Slichter SJ: Platelet transfusion therapy. Hematol Oncol Clin North Am 4:291-311, 1990