Perioperative platelet reactivity and the effects of clonidine

B. A. Rosenfeld, Nauder Faraday, D. Campbell, Todd Dorman, K. Clarkson, A. Siedler, M. J. Breslow, W. Bell

Research output: Contribution to journalArticle

Abstract

Background: Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. α2 Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregation in vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo. Methods: Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperative sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatively. Results: Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1-2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperative values, fibrinogen levels rose maximally (36%) at 72 h postoperatively and platelet counts decreased 22% at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values. Conclusions: These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet- induced perioperative arterial thrombosis.

Original languageEnglish (US)
Pages (from-to)255-261
Number of pages7
JournalAnesthesiology
Volume79
Issue number2
StatePublished - 1993

Fingerprint

Clonidine
Blood Platelets
Platelet Count
Placebos
Platelet Aggregation
Fibrinogen
Ristocetin
Local Anesthetics
Electric Impedance
Arachidonic Acid
Thrombin
Adenosine Diphosphate
General Anesthesia
Morphine
Opioid Analgesics
Thrombosis
Collagen
Biopsy
Incidence
Population

Keywords

  • Blood, coagulation: degranulation; platelet aggregation
  • Sympathetic nervous system, α agonists: clonidine
  • Sympathetic nervous system: catecholamines

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Rosenfeld, B. A., Faraday, N., Campbell, D., Dorman, T., Clarkson, K., Siedler, A., ... Bell, W. (1993). Perioperative platelet reactivity and the effects of clonidine. Anesthesiology, 79(2), 255-261.

Perioperative platelet reactivity and the effects of clonidine. / Rosenfeld, B. A.; Faraday, Nauder; Campbell, D.; Dorman, Todd; Clarkson, K.; Siedler, A.; Breslow, M. J.; Bell, W.

In: Anesthesiology, Vol. 79, No. 2, 1993, p. 255-261.

Research output: Contribution to journalArticle

Rosenfeld, BA, Faraday, N, Campbell, D, Dorman, T, Clarkson, K, Siedler, A, Breslow, MJ & Bell, W 1993, 'Perioperative platelet reactivity and the effects of clonidine', Anesthesiology, vol. 79, no. 2, pp. 255-261.
Rosenfeld BA, Faraday N, Campbell D, Dorman T, Clarkson K, Siedler A et al. Perioperative platelet reactivity and the effects of clonidine. Anesthesiology. 1993;79(2):255-261.
Rosenfeld, B. A. ; Faraday, Nauder ; Campbell, D. ; Dorman, Todd ; Clarkson, K. ; Siedler, A. ; Breslow, M. J. ; Bell, W. / Perioperative platelet reactivity and the effects of clonidine. In: Anesthesiology. 1993 ; Vol. 79, No. 2. pp. 255-261.
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abstract = "Background: Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. α2 Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregation in vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo. Methods: Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperative sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatively. Results: Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1-2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperative values, fibrinogen levels rose maximally (36{\%}) at 72 h postoperatively and platelet counts decreased 22{\%} at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values. Conclusions: These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet- induced perioperative arterial thrombosis.",
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AU - Rosenfeld, B. A.

AU - Faraday, Nauder

AU - Campbell, D.

AU - Dorman, Todd

AU - Clarkson, K.

AU - Siedler, A.

AU - Breslow, M. J.

AU - Bell, W.

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N2 - Background: Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. α2 Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregation in vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo. Methods: Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperative sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatively. Results: Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1-2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperative values, fibrinogen levels rose maximally (36%) at 72 h postoperatively and platelet counts decreased 22% at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values. Conclusions: These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet- induced perioperative arterial thrombosis.

AB - Background: Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. α2 Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregation in vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo. Methods: Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperative sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatively. Results: Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1-2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperative values, fibrinogen levels rose maximally (36%) at 72 h postoperatively and platelet counts decreased 22% at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values. Conclusions: These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet- induced perioperative arterial thrombosis.

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