Procoagulant Assessment of Topical Battlefield Hemostats Using a Novel Semi-Automated Whole Blood Clotting Assay System.

A new granular smectite hemostatic agent (WoundStat™ [WS]) is capable of producing hemostasis during high pressure arterial bleeding (Ward et al., J Trauma, 63:276–284, 2007). The mechanism by which WS and other topical hemostatic agents help achieve clotting has not been investigated. In this study, the procoagulant and hemo-compatibility functions of WS were assessed using a novel whole blood clotting time assay, and its performance compared to current hemostatic agents QuikClot® zeolite granules (QC); CELOX™ marine biopolymer hemostatic granules (CX); sterile gauze bandage (SG); and to glass beads (GB). A modified whole blood recalcified clotting time assay was developed using the Actalyke® Mini II activated clotting time (ACT) analyzer and empty G-ACT tubes devoid of contact phase activating reagents. Whole citrated blood recalcified to 10 mM with CaCl2 yielded clot times (CT) of 217+/−6 sec, 212+/−11 sec, and 236+/−5 sec, respectively, for three normal donors. Addition of WS resulted in a time and dose-dependent biphasic decrease in CT. At 0.5 mg/ml, WS lowered CT by over 40% to 124+/−7 sec, 133+/− 9 sec, and 126+/−5 sec, p 50,000 /μl while platelet counts in WS-treated specimens were similar to untreated controls (214,000/μl versus 219,000/μl) and clumped granules, presumably platelet-mediated, were visually apparent in the QC-treated bloods. Blood incubated with CX for up to 45 min also exhibited a drop in platelets from 204,000/μl to 150,000/μl. When QC, CX and WS were incubated in blood for 3 hours, corresponding to the maximal times recommended during field application prior to reapplication or surgical debridement, all hemostats resulted in an ∼ 50% reduction in platelet counts from 258,000/μl to 132,000/μl; 158,000/μl and 155,000 /μl, respectively. In summary, the data suggest that WS is hemocompatible, is moderately capable of inducing in vitro platelet aggregates, and may assist in the arrest of high-pressure arterial bleeding, at least in part by promoting the intrinsic contact phase of blood coagulation. Additional studies are required to further elucidate the potential platelet- and plasma-mediated mechanisms by which WS may help achieve hemostasis during severe arterial traumatic injury.