[swatsurgeon]

second one.....

WoundStat (WS) Safety Study Dec 12, 2008

Phase I (non survival) experiments summary report:
Background: WS has been demonstrated to be the most effective agent against arterial bleeding that otherwise are fatal with gauze treatment in swine. This mineral (smectite) agent is in granular form and approved by FDA as a hemostatic device for temporary treatment of external bleeding. When mixed with blood, it forms clay materials that adhere to soft tissues and seal bleeding vessels. In addition, the WS granules have potent procoagulant activity similar to celite, a known clotting agent. In our earlier efficacy study, in which WS was 100% successful, microscopic residues of this agent were found in the lumen of treated arteries even after extensive wound debridement. Some endothelial damage was also seen in the vessels. These observations raised the possibility of thrombosis occurrence in WS- treated vessels following vascular repair and blood reflow. The current study examined this potential side effect of WS in an experimental model in swine with both arterial and venous injuries. In addition to treated vessels, the distal organs (lung and brain) that emboli may reside were also examined. The findings with WS were compared with another hemostatic device, Combat Gauze (CG) and regular gauze (Kerlix) control.

Methods: Anesthetized pigs were instrumented for baseline blood sampling, fluid infusion and vital signs monitoring. An incision was made in the neck area and  5 cm segments of right carotid artery and external jugular vein were isolated, clamped, and injured ( 50% transection). Free bleeding was allowed for 30 seconds. The hemorrhage was then controlled by packing the wound with two packages of WS, CG or Kerlix and manual compression ( a sequence of 2, 3, 10, 15, 15, 15….. min) until hemostasis was secured. To compensate for initial bleeding and restore normal blood pressure, 500-600 ml Hextend fluid was administered IV (50 ml/min, stating at 1st compression) to each pig to raise the MAP to the target pressure of 65 mmHg.

Two hours after treatment, the hemostatic materials were removed, vessels reclamped and wounds were debrided according to standard clinical procedure using 1 L (for CG and Kerlix) or 2 L ( for WS) of saline for flushing the wound thoroughly with bulb syringes. Next, blood vessels were flushed with additional saline, removing any residues or clots in the lumens, and repaired by suturing using a monofilament nylon suture (7-0 Prolene). During anastomosis, 1 L lactated Ringer’s (LR) fluid was administered IV to produce a mild hemodilution and prevent clotting at the suture line or beyond clamped area. No heparin was given to any of the animals during the experiment. Blood flow was then restored in both vessels (first artery and then vein) and the neck wound was sutured in three layers. Two hrs after blood flow, blood samples were collected for laboratory tests and animals were CT scanned to image the neck vasculature area. Wounds were then reopened, flow (or lack of it) through the individual vessel was confirmed and vessels were recovered for histology. In addition, the entire lung and brain were harvested, carefully examined for abnormalities and samples were taken for microscopic examination. Histological examination was done by a board certified veterinarian pathologist who was initially blinded to the identity of the samples.

Results: There were no differences in baseline hemodynamic and hematological measurements among groups. Blood clotting activity was significantly increased (hypercoagulable state) 2 hrs after blood circulation through the repaired vessels in all groups with no differences among treatment. This change was measured by thrombelastography (TEG) but was not detected by standard coagulation tests (PT, aPTT, fibrinogen), suggesting possible platelet activation.

Final flow through the repaired vessels were assessed by CT angiography and confirmed by direct observation when the wounds were reopened. Based on these data, all the vessels treated with gauze and CG were patent without any measurable difference in flow rate between the two groups. In addition, no significant thrombus or blood clot was found in the lumen or on the suture line of these vessels. The repaired segments of these vessels remained partially constricted. In contrast, 7 out of 8 carotid arteries treated with WS developed occlusive thrombosis and had no blood flow when examined at 2hrs. Similarly, 6 out of 8 jugular veins treated with WS developed large occlusive red clots and had no flow. Blood flow, however, was confirmed though these vessels at the time of suture repair. A layer of red thrombus was also seen on the inner wall of one of the patent vein. When lungs were examined in this group, a blood clot (2-3 cm long and 2-3 mm thick) was found in the lower lobe of one lung and a few residues, similar to WS materials, were detected the lung of another animal treated with WS.

The histological changes of CG- and Kerlix-treated vessels were equivalent in almost every way with minimal diffuse endothelial blebbing and no significant intraluminal thrombus. Animals from the Kerlix group had a high incidence of microthrombi in their lung (6 of 9) and one animal had a thrombus in a vessel of the brain. WS caused significant endothelial and transmural injury in all vessels and most vessels had large intraluminal thrombi. Within most of the luminal thrombi (8 of 8 veins and 6 of 8 arteries), there was gray granular material visible under polarizing light that has been previously confirmed to be WS. This same material was also found to be present in the lung of one animal. A large piece of WS was associated with an arterial thrombus and there were multiple other areas that contained WS in the lung of this animal.

Conclusion: This surgical model performs as designed and is able to detect local vascular injury/thrombus and distant microthrombi caused by hemostatic treatment. While CG produces changes that are not different from regular gauze, WS causes severe endothelial injury and significant transmural damage that possibly renders the injured vessels useless for surgical repair. It is possible for WS to enter the vascular system and cause thrombosis at distal sites.

Recommendation: The use of WoundStat should be restricted only for life threatening arterial hemorrhage from compressible nontourniquetable sites that are refractory to Combat Gauze. Surgeons should strongly consider repairing all arterial injuries treated with WoundStat at the prehospital level by interposition grafts.





Personnally, I 'm sticking with quik-clot. I've used it 7 times in the body and over a dozen on the outside....it works.

ss