A point-of-care assessment of the effects of desmopressin on impaired platelet function using multiple electrode whole-blood aggregometry in patients after cardiac surgery

Anesth Analg. 2010 Mar 1;110(3):702-7. doi: 10.1213/ANE.0b013e3181c92a5c. Epub 2009 Dec 30.


Background: Blood loss after cardiac surgery can be caused by acquired platelet dysfunction after cardiopulmonary bypass. Monitoring of platelet function is clinically important for the identification of patients experiencing such platelet dysfunction. 1-Deamino-8-D-arginine vasopressin (desmopressin acetate, DDAVP) has been shown to augment platelet function and to reduce blood loss in patients with platelet dysfunction. In this study, we examined the feasibility of whole blood multiple electrode aggregometry (MEA) for the detection of cardiopulmonary bypass-induced platelet dysfunction and investigated its ability to monitor DDAVP treatment.

Methods: Fifty-eight consecutive patients with blood loss exceeding 150 mL/h in the first 2 consecutive hours after cardiac surgery were screened for suspected isolated platelet dysfunction. Twenty-two patients had suspected isolated platelet dysfunction and were enrolled in the study. Platelet dysfunction was assumed if conventional coagulation analyses (platelet count, activated partial thromboplastin time, international normalized ratio, and fibrinogen) did not show abnormal values as defined for transfusion of allogenic blood products, and no surgical cause of bleeding was suspected. Eleven patients received 0.3 microg/kg DDAVP, and 11 patients received no therapy in a nonrandomized manner. MEA was performed after stimulation with thrombin receptor-activating peptide (TRAPtest, 32 microM), adenosine diphosphate (ADPtest, 6.4 microM), and arachidonic acid (ASPItest, 0.5 mM) before and 2 hours after intervention. Conventional laboratory variables were recorded. The Mann-Whitney test was used to detect differences between the groups, and the Wilcoxon test was used to detect differences before and after intervention.

Results: All enrolled patients showed platelet dysfunction that manifested as impaired platelet aggregation in MEA before intervention. After the intervention, platelet function improved in the DDAVP group (49 U [30/72 U], median [25th/75th percentile] postintervention vs 15 U [8/21 U] preintervention for the ASPItest [P < 0.001]; 35 U [24/54 U] vs 14 U [7/28 U] for the ADPtest [P = 0.002]; and 85 U [66/115 U] vs 64 U [26/88 U] for the TRAPtest [P = 0.007]). In contrast, MEA remained unchanged in the control group (22 U [10/50 U] postintervention vs 33 U [14/57 U] preintervention for the ASPItest [P = 0.175]; 17 U [12/20 U] vs 14 U [10/28 U] for the ADPtest [P = 0.147]; and 65 U [41/89 U] vs 57 U [30/91 U] for the TRAPtest [P = 0.123]).

Conclusions: Impaired platelet function after cardiac surgery can be assessed at the bedside using MEA. The effect of DDAVP on impaired platelet function can also be detected as significant improvement in platelet aggregation to all activators. This device might be helpful for the identification of patients who may benefit from DDAVP therapy.

Publication types

  • Controlled Clinical Trial

MeSH terms

  • Adenosine Diphosphate
  • Aged
  • Aged, 80 and over
  • Arachidonic Acid
  • Cardiac Surgical Procedures*
  • Cardiopulmonary Bypass / adverse effects*
  • Deamino Arginine Vasopressin / therapeutic use*
  • Drug Monitoring / methods*
  • Feasibility Studies
  • Female
  • Hemostatics / therapeutic use*
  • Humans
  • Male
  • Peptide Fragments
  • Platelet Aggregation / drug effects*
  • Point-of-Care Systems*
  • Postoperative Hemorrhage / blood
  • Postoperative Hemorrhage / etiology
  • Postoperative Hemorrhage / prevention & control*
  • Predictive Value of Tests
  • Prospective Studies
  • Time Factors
  • Treatment Outcome


  • Hemostatics
  • Peptide Fragments
  • thrombin receptor peptide (42-47)
  • Arachidonic Acid
  • Adenosine Diphosphate
  • Deamino Arginine Vasopressin