Platelet activation and function after trauma

R. C. Jacoby, John T Owings, James F Holmes Jr, F. D. Battistella, R. C. Gosselin, T. G. Paglieroni

Research output: Contribution to journalArticle

134 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)639-647
Number of pages9
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume51
Issue number4
StatePublished - 2001

Fingerprint

Platelet Activation
Blood Platelets
Wounds and Injuries
Epinephrine
Collagen
Hemostasis
Brain Injuries
Reference Values
Nonpenetrating Wounds
Glasgow Coma Scale
Platelet Glycoprotein GPIIb-IIIa Complex
Injury Severity Score
P-Selectin
Mortality
Disseminated Intravascular Coagulation
Pulmonary Embolism
Venous Thrombosis
Survivors
Hospital Emergency Service
Flow Cytometry

Keywords

  • Flow cytometry
  • Head injury
  • Platelet activation
  • Platelet function
  • Platelet function analyzer
  • Trauma

ASJC Scopus subject areas

  • Surgery

Cite this

Jacoby, R. C., Owings, J. T., Holmes Jr, J. F., Battistella, F. D., Gosselin, R. C., & Paglieroni, T. G. (2001). Platelet activation and function after trauma. Journal of Trauma - Injury, Infection and Critical Care, 51(4), 639-647.

Platelet activation and function after trauma. / Jacoby, R. C.; Owings, John T; Holmes Jr, James F; Battistella, F. D.; Gosselin, R. C.; Paglieroni, T. G.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 51, No. 4, 2001, p. 639-647.

Research output: Contribution to journalArticle

Jacoby, RC, Owings, JT, Holmes Jr, JF, Battistella, FD, Gosselin, RC & Paglieroni, TG 2001, 'Platelet activation and function after trauma', Journal of Trauma - Injury, Infection and Critical Care, vol. 51, no. 4, pp. 639-647.
Jacoby, R. C. ; Owings, John T ; Holmes Jr, James F ; Battistella, F. D. ; Gosselin, R. C. ; Paglieroni, T. G. / Platelet activation and function after trauma. In: Journal of Trauma - Injury, Infection and Critical Care. 2001 ; Vol. 51, No. 4. pp. 639-647.
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abstract = "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.",
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AU - Paglieroni, T. G.

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N2 - 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.

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