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 language | English (US) |
|---|---|
| Pages (from-to) | 255-261 |
| Number of pages | 7 |
| Journal | Anesthesiology |
| Volume | 79 |
| Issue number | 2 |
| State | Published - 1993 |
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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
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 journal › Article
}
TY - JOUR
T1 - Perioperative platelet reactivity and the effects of clonidine
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.
PY - 1993
Y1 - 1993
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.
KW - Blood, coagulation: degranulation; platelet aggregation
KW - Sympathetic nervous system, α agonists: clonidine
KW - Sympathetic nervous system: catecholamines
UR - http://www.scopus.com/inward/record.url?scp=0027194585&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027194585&partnerID=8YFLogxK
M3 - Article
C2 - 8342838
AN - SCOPUS:0027194585
VL - 79
SP - 255
EP - 261
JO - Anesthesiology
JF - Anesthesiology
SN - 0003-3022
IS - 2
ER -