BACKGROUND: Abnormal hemostasis is associated with many of the complications of trauma-associated morbidity and mortality. Platelets are integral in the maintenance of hemostasis. METHODS: Samples were obtained from 100 trauma patients on arrival at the emergency room (initial time) and at 24, 48, and 72 hours later. Samples were also obtained from 10 healthy controls at the same time intervals. Using flow cytometry, three parameters were used to measure platelet activation: platelet microparticles, expression of P-selectin (CD62P), and expression of the activated conformation of glycoprotein IIb-IIIa (PAC-1 binding). Platelet function was measured using a platelet function analyzer (PFA-100, Dade International Inc., Miami, FL). RESULTS: One hundred trauma patients were enrolled. The average age was 40 years, 75% were men, and 84% had blunt injuries. The mean Injury Severity Score was 22.3 +/- 10.9 (mean +/- SD) and the average Glasgow Coma Scale score was 11 +/- 4. All three platelet activation parameters were increased in trauma patients versus controls for all time periods (p < 0.001). Trauma patients had a trend toward a shorter initial collagen/epinephrine closure time versus controls (p = 0.096). Compared with the 24-, 48-, and 72-hour time intervals, initial collagen/epinephrine closure times were shortened (p < 0.001, p < 0.001, and p < 0.001). Platelet function returned to normal reference ranges within 24 hours but platelet activation parameters remained elevated at least 72 hours after initial trauma. In contrast, when trauma patients with and without brain injury were compared, brain injury patients had increased platelet activation but decreased platelet function (increased collagen/epinephrine closure times). In addition, there was a significant prolongation in collagen/epinephrine closure times for the 24-, 48-, and 72-hour time points in nonsurviving patients versus survivors. There was no association between platelet activation and function and other adverse outcomes including pulmonary embolism, deep venous thrombosis, and disseminated intravascular coagulation. CONCLUSION: Severe injury usually results in increased platelet activation and function. However, the combination of increased platelet activation with decreased function was associated with increased mortality.
BACKGROUND:Abnormal hemostasis is associated with many of the complications of trauma-associated morbidity and mortality. Platelets are integral in the maintenance of hemostasis. METHODS: Samples were obtained from 100 traumapatients on arrival at the emergency room (initial time) and at 24, 48, and 72 hours later. Samples were also obtained from 10 healthy controls at the same time intervals. Using flow cytometry, three parameters were used to measure platelet activation: platelet microparticles, expression of P-selectin (CD62P), and expression of the activated conformation of glycoprotein IIb-IIIa (PAC-1 binding). Platelet function was measured using a platelet function analyzer (PFA-100, Dade International Inc., Miami, FL). RESULTS: One hundred traumapatients were enrolled. The average age was 40 years, 75% were men, and 84% had blunt injuries. The mean Injury Severity Score was 22.3 +/- 10.9 (mean +/- SD) and the average Glasgow Coma Scale score was 11 +/- 4. All three platelet activation parameters were increased in traumapatients versus controls for all time periods (p < 0.001). Traumapatients had a trend toward a shorter initial collagen/epinephrine closure time versus controls (p = 0.096). Compared with the 24-, 48-, and 72-hour time intervals, initial collagen/epinephrine closure times were shortened (p < 0.001, p < 0.001, and p < 0.001). Platelet function returned to normal reference ranges within 24 hours but platelet activation parameters remained elevated at least 72 hours after initial trauma. In contrast, when traumapatients with and without brain injury were compared, brain injurypatients had increased platelet activation but decreased platelet function (increased collagen/epinephrine closure times). In addition, there was a significant prolongation in collagen/epinephrine closure times for the 24-, 48-, and 72-hour time points in nonsurviving patients versus survivors. There was no association between platelet activation and function and other adverse outcomes including pulmonary embolism, deep venous thrombosis, and disseminated intravascular coagulation. CONCLUSION: Severe injury usually results in increased platelet activation and function. However, the combination of increased platelet activation with decreased function was associated with increased mortality.
Authors: Lisa M Brown; Mariah S Call; M Margaret Knudson; Mitchell J Cohen; J B Holcomb; C E Wade; K J Brasel; G Vercruysse; J MacLeod; R P Dutton; J R Hess; J C Duchesne; N E McSwain; P Muskat; J Johannigamn; H M Cryer; A Tillou; J F Pittet; M A De Moya; M A Schreiber; B Tieu; S Brundage; L M Napolitano; M Brunsvold; M Brunsvold; G Beilman; A B Peitzman; M S Zenait; J Sperry; L Alarcon; M A Croce; J P Minei; R Kozar; E A Gonzalez; R M Stewart; S M Cohn; J E Mickalek; E M Bulger; B A Cotton; T C Nunez; R Ivatury; J W Meredith; P Miller; G J Pomper; B Marin Journal: J Trauma Date: 2011-08
Authors: N J White; D Contaifer; E J Martin; J C Newton; B M Mohammed; J L Bostic; G M Brophy; B D Spiess; A E Pusateri; K R Ward; D F Brophy Journal: J Thromb Haemost Date: 2015-05-09 Impact factor: 5.824
Authors: Deborah L Donahue; Julia Beck; Braxton Fritz; Patrick Davis; Mayra J Sandoval-Cooper; Scott G Thomas; Robert A Yount; Mark Walsh; Victoria A Ploplis; Francis J Castellino Journal: J Neurotrauma Date: 2013-11-21 Impact factor: 5.269
Authors: Patrick K Davis; Harsha Musunuru; Mark Walsh; Robert Cassady; Robert Yount; Andrew Losiniecki; Ernest E Moore; Max V Wohlauer; Janet Howard; Victoria A Ploplis; Francis J Castellino; Scott G Thomas Journal: Neurocrit Care Date: 2013-04 Impact factor: 3.210