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Background: Plasmatic coagulation disorders in trauma patients are common and their management is subject to current guidelines. Less evidence exists for platelet function. Although it is known that several trauma-associated factors have a negative influence on platelet function, routine monitoring has not yet become established.Methods: A retrospective single center study was carried out at a German level 1 trauma center from 2010 to 2016. In all patients fulfilling the requirements for the German Trauma Society (DGU) Traumaregister® who were admitted directly from the scene of the incident, platelet function was analyzed using the Platelet Function Analyzer (PFA 100®) with adenosine diphosphate (ADP) and epinephrine as activation factors. After exclusion of patients with intake of long-term anticoagulant and antiaggregant medication, possible influencing factors of a reduced platelet function were identified.Results: The results from 310 patients (44.0 ± 14.7 years, 76% male, Injury Severity Score, ISS 28.4 ± 14.2 points) were available. A delayed platelet activation was found in 25.5% using ADP and 31% using epinephrine. Laboratory parameters indicated a greater blood loss. Prolonged closure times were associated with an increased transfusion rate of packed red blood cell concentrates and a higher mortality rate. Logistic regression revealed hemoglobin (Hb) and fibrinogen levels at admission to be independent predictors for a decreased platelet activation in the assay with ADP (p < 0.001, Cohen's f = 0.61) and with epinephrine (p < 0.001, f = 0.42).Conclusion: Approximately one quarter to one third of primarily admitted trauma patients without long-term anticoagulation medication showed a delayed platelet activation in the PFA-100 test. By considering all trauma patients an even higher rate can be expected. The Hb and fibrinogen levels at admission can be helpful to estimate platelet disorders. The development of platelet assays to guide the resuscitation of individual patients seems to be absolutely necessary. The contribution of platelet disorders to trauma-induced coagulopathy is not sufficiently understood. Regarding the importance assigned to platelet transfusion or administration of desmopressin, these aspects should be the subject of further research. [ABSTRACT FROM AUTHOR]

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The investigation of in vitro platelet functions from patients with SLE and rheumatoid arthritis (RA) revealed a distinctly reduced aggregation mass after both collagen und ADP induction. The platelet serotonin contents were significantly decreased in both groups. An 'aspirin-like' platelet defect could be excluded by finding a normal malonyldialdehyde release of patients' platelets upon thrombin stimulation. Significantly increased platelet associated IgG was also detected, whereas platelet associated IgM remained within normal limits. These results are interpreted as indicating an ongoing platelet release reaction induced by IgG platelet antibodies, which induce the observed impairment of platelet functions and may also lead to the release of proinflammatory platelet mediators. [ABSTRACT FROM AUTHOR]

About 50% of the circulating platelets can be taken from healthy donors by means of the cell separation technique. In order to investigate the effect of cell separation on thrombopoesis bone marrow samples were taken from 12 voluntary donors up to 5 times. The megacaryocytes were analyzed before and after cell separation by morphometric measures and determinations of platelet count and platelet function (adhesion, aggregation, spreading, retraction) were carried out. Removing of large amounts of platelets form the circulation by stimulation of thrombopoesis resulted in an increase of the peripherical platelet count already 48 h after cell separation. Of the platelet functions tested only aggregation induced by collagen was found to be increased after cell separation as compared to that before the procedure. [ABSTRACT FROM AUTHOR]

In man, a single oral dose of 100-300 mg ASA leads to irreversible and almost total inhibition of cyclo-oxygenase in the platelets. The ensuing inhibition of thromboxane-formation results in a reduction of ADP- or collagen-induced or spontaneous platelet aggregation, which lasts for up to 7-9 days. Application of ASA in small doses ranging between 50-200 mg/day are sufficient to inhibit platelet aggregation continuously. Spontaneous platelet shape change after blood sampling and tissue extract-induced platelet stimulation are inhibited after single oral ASA-dosis of 500-1000 mg for also 8-12 h. Oral administration of 500 mg ASA to four healthy volunteers resulted in a rapid increase in the blood levels of ASA, salicyluric acid (SUA) and salicylic acid (SA). SUA and SA levels remained high for several hours. Platelet shape change was inhibited 30 min after ASA ingestion and after 480 min some inhibitory effect was still present. Administration of 500 mg salicylic acid led to similar blood levels of SUa and SA, but platelet shape change was not inhibited. The inhibition of platelet shape change apparently also is a specific effect of ASA, its mechanism is not yet known. If the inhibition of platelet shape change essentially contributes to the antithrombotic effect of ASA, as is made likely by animal thrombosis studies, ASA has to be administered in much higher doses than those needed for the inhibition of thromboxane-formation in the platelets. [ABSTRACT FROM AUTHOR]

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Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Plasmatic coagulation disorders in trauma patients are common and their management is subject to current guidelines. Less evidence exists for platelet function. Although it is known that several trauma-associated factors have a negative influence on platelet function, routine monitoring has not yet become established., Methods: A retrospective single center study was carried out at a German level 1 trauma center from 2010 to 2016. In all patients fulfilling the requirements for the German Trauma Society (DGU) Traumaregister® who were admitted directly from the scene of the incident, platelet function was analyzed using the Platelet Function Analyzer (PFA 100®) with adenosine diphosphate (ADP) and epinephrine as activation factors. After exclusion of patients with intake of long-term anticoagulant and antiaggregant medication, possible influencing factors of a reduced platelet function were identified., Results: The results from 310 patients (44.0 ± 14.7 years, 76% male, Injury Severity Score, ISS 28.4 ± 14.2 points) were available. A delayed platelet activation was found in 25.5% using ADP and 31% using epinephrine. Laboratory parameters indicated a greater blood loss. Prolonged closure times were associated with an increased transfusion rate of packed red blood cell concentrates and a higher mortality rate. Logistic regression revealed hemoglobin (Hb) and fibrinogen levels at admission to be independent predictors for a decreased platelet activation in the assay with ADP (p < 0.001, Cohen's f = 0.61) and with epinephrine (p < 0.001, f = 0.42)., Conclusion: Approximately one quarter to one third of primarily admitted trauma patients without long-term anticoagulation medication showed a delayed platelet activation in the PFA-100 test. By considering all trauma patients an even higher rate can be expected. The Hb and fibrinogen levels at admission can be helpful to estimate platelet disorders. The development of platelet assays to guide the resuscitation of individual patients seems to be absolutely necessary. The contribution of platelet disorders to trauma-induced coagulopathy is not sufficiently understood. Regarding the importance assigned to platelet transfusion or administration of desmopressin, these aspects should be the subject of further research.

Copyright of Langenbecks Archiv fuer Chirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)