SummaryHypothermia and acidosis lead to an impairment of coagulation. It has been demonstrated that desmopressin improves platelet function under hypothermia. We tested platelet function ex vivo during hypothermia and acidosis. Blood samples were taken from 12 healthy subjects and assigned as follows: normal pH, pH 7.2, and pH 7.0, each with and without incubation with desmopressin. Platelet aggregation was assessed by multiple electrode aggregometry. Baseline was normal pH and 36°C. The other samples were incubated for 30 min and measured at 32°C. Acidosis significantly impaired aggregation. Desmopressin significantly increased aggregability during hypothermia and acidosis regardless of pH, but did not return it to normal values at low pH. During acidosis and hypothermia, acidosis should be corrected first; desmopressin can then be administered to improve platelet function as a bridge until normothermia can be achieved. Hypothermia and acidosis are common complications in severely injured patients [1,2]. The negative impact of these conditions on coagulation resulting in coagulopathy has been well described [3][4][5][6][7][8][9].Desmopressin is a synthetic analogue of vasopressin (1-deamino-8-D-aginine vasopressin, DDAVP). Beside its first indication for treatment of cranial diabetes insipidus, it has become the treatment of choice for von Willebrand disease (Type I) and mild haemophilia A after it was shown that DDAVP leads to increased levels of coagulation factor (F) VIII, von Willebrand factor (vWF), and tissue plasminogen activator [10]. It also has been shown to improve platelet function [11][12][13] even under anti-platelet drug therapy [14] or after cardiopulmonary bypass [15]. DDAVP has been shown to correct hypothermia-induced impairment of primary haemostasis partially [16]. The effect of DDAVP under hypothermia and acidosis has not been evaluated to date. Thus, we tested the hypothesis that DDAVP is able to improve platelet function under both hypothermia and acidosis. Anaesthesia, 2010Anaesthesia, , 65, pages 688-691 doi:10.1111Anaesthesia, /j.1365Anaesthesia, -2044Anaesthesia, .2010 Twelve healthy volunteers of Caucasian origin participated in the study after oral and written information and written consent. All volunteers were healthy and with no history of abnormal bleeding nor taking coagulation impairing drugs. Blood was drawn into four 4.5-ml tubes containing 20 lg.ml )1 recombinant hirudin (Dynabyte, Munich, Germany) from a basilic vein using a 18-G cannula. Seven polypropylene tubes were labelled (Tube 1-7) and the collected hirudinised blood was immediately aliquoted into these tubes in 2.7-ml split samples. The test group (DDAVP+) was defined as samples treated with DDAVP. These samples were prepared yielding a final concentration of 1 nM representing an approximate plasma concentration after recommended treatment with DDAVP of 0.3 lg.kg )1 [17]. Samples without treatment with DDAVP were assigned to the control group (DDAVP)). Baseline was defined as a sample without DDAVP treatment ...
DDAVP and fibrinogen increased whole blood coagulation under hypothermia. Acidosis diminished this effect. Thus, acidosis should be corrected first and then both substances could be used for bridging until normothermia can be achieved. In combination, the effects of fibrinogen were overwhelming DDAVP effects. Thus, combined administration did not show any benefit compared to fibrinogen administration alone.
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