doc, any long term hepatic or renal complications due to the disruption of the hemofibral thread dissolution from the prevention of the clot breakdown?
First, SERIOUS DISCLAIMER: I am by no means an expert on the use of TXA and the long term effects after resuscitation. So what I'm giving you is what I know and recall, having been trained by the authors of the MATTERS study and by the invited critique author, Dr. Kenji Inaba.
Caveat lector.
Short answer? Theoretically, yes, but no one really knows, because there just isn't enough data
Long answer, no long term hepatic or renal complications are known in non-trauma use, but recall that the majority of use has been in clotting disorders, a population where major thrombosis or embolus is not at issue. Large vessel issues would need to have patients that are already in some type hypercoagulable state, and the TXA then aids clot propagation, which would be statistically quite rare as those patient would not likely be taking TXA. In terms of small vessel or microthrombosis or emboli, it would likely cause problems, but again not too many patients in that category. Mechanistically it makes sense that TXA induced, arteriole sited, damage could be a problem, because the plasminogen activation inhibition is more effective in the small vessels, but that's me spitballing.
The two ways in which renal/hepatic impairment would occur in trauma use would be either in the large vessel obstruction or small vessel. This is why TXA can only be used in the initial 3 hours of trauma, just as it can only be used in the hemorrhage stage of septic DIC in the fibrinolytic stage. During that period, the primary necessity is to counter the bleeding. Mostly the TXA is used to buy time to correct the underlying cause of hemorrhage. Even in that 3 hour window, the rates of DVT and PE were higher in the treatment group. After the 3 hour window, bleeding rates actually INCREASED. Was this because of unknown site of surgically treatable bleeding? Was this because the TXA increased consumption of transfused coagulation factors, in essence CREATING a DIC like-state (which is why in septic DIC TXA is given with heparin to anticoagulate at the same time)? No one really knows. After that period, theoretically, all the TXA would be doing is propagating clot initiated by exposed tissue factor, contributing to MSOF. But I don't think there's enough data out there for anyone to authoritatively comment on long term hepatic or renal sequelae. Although I will say hepatic sequealae are rather rare in similar situations, renal complications far more common.
I'm about to go on leave, so I'll get in touch with Kenji and ask him. And give him shit about volunteering to get Tased for demonstration purposes. Maybe they need a clinical fellow next year. Hmmmm...
I don't know if that helped any.