Hemorrhage Control / Clotting Agent

[CA_TacMedic]

Student creates substance that stops bleeding instantly

Just found this on the web. http://www.ksl.com/?sid=24448294&section=local

There is not a lot of information in the article, however it appears to be a rapid catalyst for the activation of clotting mechanisms.

@Syd...have you seen or heard of this product? And if so can you possibly elaborate on the mechanism and possible side effects? IE: exothermic properties, or complications with post application removal etc. as these have been common obstacles with current and former clotting agents.

Thanks in advance for any further input or information.


Wallace

[swatsurgeon]

Interesting......have to wait for more detailed Information, not much available right now.

[PrimalAndrew]

If you can stand the guy's voice, here's a little extra information:

http://www.youtube.com/watch?v=PCDStwS6Is8


Interestingly, for people with some coagulopathies, this type of material might not activate the coagulation cascade (Hemophilia A, Hemophilia B, Inhibitor mutations, Factor 5 Leiden). For others this miiiight do such a thing (Factor 13th deficiency, Lupus Anticoagulant, van Willebrand's disease...)
Having something to act as skin to stop bleeding, may be useful though.

[PedOncoDoc]

Interestingly, for people with some coagulopathies, this type of material might not activate the coagulation cascade (Hemophilia A, Hemophilia B, Inhibitor mutations, Factor 5 Leiden). For others this miiiight do such a thing (Factor 13th deficiency, Lupus Anticoagulant, van Willebrand's disease...)

Having something to act as skin to stop bleeding, may be useful though.

Factor V Leiden is not a coagulopathy - most the time it's not even a thrombophilic condition, although in the homozygous form (and on occasion in the heterozygous case with likely other genetic modifiers) can cause blood clots. Also - what "inhibitor mutations" are you speaking about? Inhibitors typically either arise spontaneously in healthy individuals and are typically transient, or develop in patients who do not make a specific clotting factor (most classically against FVIII in Hemophilia A).

Get your facts straight before adding medical/scientific opinions on subjects.

ECM serves as an initiator for platelet plug formation, and platelet-platelet binding is facilitated through von Willebrand factor which leads to the platelet plug. The coagulation cascade leads to fibrin deposition and crosslinking which makes the stable clot.

This product would be unlikely to work in patients with inherent platelet defects (e.g. Glanzman's thrombasthenia or Bernard-Soulier) or von Willebrand's disease (type 2s, type 3, and severe Type 1s due to the inability to make a primary platelet plug, and any moderate-to-severe factor deficiency that culminates in bleeding due to the inability to make a stable clot, although the latter would have temporary cessation of bleeding only to have recurrence later.

[PrimalAndrew]

As far as what Inhibitor mutations- I was alluding to many cases of HIV-1 having some sort of thrombocytopenia.

As far as everything else- you're absolutely right. I did some research and realized Factor V Leiden is not a coagulopathy but a hypercoagulability disorder.
(Boy did THAT make me feel dumb when I cracked a damn book and read up on it. . .)
It's been a long time since I've worked in a hospital. I've never professionally studied medicine either so thank you for your quick response; because without it I'd never had known otherwise.